A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN.
A condition of inadequate circulating red blood cells (ANEMIA) or insufficient HEMOGLOBIN due to premature destruction of red blood cells (ERYTHROCYTES).
Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.
Hemolytic anemia due to various intrinsic defects of the erythrocyte.
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.
A form of anemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements.
Substances that are toxic to blood in general, including the clotting mechanism; hematotoxins may refer to the hematopoietic system.
Congenital disorder affecting all bone marrow elements, resulting in ANEMIA; LEUKOPENIA; and THROMBOPENIA, and associated with cardiac, renal, and limb malformations as well as dermal pigmentary changes. Spontaneous CHROMOSOME BREAKAGE is a feature of this disease along with predisposition to LEUKEMIA. There are at least 7 complementation groups in Fanconi anemia: FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, and FANCL. (from Online Mendelian Inheritance in Man, http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=227650, August 20, 2004)
Any one of a group of congenital hemolytic anemias in which there is no abnormal hemoglobin or spherocytosis and in which there is a defect of glycolysis in the erythrocyte. Common causes include deficiencies in GLUCOSE-6-PHOSPHATE ISOMERASE; PYRUVATE KINASE; and GLUCOSE-6-PHOSPHATE DEHYDROGENASE.
A syndrome that is associated with microvascular diseases of the KIDNEY, such as RENAL CORTICAL NECROSIS. It is characterized by hemolytic anemia (ANEMIA, HEMOLYTIC); THROMBOCYTOPENIA; and ACUTE RENAL FAILURE.
Anemia characterized by a decrease in the ratio of the weight of hemoglobin to the volume of the erythrocyte, i.e., the mean corpuscular hemoglobin concentration is less than normal. The individual cells contain less hemoglobin than they could have under optimal conditions. Hypochromic anemia may be caused by iron deficiency from a low iron intake, diminished iron absorption, or excessive iron loss. It can also be caused by infections or other diseases, therapeutic drugs, lead poisoning, and other conditions. (Stedman, 25th ed; from Miale, Laboratory Medicine: Hematology, 6th ed, p393)
Anemia characterized by larger than normal erythrocytes, increased mean corpuscular volume (MCV) and increased mean corpuscular hemoglobin (MCH).
A megaloblastic anemia occurring in children but more commonly in later life, characterized by histamine-fast achlorhydria, in which the laboratory and clinical manifestations are based on malabsorption of vitamin B 12 due to a failure of the gastric mucosa to secrete adequate and potent intrinsic factor. (Dorland, 27th ed)
A disease characterized by chronic hemolytic anemia, episodic painful crises, and pathologic involvement of many organs. It is the clinical expression of homozygosity for hemoglobin S.
Proteins from BACTERIA and FUNGI that are soluble enough to be secreted to target ERYTHROCYTES and insert into the membrane to form beta-barrel pores. Biosynthesis may be regulated by HEMOLYSIN FACTORS.
The oxygen-carrying proteins of ERYTHROCYTES. They are found in all vertebrates and some invertebrates. The number of globin subunits in the hemoglobin quaternary structure differs between species. Structures range from monomeric to a variety of multimeric arrangements.
Anemia characterized by the presence of erythroblasts containing excessive deposits of iron in the marrow.
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.
A test to detect non-agglutinating ANTIBODIES against ERYTHROCYTES by use of anti-antibodies (the Coombs' reagent.) The direct test is applied to freshly drawn blood to detect antibody bound to circulating red cells. The indirect test is applied to serum to detect the presence of antibodies that can bind to red blood cells.
A disorder characterized by the presence of ANEMIA, abnormally large red blood cells (megalocytes or macrocytes), and MEGALOBLASTS.
A species of LENTIVIRUS, subgenus equine lentiviruses (LENTIVIRUSES, EQUINE), causing acute and chronic infection in horses. It is transmitted mechanically by biting flies, mosquitoes, and midges, and iatrogenically through unsterilized equipment. Chronic infection often consists of acute episodes with remissions.
A severe sometimes chronic anemia, usually macrocytic in type, that does not respond to ordinary antianemic therapy.
A screening assay for circulating COMPLEMENT PROTEINS. Diluted SERUM samples are added to antibody-coated ERYTHROCYTES and the percentage of cell lysis is measured. The values are expressed by the so called CH50, in HEMOLYTIC COMPLEMENT units per milliliter, which is the dilution of serum required to lyse 50 percent of the erythrocytes in the assay.
Glycoprotein hormone, secreted chiefly by the KIDNEY in the adult and the LIVER in the FETUS, that acts on erythroid stem cells of the BONE MARROW to stimulate proliferation and differentiation.
A method to identify and enumerate cells that are synthesizing ANTIBODIES against ANTIGENS or HAPTENS conjugated to sheep RED BLOOD CELLS. The sheep red blood cells surrounding cells secreting antibody are lysed by added COMPLEMENT producing a clear zone of HEMOLYSIS. (From Illustrated Dictionary of Immunology, 3rd ed)
Viral disease of horses caused by the equine infectious anemia virus (EIAV; INFECTIOUS ANEMIA VIRUS, EQUINE). It is characterized by intermittent fever, weakness, and anemia. Chronic infection consists of acute episodes with remissions.
A condition characterized by the abnormal presence of ERYTHROBLASTS in the circulation of the FETUS or NEWBORNS. It is a disorder due to BLOOD GROUP INCOMPATIBILITY, such as the maternal alloimmunization by fetal antigen RH FACTORS leading to HEMOLYSIS of ERYTHROCYTES, hemolytic anemia (ANEMIA, HEMOLYTIC), general edema (HYDROPS FETALIS), and SEVERE JAUNDICE IN NEWBORN.
Diazo derivatives of aniline, used as a reagent for sugars, ketones, and aldehydes. (Dorland, 28th ed)
The type species of GYROVIRUS, a small, non-enveloped DNA virus originally isolated from contaminated vaccines in Japan. It causes chicken infectious anemia and may possibly play a key role in hemorrhagic anemia syndrome, anemia dermatitis, and blue wing disease.
A group of familial congenital hemolytic anemias characterized by numerous abnormally shaped erythrocytes which are generally spheroidal. The erythrocytes have increased osmotic fragility and are abnormally permeable to sodium ions.
A familial disorder characterized by ANEMIA with multinuclear ERYTHROBLASTS, karyorrhexis, asynchrony of nuclear and cytoplasmic maturation, and various nuclear abnormalities of bone marrow erythrocyte precursors (ERYTHROID PRECURSOR CELLS). Type II is the most common of the 3 types; it is often referred to as HEMPAS, based on the Hereditary Erythroblast Multinuclearity with Positive Acidified Serum test.
A metallic element with atomic symbol Fe, atomic number 26, and atomic weight 55.85. It is an essential constituent of HEMOGLOBINS; CYTOCHROMES; and IRON-BINDING PROTEINS. It plays a role in cellular redox reactions and in the transport of OXYGEN.
Abnormal intracellular inclusions, composed of denatured hemoglobin, found on the membrane of red blood cells. They are seen in thalassemias, enzymopathies, hemoglobinopathies, and after splenectomy.
The number of RED BLOOD CELLS per unit volume in a sample of venous BLOOD.
A rare congenital hypoplastic anemia that usually presents early in infancy. The disease is characterized by a moderate to severe macrocytic anemia, occasional neutropenia or thrombocytosis, a normocellular bone marrow with erythroid hypoplasia, and an increased risk of developing leukemia. (Curr Opin Hematol 2000 Mar;7(2):85-94)
A diverse group of proteins whose genetic MUTATIONS have been associated with the chromosomal instability syndrome FANCONI ANEMIA. Many of these proteins play important roles in protecting CELLS against OXIDATIVE STRESS.
The co-occurrence of pregnancy and a blood disease (HEMATOLOGIC DISEASES) which involves BLOOD CELLS or COAGULATION FACTORS. The hematologic disease may precede or follow FERTILIZATION and it may or may not have a deleterious effect on the pregnant woman or FETUS.
The number of RETICULOCYTES per unit volume of BLOOD. The values are expressed as a percentage of the ERYTHROCYTE COUNT or in the form of an index ("corrected reticulocyte index"), which attempts to account for the number of circulating erythrocytes.
The volume of packed RED BLOOD CELLS in a blood specimen. The volume is measured by centrifugation in a tube with graduated markings, or with automated blood cell counters. It is an indicator of erythrocyte status in disease. For example, ANEMIA shows a low value; POLYCYTHEMIA, a high value.
The senescence of RED BLOOD CELLS. Lacking the organelles that make protein synthesis possible, the mature erythrocyte is incapable of self-repair, reproduction, and carrying out certain functions performed by other cells. This limits the average life span of an erythrocyte to 120 days.
RED BLOOD CELL sensitivity to change in OSMOTIC PRESSURE. When exposed to a hypotonic concentration of sodium in a solution, red cells take in more water, swell until the capacity of the cell membrane is exceeded, and burst.
The production of red blood cells (ERYTHROCYTES). In humans, erythrocytes are produced by the YOLK SAC in the first trimester; by the liver in the second trimester; by the BONE MARROW in the third trimester and after birth. In normal individuals, the erythrocyte count in the peripheral blood remains relatively constant implying a balance between the rate of erythrocyte production and rate of destruction.
Oxygen-carrying RED BLOOD CELLS in mammalian blood that are abnormal in structure or function.
The mildest form of erythroblastosis fetalis in which anemia is the chief manifestation.
The introduction of whole blood or blood component directly into the blood stream. (Dorland, 27th ed)
A disease-producing enzyme deficiency subject to many variants, some of which cause a deficiency of GLUCOSE-6-PHOSPHATE DEHYDROGENASE activity in erythrocytes, leading to hemolytic anemia.
Agents which improve the quality of the blood, increasing the hemoglobin level and the number of erythrocytes. They are used in the treatment of anemias.
Chronic refractory anemia with granulocytopenia, and/or thrombocytopenia. Myeloblasts and progranulocytes constitute 5 to 40 percent of the nucleated marrow cells.
ERYTHROCYTE size and HEMOGLOBIN content or concentration, usually derived from ERYTHROCYTE COUNT; BLOOD hemoglobin concentration; and HEMATOCRIT. The indices include the mean corpuscular volume (MCV), the mean corpuscular hemoglobin (MCH), and the mean corpuscular hemoglobin concentration (MCHC).
The semi-permeable outer structure of a red blood cell. It is known as a red cell 'ghost' after HEMOLYSIS.
A Fanconi anemia complementation group protein that regulates the activities of CYTOCHROME P450 REDUCTASE and GLUTATHIONE S-TRANSFERASE. It is found predominately in the CYTOPLASM, but moves to the CELL NUCLEUS in response to FANCE PROTEIN.
Erythrocyte isoantigens of the Rh (Rhesus) blood group system, the most complex of all human blood groups. The major antigen Rh or D is the most common cause of erythroblastosis fetalis.
A Fanconi anemia complementation group protein that undergoes mono-ubiquitination by FANCL PROTEIN in response to DNA DAMAGE. Also, in response to IONIZING RADIATION it can undergo PHOSPHORYLATION by ataxia telangiectasia mutated protein. Modified FANCD2 interacts with BRCA2 PROTEIN in a stable complex with CHROMATIN, and it is involved in DNA REPAIR by homologous RECOMBINATION.
A Fanconi anemia complementation group protein that is the most commonly mutated protein in FANCONI ANEMIA. It undergoes PHOSPHORYLATION by PROTEIN KINASE B and forms a complex with FANCC PROTEIN in the CELL NUCLEUS.
Measurement of hemoglobin concentration in blood.
Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).
Exotoxins produced by certain strains of streptococci, particularly those of group A (STREPTOCOCCUS PYOGENES), that cause HEMOLYSIS.
Iron-containing proteins that are widely distributed in animals, plants, and microorganisms. Their major function is to store IRON in a nontoxic bioavailable form. Each ferritin molecule consists of ferric iron in a hollow protein shell (APOFERRITINS) made of 24 subunits of various sequences depending on the species and tissue types.
A clinical manifestation consisting of an unnatural paleness of the skin.
The transfer of erythrocytes from a donor to a recipient or reinfusion to the donor.
An important soluble regulator of the alternative pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It is a 139-kDa glycoprotein expressed by the liver and secreted into the blood. It binds to COMPLEMENT C3B and makes iC3b (inactivated complement 3b) susceptible to cleavage by COMPLEMENT FACTOR I. Complement factor H also inhibits the association of C3b with COMPLEMENT FACTOR B to form the C3bB proenzyme, and promotes the dissociation of Bb from the C3bBb complex (COMPLEMENT C3 CONVERTASE, ALTERNATIVE PATHWAY).
A toxin produced by SHIGELLA DYSENTERIAE. It is the prototype of class of toxins that inhibit protein synthesis by blocking the interaction of ribosomal RNA; (RNA, RIBOSOMAL) with PEPTIDE ELONGATION FACTORS.
An antigenic mismatch between donor and recipient blood. Antibodies present in the recipient's serum may be directed against antigens in the donor product. Such a mismatch may result in a transfusion reaction in which, for example, donor blood is hemolyzed. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984).
Hemoglobins characterized by structural alterations within the molecule. The alteration can be either absence, addition or substitution of one or more amino acids in the globin part of the molecule at selected positions in the polypeptide chains.
Surgical procedure involving either partial or entire removal of the spleen.
Small cationic peptides that are an important component, in most species, of early innate and induced defenses against invading microbes. In animals they are found on mucosal surfaces, within phagocytic granules, and on the surface of the body. They are also found in insects and plants. Among others, this group includes the DEFENSINS, protegrins, tachyplesins, and thionins. They displace DIVALENT CATIONS from phosphate groups of MEMBRANE LIPIDS leading to disruption of the membrane.
Enlargement of the spleen.
Substances that are toxic to cells; they may be involved in immunity or may be contained in venoms. These are distinguished from CYTOSTATIC AGENTS in degree of effect. Some of them are used as CYTOTOXIC ANTIBIOTICS. The mechanism of action of many of these are as ALKYLATING AGENTS or MITOSIS MODULATORS.
Diseases that result in THROMBOSIS in MICROVASCULATURE. The two most prominent diseases are PURPURA, THROMBOTIC THROMBOCYTOPENIC; and HEMOLYTIC-UREMIC SYNDROME. Multiple etiological factors include VASCULAR ENDOTHELIAL CELL damage due to SHIGA TOXIN; FACTOR H deficiency; and aberrant VON WILLEBRAND FACTOR formation.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A condition characterized by the recurrence of HEMOGLOBINURIA caused by intravascular HEMOLYSIS. In cases occurring upon cold exposure (paroxysmal cold hemoglobinuria), usually after infections, there is a circulating antibody which is also a cold hemolysin. In cases occurring during or after sleep (paroxysmal nocturnal hemoglobinuria), the clonal hematopoietic stem cells exhibit a global deficiency of cell membrane proteins.
Immature ERYTHROCYTES. In humans, these are ERYTHROID CELLS that have just undergone extrusion of their CELL NUCLEUS. They still contain some organelles that gradually decrease in number as the cells mature. RIBOSOMES are last to disappear. Certain staining techniques cause components of the ribosomes to precipitate into characteristic "reticulum" (not the same as the ENDOPLASMIC RETICULUM), hence the name reticulocytes.
The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.
The process by which fetal Rh+ erythrocytes enter the circulation of an Rh- mother, causing her to produce IMMUNOGLOBULIN G antibodies, which can cross the placenta and destroy the erythrocytes of Rh+ fetuses. Rh isoimmunization can also be caused by BLOOD TRANSFUSION with mismatched blood.
Toxic substances formed in or elaborated by bacteria; they are usually proteins with high molecular weight and antigenicity; some are used as antibiotics and some to skin test for the presence of or susceptibility to certain diseases.
A Fanconi anemia complementation group protein that undergoes PHOSPHORYLATION by CDC2 PROTEIN KINASE during MITOSIS. It forms a complex with other FANCONI ANEMIA PROTEINS and helps protect CELLS from DNA DAMAGE by genotoxic agents.
A subnormal level of BLOOD PLATELETS.
Large, hoofed mammals of the family EQUIDAE. Horses are active day and night with most of the day spent seeking and consuming food. Feeding peaks occur in the early morning and late afternoon, and there are several daily periods of rest.
Removal of plasma and replacement with various fluids, e.g., fresh frozen plasma, plasma protein fractions (PPF), albumin preparations, dextran solutions, saline. Used in treatment of autoimmune diseases, immune complex diseases, diseases of excess plasma factors, and other conditions.
A group of hereditary hemolytic anemias in which there is decreased synthesis of one or more hemoglobin polypeptide chains. There are several genetic types with clinical pictures ranging from barely detectable hematologic abnormality to severe and fatal anemia.
Any of the ruminant mammals with curved horns in the genus Ovis, family Bovidae. They possess lachrymal grooves and interdigital glands, which are absent in GOATS.
A class of Echinodermata characterized by long, slender bodies.
Stable chromium atoms that have the same atomic number as the element chromium, but differ in atomic weight. Cr-50, 53, and 54 are stable chromium isotopes.
A disorder characterized by reduced synthesis of the beta chains of hemoglobin. There is retardation of hemoglobin A synthesis in the heterozygous form (thalassemia minor), which is asymptomatic, while in the homozygous form (thalassemia major, Cooley's anemia, Mediterranean anemia, erythroblastic anemia), which can result in severe complications and even death, hemoglobin A synthesis is absent.
The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells.
ATP:pyruvate 2-O-phosphotransferase. A phosphotransferase that catalyzes reversibly the phosphorylation of pyruvate to phosphoenolpyruvate in the presence of ATP. It has four isozymes (L, R, M1, and M2). Deficiency of the enzyme results in hemolytic anemia. EC 2.7.1.40.
Small, abnormal spherical red blood cells with more than the normal amount of hemoglobin.
Iron or iron compounds used in foods or as food. Dietary iron is important in oxygen transport and the synthesis of the iron-porphyrin proteins hemoglobin, myoglobin, cytochromes, and cytochrome oxidase. Insufficient amounts of dietary iron can lead to iron-deficiency anemia.
Infections with bacteria of the species ESCHERICHIA COLI.
A group of inherited disorders characterized by structural alterations within the hemoglobin molecule.
In utero transfusion of BLOOD into the FETUS for the treatment of FETAL DISEASES, such as fetal erythroblastosis (ERYTHROBLASTOSIS, FETAL).
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
A verocytotoxin-producing serogroup belonging to the O subfamily of Escherichia coli which has been shown to cause severe food-borne disease. A strain from this serogroup, serotype H7, which produces SHIGA TOXINS, has been linked to human disease outbreaks resulting from contamination of foods by E. coli O157 from bovine origin.
The number of LEUKOCYTES and ERYTHROCYTES per unit volume in a sample of venous BLOOD. A complete blood count (CBC) also includes measurement of the HEMOGLOBIN; HEMATOCRIT; and ERYTHROCYTE INDICES.
Organic and inorganic compounds that contain iron as an integral part of the molecule.
Forms of hepcidin, a cationic amphipathic peptide synthesized in the liver as a prepropeptide which is first processed into prohepcidin and then into the biologically active hepcidin forms, including in human the 20-, 22-, and 25-amino acid residue peptide forms. Hepcidin acts as a homeostatic regulators of iron metabolism and also possesses antimicrobial activity.
Hemolytic anemia due to the ingestion of fava beans or after inhalation of pollen from the Vicia fava plant by persons with glucose-6-phosphate dehydrogenase deficient erythrocytes.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
An aminoquinoline that is given by mouth to produce a radical cure and prevent relapse of vivax and ovale malarias following treatment with a blood schizontocide. It has also been used to prevent transmission of falciparum malaria by those returning to areas where there is a potential for re-introduction of malaria. Adverse effects include anemias and GI disturbances. (From Martindale, The Extra Pharmacopeia, 30th ed, p404)
The major component of hemoglobin in the fetus. This HEMOGLOBIN has two alpha and two gamma polypeptide subunits in comparison to normal adult hemoglobin, which has two alpha and two beta polypeptide subunits. Fetal hemoglobin concentrations can be elevated (usually above 0.5%) in children and adults affected by LEUKEMIA and several types of ANEMIA.
The presence of free HEMOGLOBIN in the URINE, indicating hemolysis of ERYTHROCYTES within the vascular system. After saturating the hemoglobin-binding proteins (HAPTOGLOBINS), free hemoglobin begins to appear in the urine.
Proteins prepared by recombinant DNA technology.
A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.
A high molecular weight (220-250 kDa) water-soluble protein which can be extracted from erythrocyte ghosts in low ionic strength buffers. The protein contains no lipids or carbohydrates, is the predominant species of peripheral erythrocyte membrane proteins, and exists as a fibrous coating on the inner, cytoplasmic surface of the membrane.
A disorder characterized by reduced synthesis of the alpha chains of hemoglobin. The severity of this condition can vary from mild anemia to death, depending on the number of genes deleted.
The total number of cases of a given disease in a specified population at a designated time. It is differentiated from INCIDENCE, which refers to the number of new cases in the population at a given time.
Immature, nucleated ERYTHROCYTES occupying the stage of ERYTHROPOIESIS that follows formation of ERYTHROID PRECURSOR CELLS and precedes formation of RETICULOCYTES. The normal series is called normoblasts. Cells called MEGALOBLASTS are a pathologic series of erythroblasts.
An infant during the first month after birth.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
An abnormal hemoglobin resulting from the substitution of valine for glutamic acid at position 6 of the beta chain of the globin moiety. The heterozygous state results in sickle cell trait, the homozygous in sickle cell anemia.
A toxin produced by certain pathogenic strains of ESCHERICHIA COLI such as ESCHERICHIA COLI O157. It shares 50-60% homology with SHIGA TOXIN and SHIGA TOXIN 1.
Disorders of the blood and blood forming tissues.
A plasma serine proteinase that cleaves the alpha-chains of C3b and C4b in the presence of the cofactors COMPLEMENT FACTOR H and C4-binding protein, respectively. It is a 66-kDa glycoprotein that converts C3b to inactivated C3b (iC3b) followed by the release of two fragments, C3c (150-kDa) and C3dg (41-kDa). It was formerly called KAF, C3bINF, or enzyme 3b inactivator.
A nutritional condition produced by a deficiency of VITAMIN B 12 in the diet, characterized by megaloblastic anemia. Since vitamin B 12 is not present in plants, humans have obtained their supply from animal products, from multivitamin supplements in the form of pills, and as additives to food preparations. A wide variety of neuropsychiatric abnormalities is also seen in vitamin B 12 deficiency and appears to be due to an undefined defect involving myelin synthesis. (From Cecil Textbook of Medicine, 19th ed, p848)
C5 plays a central role in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C5 is cleaved by C5 CONVERTASE into COMPLEMENT C5A and COMPLEMENT C5B. The smaller fragment C5a is an ANAPHYLATOXIN and mediator of inflammatory process. The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX.
A protozoan disease caused in humans by four species of the PLASMODIUM genus: PLASMODIUM FALCIPARUM; PLASMODIUM VIVAX; PLASMODIUM OVALE; and PLASMODIUM MALARIAE; and transmitted by the bite of an infected female mosquito of the genus ANOPHELES. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high FEVER; SWEATING; shaking CHILLS; and ANEMIA. Malaria in ANIMALS is caused by other species of plasmodia.
An encapsulated lymphatic organ through which venous blood filters.
An increase in circulating RETICULOCYTES, which is among the simplest and most reliable signs of accelerated ERYTHROCYTE production. Reticulocytosis occurs during active BLOOD regeneration (stimulation of red bone marrow) and in certain types of ANEMIA, particularly CONGENITAL HEMOLYTIC ANEMIA.
A toxin produced by certain pathogenic strains of ESCHERICHIA COLI such as ESCHERICHIA COLI O157. It is closely related to SHIGA TOXIN produced by SHIGELLA DYSENTERIAE.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.
A genus in the family ORTHOMYXOVIRIDAE containing one species: Infectious salmon anemia virus.
Elements of limited time intervals, contributing to particular results or situations.
Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
An excessive accumulation of iron in the body due to a greater than normal absorption of iron from the gastrointestinal tract or from parenteral injection. This may arise from idiopathic hemochromatosis, excessive iron intake, chronic alcoholism, certain types of refractory anemia, or transfusional hemosiderosis. (From Churchill's Illustrated Medical Dictionary, 1989)
Testing erythrocytes to determine presence or absence of blood-group antigens, testing of serum to determine the presence or absence of antibodies to these antigens, and selecting biocompatible blood by crossmatching samples from the donor against samples from the recipient. Crossmatching is performed prior to transfusion.
A sulfone active against a wide range of bacteria but mainly employed for its actions against MYCOBACTERIUM LEPRAE. Its mechanism of action is probably similar to that of the SULFONAMIDES which involves inhibition of folic acid synthesis in susceptible organisms. It is also used with PYRIMETHAMINE in the treatment of malaria. (From Martindale, The Extra Pharmacopoeia, 30th ed, p157-8)
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.
Strains of ESCHERICHIA COLI with the ability to produce at least one or more of at least two antigenically distinct, usually bacteriophage-mediated cytotoxins: SHIGA TOXIN 1 and SHIGA TOXIN 2. These bacteria can cause severe disease in humans including bloody DIARRHEA and HEMOLYTIC UREMIC SYNDROME.
A Fanconi anemia complementation group protein. It is an essential component of a nuclear core complex that protects the GENOME against CHROMOSOMAL INSTABILITY. It interacts directly with FANCG PROTEIN and helps stabilize a complex with FANCA PROTEIN and FANCC PROTEIN.
Suppression of erythropoiesis with little or no abnormality of leukocyte or platelet production.
Proteins found in any species of bacterium.
A Fanconi anemia complementation group protein that interacts with FANCC PROTEIN and FANCD2 PROTEIN. It promotes the accumulation of FANCC protein in the CELL NUCLEUS.
A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B.
Thrombocytopenia occurring in the absence of toxic exposure or a disease associated with decreased platelets. It is mediated by immune mechanisms, in most cases IMMUNOGLOBULIN G autoantibodies which attach to platelets and subsequently undergo destruction by macrophages. The disease is seen in acute (affecting children) and chronic (adult) forms.
The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenic capacity of an organism is determined by its VIRULENCE FACTORS.
Plasmids controlling the synthesis of hemolysin by bacteria.
Antibodies from an individual that react with ISOANTIGENS of another individual of the same species.
The type species of ERYTHROVIRUS and the etiological agent of ERYTHEMA INFECTIOSUM, a disease most commonly seen in school-age children.
A nutritional condition produced by a deficiency of FOLIC ACID in the diet. Many plant and animal tissues contain folic acid, abundant in green leafy vegetables, yeast, liver, and mushrooms but destroyed by long-term cooking. Alcohol interferes with its intermediate metabolism and absorption. Folic acid deficiency may develop in long-term anticonvulsant therapy or with use of oral contraceptives. This deficiency causes anemia, macrocytic anemia, and megaloblastic anemia. It is indistinguishable from vitamin B 12 deficiency in peripheral blood and bone marrow findings, but the neurologic lesions seen in B 12 deficiency do not occur. (Merck Manual, 16th ed)
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.
Virus infections caused by the PARVOVIRIDAE.
Ability of ERYTHROCYTES to change shape as they pass through narrow spaces, such as the microvasculature.
Repetitive withdrawal of small amounts of blood and replacement with donor blood until a large proportion of the blood volume has been exchanged. Used in treatment of fetal erythroblastosis, hepatic coma, sickle cell anemia, disseminated intravascular coagulation, septicemia, burns, thrombotic thrombopenic purpura, and fulminant malaria.
An individual in which both alleles at a given locus are identical.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
An intrinsic defect of erythrocytes inherited as an autosomal dominant trait. The erythrocytes assume an oval or elliptical shape.
A cobalt-containing coordination compound produced by intestinal micro-organisms and found also in soil and water. Higher plants do not concentrate vitamin B 12 from the soil and so are a poor source of the substance as compared with animal tissues. INTRINSIC FACTOR is important for the assimilation of vitamin B 12.
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)
A bile pigment that is a degradation product of HEME.
An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.
Endogenous proteins that inhibit or inactivate COMPLEMENT C3B. They include COMPLEMENT FACTOR H and COMPLEMENT FACTOR I (C3b/C4b inactivator). They cleave or promote the cleavage of C3b into inactive fragments, and thus are important in the down-regulation of COMPLEMENT ACTIVATION and its cytolytic sequence.
Venoms produced by FISHES, including SHARKS and sting rays, usually delivered by spines. They contain various substances, including very labile toxins that affect the HEART specifically and all MUSCLES generally.
Glycosphingolipids which contain as their polar head group a trisaccharide (galactose-galactose-glucose) moiety bound in glycosidic linkage to the hydroxyl group of ceramide. Their accumulation in tissue, due to a defect in ceramide trihexosidase, is the cause of angiokeratoma corporis diffusum (FABRY DISEASE).
Plasma glycoproteins that form a stable complex with hemoglobin to aid the recycling of heme iron. They are encoded in man by a gene on the short arm of chromosome 16.
Abnormal accumulation of serous fluid in two or more fetal compartments, such as SKIN; PLEURA; PERICARDIUM; PLACENTA; PERITONEUM; AMNIOTIC FLUID. General fetal EDEMA may be of non-immunologic origin, or of immunologic origin as in the case of ERYTHROBLASTOSIS FETALIS.
The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.
Sets of cell surface antigens located on BLOOD CELLS. They are usually membrane GLYCOPROTEINS or GLYCOLIPIDS that are antigenically distinguished by their carbohydrate moieties.
Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.
Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging.
The aggregation of ERYTHROCYTES by AGGLUTININS, including antibodies, lectins, and viral proteins (HEMAGGLUTINATION, VIRAL).
Basic polypeptide from the venom of the honey bee (Apis mellifera). It contains 26 amino acids, has cytolytic properties, causes contracture of muscle, releases histamine, and disrupts surface tension, probably due to lysis of cell and mitochondrial membranes.
A major integral transmembrane protein of the ERYTHROCYTE MEMBRANE. It is the anion exchanger responsible for electroneutral transporting in CHLORIDE IONS in exchange of BICARBONATE IONS allowing CO2 uptake and transport from tissues to lungs by the red blood cells. Genetic mutations that result in a loss of the protein function have been associated with type 4 HEREDITARY SPHEROCYTOSIS.
Serum containing GAMMA-GLOBULINS which are antibodies for lymphocyte ANTIGENS. It is used both as a test for HISTOCOMPATIBILITY and therapeutically in TRANSPLANTATION.
A genus of large SEA CUCUMBERS possessing the primitive radial configuration of podia in all five ambulacral areas.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
The presence of parasites (especially malarial parasites) in the blood. (Dorland, 27th ed)
Inorganic or organic compounds that contain divalent iron.
A subspecialty of internal medicine concerned with morphology, physiology, and pathology of the blood and blood-forming tissues.
An increased liquidity or decreased consistency of FECES, such as running stool. Fecal consistency is related to the ratio of water-holding capacity of insoluble solids to total water, rather than the amount of water present. Diarrhea is not hyperdefecation or increased fecal weight.
The condition of being heterozygous for hemoglobin S.
Infection of humans or animals with hookworms other than those caused by the genus Ancylostoma or Necator, for which the specific terms ANCYLOSTOMIASIS and NECATORIASIS are available.
Membrane glycoproteins found in high concentrations on iron-utilizing cells. They specifically bind iron-bearing transferrin, are endocytosed with its ligand and then returned to the cell surface where transferrin without its iron is released.
Specific, characterizable, poisonous chemicals, often PROTEINS, with specific biological properties, including immunogenicity, produced by microbes, higher plants (PLANTS, TOXIC), or ANIMALS.
Substances that reduce the growth or reproduction of BACTERIA.
Therapy for the insufficient cleansing of the BLOOD by the kidneys based on dialysis and including hemodialysis, PERITONEAL DIALYSIS, and HEMODIAFILTRATION.
A genus of gram-positive, coccoid bacteria whose organisms occur in pairs or chains. No endospores are produced. Many species exist as commensals or parasites on man or animals with some being highly pathogenic. A few species are saprophytes and occur in the natural environment.
A genus of gram-negative, facultatively anaerobic, rod-shaped bacteria that occurs singly, in pairs, or in short chains. Its organisms are found in fresh water and sewage and are pathogenic to humans, frogs, and fish.
Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.
A disease characterized by compensated hemolysis with a normal hemoglobin level or a mild to moderate anemia. There may be intermittent abdominal discomfort, splenomegaly, and slight jaundice.
A phenylacetamide that was formerly used in ANALGESICS but nephropathy and METHEMOGLOBINEMIA led to its withdrawal from the market. (From Smith and Reynard, Textbook of Pharmacology,1991, p431)
A 150-kDa serum glycoprotein composed of three subunits with each encoded by a different gene (C8A; C8B; and C8G). This heterotrimer contains a disulfide-linked C8alpha-C8gamma heterodimer and a noncovalently associated C8beta chain. C8 is the next component to bind the C5-7 complex forming C5b-8 that binds COMPLEMENT C9 and acts as a catalyst in the polymerization of C9.
Malaria caused by PLASMODIUM FALCIPARUM. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations.
The presence of methemoglobin in the blood, resulting in cyanosis. A small amount of methemoglobin is present in the blood normally, but injury or toxic agents convert a larger proportion of hemoglobin into methemoglobin, which does not function reversibly as an oxygen carrier. Methemoglobinemia may be due to a defect in the enzyme NADH methemoglobin reductase (an autosomal recessive trait) or to an abnormality in hemoglobin M (an autosomal dominant trait). (Dorland, 27th ed)
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
Volume of circulating ERYTHROCYTES . It is usually measured by RADIOISOTOPE DILUTION TECHNIQUE.
The transference of BONE MARROW from one human or animal to another for a variety of purposes including HEMATOPOIETIC STEM CELL TRANSPLANTATION or MESENCHYMAL STEM CELL TRANSPLANTATION.
Venoms from jellyfish; CORALS; SEA ANEMONES; etc. They contain hemo-, cardio-, dermo- , and neuro-toxic substances and probably ENZYMES. They include palytoxin, sarcophine, and anthopleurine.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
A glycoprotein secreted by the cells of the GASTRIC GLANDS that is required for the absorption of VITAMIN B 12 (cyanocobalamin). Deficiency of intrinsic factor leads to VITAMIN B 12 DEFICIENCY and ANEMIA, PERNICIOUS.
A ubiquitously expressed complement receptor that binds COMPLEMENT C3B and COMPLEMENT C4B and serves as a cofactor for their inactivation. CD46 also interacts with a wide variety of pathogens and mediates immune response.
The larger fragment generated from the cleavage of COMPLEMENT C3 by C3 CONVERTASE. It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. C3b participates in IMMUNE ADHERENCE REACTION and enhances PHAGOCYTOSIS. It can be inactivated (iC3b) or cleaved by various proteases to yield fragments such as COMPLEMENT C3C; COMPLEMENT C3D; C3e; C3f; and C3g.
Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.

Complement receptor 1 (CD35) on human reticulocytes: normal expression in systemic lupus erythematosus and HIV-infected patients. (1/384)

The low levels of complement receptor 1 (CR1) on erythrocytes in autoimmune diseases and AIDS may be due to accelerated loss in the circulation, or to a diminished expression of CR1 on the red cell lineage. Therefore, we analyzed the expression of CR1 on reticulocytes (R) vs erythrocytes (E). Healthy subjects had a significant higher CR1 number per cell on R (919 +/- 99 CR1/cell) than on E (279 +/- 30 CR1/cell, n = 23), which corresponded to a 3. 5- +/- 1.3-fold loss of CR1. This intravascular loss was confirmed by FACS analysis, which showed that all R expressed CR1, whereas a large fraction of E was negative. The systemic lupus erythematosus (SLE), HIV-infected, and cold hemolytic Ab disease (CHAD) patients had a CR1 number on R identical to the healthy subjects, contrasting with a lower CR1 on their E. The data indicated a significantly higher loss of CR1 in the three diseases, i.e., 7.0- +/- 3.8-, 6.1- +/- 2.9-, and 9.6- +/- 5.6-fold, respectively. The intravascular loss was best exemplified in a patient with factor I deficiency whose CR1 dropped from 520 CR1/R to 28 CR1/E, i.e., 18.6-fold loss. In one SLE patient and in the factor I-deficient patient, the FACS data were consistent with a loss of CR1 already on some R. In conclusion, CR1 is lost progressively from normal E during in vivo aging so that old E are almost devoid of CR1. The low CR1 of RBC in autoimmune diseases and HIV-infection is due to a loss occurring in the circulation by an active process that remains to be defined.  (+info)

Requirement of IL-5 for induction of autoimmune hemolytic anemia in anti-red blood cell autoantibody transgenic mice. (2/384)

IL-5, IL-10 and lipopolysaccharide (LPS) are known to activate B-1 cells in vivo in normal mice and anti-red blood cell autoantibody transgenic mice (HL mice). To assess the exact role of IL-5 in proliferation and activation of peritoneal B-1 cells, we analyzed IL-5 receptor alpha chain-deficient HL (IL-5Ralpha-/- x HL) mice generated by the cross between IL-5Ralpha-/- and HL mice. In IL-5Ralpha-/- x HL mice, Ig-producing B-1 cells in the peritoneal cavity were negligible, although the total number of B-1 cells in the peritoneal cavity were as many as 30% of that in HL mice. Moreover, LPS- or IL-10-induced differentiation of B-1 cells into antibody-producing cells was severely impaired in IL-5Ralpha-/- x HL mice. We also used in vivo 5-bromo-2'-deoxyuridine labeling to estimate the proliferation of B-1 cells in IL-5Ralpha-/- mice. The absence of IL-5Ralpha did not affect spontaneous proliferation of peritoneal B-1 cells. However, induced proliferation of peritoreal B-1 cells by oral administration of LPS was markedly impaired in IL-5Ralpha-/- mice. These results suggest that IL-5 is required for activation-associated proliferation of B-1 cells but not for their spontaneous proliferation and support the idea that IL-5 plays an important role on the induction of autoantibody production from B-1 cells.  (+info)

Cardiac changes in fetuses secondary to immune hemolytic anemia and their relation to hemoglobin and catecholamine concentrations in fetal blood. (3/384)

OBJECTIVES: Immune hemolytic anemia in the fetus may cause cardiac decompensation and intrauterine death. Postnatally, norepinephrine (noradrenaline) is released in chronic heart failure, and may lead to myocardial hypertrophy. The aim of this study was to determine fetal cardiac changes associated with immune hemolytic anemia by means of echocardiography, and to relate them to fetal hemoglobin and norepinephrine levels. DESIGN: Thirty anemic fetuses underwent a total of 76 umbilical venous transfusions. Before the procedure, fetal echocardiography was performed, and end-diastolic myocardial wall thicknesses and ventricular dimensions together with Doppler flow patterns at the atrioventricular and semilunar valves were measured. Fetal hemoglobin, epinephrine and norepinephrine concentrations were determined before the transfusion. Statistical analysis of this prospective study comprised descriptive statistics including linear regression and correlation analyses. Two samples of measurements were compared by the Mann-Whitney U test. RESULTS: The mean hemoglobin concentration before the first transfusion was 6.9 g% at a mean gestational age of 26.8 weeks. Norepinephrine values were elevated in comparison to a reference range, and were higher than epinephrine values. The most striking echocardiographic finding was myocardial hypertrophy of all ventricular walls. Mean blood flow velocities were increased; at the left ventricle, they were negatively related to the hemoglobin concentrations, and positively to the norepinephrine values. CONCLUSIONS: Fetal myocardial hypertrophy in anemia may be the result of an augmented cardiac workload, indicated by the increased left ventricular mean velocities. This reaction reflects the redistribution of blood flow that may depend on hemoglobin and norepinephrine concentrations.  (+info)

Autologous CD34+ cells transplantation after FAMP treatment in a patient with CLL and persisting AIHA: complete remission of lymphoma with control of autoimmune complications. (4/384)

A 48-year-old male with CLL and concomitant AIHA unresponsive to chlorambucil was treated with fludarabine. The remission of CLL and improvement of the AIHA was achieved, but the patient remained steroid dependent. Therefore, high-dose chemotherapy followed by CD34-selected autologous peripheral blood stem cells transplantation was performed and this led to long-term clinical, immunophenotypic and molecular remission with disappearance of AIHA. Twenty-three months later, the CLL recurred with signs of AIHA. In this patient with AIHA, HDC and selected CD34+ cells completely, though temporarily, controlled both CLL and associated immune complications. This case illustrates the potential application of this approach in the management of CLL patients with immune complications.  (+info)

Galactosylation of serum IgG and autoantibodies in murine models of autoimmune haemolytic anaemia. (5/384)

A number of systemic autoimmune diseases are associated with increased levels of the agalactosyl (G0) IgG isoforms that lack a terminal galactose from the CH2 domain oligosaccharide. The current aim was to determine whether the galactosylation of serum IgG is also reduced in a classic antibody-mediated, organ-specific autoimmune condition, and whether the pathogenic autoantibodies are preferentially G0. In two murine forms of autoimmune haemolytic anaemia (AIHA), sera and autoantibodies eluted from erythrocytes were obtained, and the levels of G0 measured using a lectin-binding assay. Serum IgG galactosylation was unaffected following the induction of AIHA in CBA/Igb mice by immunization with rat erythrocytes, but in all animals with the disease the IgG autoantibodies generated were more G0 than the sera. The anti-rat erythrocyte antibodies were similar to the autoantibodies in being preferentially G0, and when CBA/Igb mice were immunized with canine erythrocytes as a control foreign antigen, there was again a bias towards the production of G0 IgG antibodies. In NZB mice with chronic, spontaneous AIHA, the concentration and galactosylation of both serum IgG and autoantibodies were lower than in the induced model, and the ratio of G0 IgG in the serum and erythrocyte eluates varied markedly between different individuals. Our interpretation of these results is that changes in serum IgG or autoantibody galactosylation are not consistent in different models of AIHA, and that production of low galactosyl antibodies can be a feature of a normal immune response.  (+info)

A persistent severe autoimmune hemolytic anemia despite apparent direct antiglobulin test negativization. (6/384)

BACKGROUND AND OBJECTIVE: Not all cases of autoimmune hemolytic anemia (AIHA) are diagnosed by the direct antiglobulin test (DAT). We present and discuss a simple method of enhancing the sensitivity of the standard DAT. DESIGN AND METHODS: We report the case of a five-month-old child diagnosed with a severe IgG-mediated AIHA, characterized by quick DAT negativization despite clinical worsening. Warm AIHA with negative DAT, possibly due to a low affinity autoantibody, unresponsive to conventional therapy, was hypothesized. RESULTS: The DAT resulted strongly positive with anti-IgG serum using a 4C saline for erythrocyte washing, to reduce the dissociation of the supposed low affinity autoantibody. Very intensive cytoreductive treatment was administered twice until clinical remission was obtained. INTERPRETATION AND CONCLUSIONS: The clinical course of AIHA can be dissociated by the DAT. Since autoantibody-mediated hemolysis with negative DAT rarely occurs, once other causes of high reticulocyte count anemia have been ruled out, the DAT after ice-cold saline washing could be a useful and easy means of corroborating the diagnosis of AHIA, when traditional methods fail.  (+info)

Autoimmune hemolytic anemia in patients with SCID after T cell-depleted BM and PBSC transplantation. (7/384)

We report a high incidence (19.5%) of autoimmune hemolytic anemia (AIHA) in 41 patients with SCID who underwent a T cell-depleted haploidentical transplant. Other than infections, AIHA was the most common post-transplant complication in this patient cohort. Clinical characteristics and treatment of eight patients who developed AIHA at a median of 8 months after the first T cell-depleted transplant are presented. All patients had warm-reacting autoantibodies, and two of eight had concurrent cold and warm autoantibodies. Clinical course was most severe in two patients who had cold and warm autoantibodies. Five patients received specific therapy for AIHA. Successful taper off immunosuppressive therapy for AIHA coincided with T cell reconstitution. Delayed reconstitution of T cell immunity, due to T cell depletion, immunosuppressive conditioning and CsA, as well as paucity of regulatory T cells, are the likely explanations for the occurrence of AIHA in our patient cohort. Screening of the population at risk may prevent morbidity and mortality from AIHA.  (+info)

High pathogenic potential of low-affinity autoantibodies in experimental autoimmune hemolytic anemia. (8/384)

To assess the potency of low-affinity anti-red blood cell (RBC) autoantibodies in the induction of anemia, we generated an immunoglobulin (Ig)G2a class-switch variant of a 4C8 IgM anti-mouse RBC autoantibody, and compared its pathogenic potential with that of its IgM isotype and a high-affinity 34-3C IgG2a autoantibody. The RBC-binding activity of the 4C8 IgG2a variant was barely detectable, at least 1,000 times lower than that of its IgM isotype, having a high-binding avidity, and that of the 34-3C IgG2a monoclonal antibody (mAb). This low-affinity feature of the 4C8 mAb was consistent with the lack of detection of opsonized RBCs in the circulating blood from the 4C8 IgG2a-injected mice. However, the 4C8 IgG2a variant was highly pathogenic, as potent as its IgM isotype and the 34-3C IgG2a mAb, due to its capacity to interact with Fc receptors involved in erythrophagocytosis. In addition, our results indicated that the pentameric form of the low-affinity IgM isotype, by promoting the binding and agglutination of RBCs, is critical for its pathogenic activity. Demonstration of the remarkably high pathogenic potency of low-affinity autoantibodies, if combined with appropriate heavy chain effector functions, highlights the critical role of the Ig heavy chain constant regions, but the relatively minor role of autoantigen-binding affinities, in autoimmune hemolytic anemia.  (+info)

There are many different types of anemia, each with its own set of causes and symptoms. Some common types of anemia include:

1. Iron-deficiency anemia: This is the most common type of anemia and is caused by a lack of iron in the diet or a problem with the body's ability to absorb iron. Iron is essential for making hemoglobin.
2. Vitamin deficiency anemia: This type of anemia is caused by a lack of vitamins, such as vitamin B12 or folate, that are necessary for red blood cell production.
3. Anemia of chronic disease: This type of anemia is seen in people with chronic diseases, such as kidney disease, rheumatoid arthritis, and cancer.
4. Sickle cell anemia: This is a genetic disorder that affects the structure of hemoglobin and causes red blood cells to be shaped like crescents or sickles.
5. Thalassemia: This is a genetic disorder that affects the production of hemoglobin and can cause anemia, fatigue, and other health problems.

The symptoms of anemia can vary depending on the type and severity of the condition. Common symptoms include fatigue, weakness, pale skin, shortness of breath, and dizziness or lightheadedness. Anemia can be diagnosed with a blood test that measures the number and size of red blood cells, as well as the levels of hemoglobin and other nutrients.

Treatment for anemia depends on the underlying cause of the condition. In some cases, dietary changes or supplements may be sufficient to treat anemia. For example, people with iron-deficiency anemia may need to increase their intake of iron-rich foods or take iron supplements. In other cases, medical treatment may be necessary to address underlying conditions such as kidney disease or cancer.

Preventing anemia is important for maintaining good health and preventing complications. To prevent anemia, it is important to eat a balanced diet that includes plenty of iron-rich foods, vitamin C-rich foods, and other essential nutrients. It is also important to avoid certain substances that can interfere with the absorption of nutrients, such as alcohol and caffeine. Additionally, it is important to manage any underlying medical conditions and seek medical attention if symptoms of anemia persist or worsen over time.

In conclusion, anemia is a common blood disorder that can have significant health implications if left untreated. It is important to be aware of the different types of anemia, their causes, and symptoms in order to seek medical attention if necessary. With proper diagnosis and treatment, many cases of anemia can be successfully managed and prevented.

Symptoms of hemolytic anemia may include fatigue, weakness, shortness of breath, dizziness, headaches, and pale or yellowish skin. Treatment options depend on the underlying cause but may include blood transfusions, medication to suppress the immune system, antibiotics for infections, and removal of the spleen (splenectomy) in severe cases.

Prevention strategies for hemolytic anemia include avoiding triggers such as certain medications or infections, maintaining good hygiene practices, and seeking early medical attention if symptoms persist or worsen over time.

It is important to note that while hemolytic anemia can be managed with proper treatment, it may not be curable in all cases, and ongoing monitoring and care are necessary to prevent complications and improve quality of life.

Autoimmune hemolytic anemia (AIHA) is a specific type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells. This can happen due to various underlying causes such as infections, certain medications, and some types of cancer.

In autoimmune hemolytic anemia, the immune system produces antibodies that coat the surface of red blood cells and mark them for destruction by other immune cells called complement proteins. This leads to the premature destruction of red blood cells in the spleen, liver, and other organs.

Symptoms of autoimmune hemolytic anemia can include fatigue, weakness, shortness of breath, jaundice (yellowing of the skin and eyes), dark urine, and a pale or yellowish complexion. Treatment options for AIHA depend on the underlying cause of the disorder, but may include medications to suppress the immune system, plasmapheresis to remove antibodies from the blood, and in severe cases, splenectomy (removal of the spleen) or bone marrow transplantation.

In summary, autoimmune hemolytic anemia is a type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells, leading to premature destruction of red blood cells and various symptoms such as fatigue, weakness, and jaundice. Treatment options depend on the underlying cause of the disorder and may include medications, plasmapheresis, and in severe cases, splenectomy or bone marrow transplantation.

Prevalence: Anemia, hemolytic, congenital is a rare disorder, affecting approximately 1 in 100,000 to 1 in 200,000 births.

Causes: The condition is caused by mutations in genes that code for proteins involved in hemoglobin synthesis or red blood cell membrane structure. These mutations can lead to abnormal hemoglobin formation, red blood cell membrane instability, and increased susceptibility to oxidative stress, which can result in hemolytic anemia.

Symptoms: Symptoms of anemia, hemolytic, congenital may include jaundice (yellowing of the skin and eyes), fatigue, weakness, pale skin, and shortness of breath. In severe cases, the condition can lead to life-threatening complications such as anemia, infections, and kidney failure.

Diagnosis: Anemia, hemolytic, congenital is typically diagnosed through a combination of physical examination, medical history, and laboratory tests, including blood smear examination, hemoglobin electrophoresis, and mutation analysis.

Treatment: Treatment for anemia, hemolytic, congenital depends on the specific underlying genetic cause and may include blood transfusions, folic acid supplements, antibiotics, and/or surgery to remove the spleen. In some cases, bone marrow transplantation may be necessary.

Prognosis: The prognosis for anemia, hemolytic, congenital varies depending on the specific underlying genetic cause and the severity of the condition. With appropriate treatment, many individuals with this condition can lead relatively normal lives, but in severe cases, the condition can be life-threatening.

There are two main types of hemolysis:

1. Intravascular hemolysis: This type occurs within the blood vessels and is caused by factors such as mechanical injury, oxidative stress, and certain infections.
2. Extravascular hemolysis: This type occurs outside the blood vessels and is caused by factors such as bone marrow disorders, splenic rupture, and certain medications.

Hemolytic anemia is a condition that occurs when there is excessive hemolysis of RBCs, leading to a decrease in the number of healthy red blood cells in the body. This can cause symptoms such as fatigue, weakness, pale skin, and shortness of breath.

Some common causes of hemolysis include:

1. Genetic disorders such as sickle cell anemia and thalassemia.
2. Autoimmune disorders such as autoimmune hemolytic anemia (AIHA).
3. Infections such as malaria, babesiosis, and toxoplasmosis.
4. Medications such as antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners.
5. Bone marrow disorders such as aplastic anemia and myelofibrosis.
6. Splenic rupture or surgical removal of the spleen.
7. Mechanical injury to the blood vessels.

Diagnosis of hemolysis is based on a combination of physical examination, medical history, and laboratory tests such as complete blood count (CBC), blood smear examination, and direct Coombs test. Treatment depends on the underlying cause and may include supportive care, blood transfusions, and medications to suppress the immune system or prevent infection.

Symptoms of aplastic anemia may include fatigue, weakness, shortness of breath, pale skin, and increased risk of bleeding or infection. Treatment options for aplastic anemia typically involve blood transfusions and immunosuppressive drugs to stimulate the bone marrow to produce new blood cells. In severe cases, a bone marrow transplant may be necessary.

Overall, aplastic anemia is a rare and serious condition that requires careful management by a healthcare provider to prevent complications and improve quality of life.

There are currently no cures for Fanconi anemia, but bone marrow transplantation and other supportive therapies can help manage some of the symptoms and improve quality of life. Research into the genetics and molecular biology of Fanconi anemia is ongoing to better understand the disorder and develop new treatments.

Some of the common symptoms of Fanconi anemia include short stature, limb deformities, hearing loss, vision problems, and an increased risk of infections and cancer. Children with Fanconi anemia may also experience developmental delays, learning disabilities, and social and emotional challenges.

The diagnosis of Fanconi anemia is typically made based on a combination of clinical findings, laboratory tests, and genetic analysis. Treatment options for Fanconi anemia depend on the severity of the disorder and may include bone marrow transplantation, blood transfusions, antibiotics, and other supportive therapies.

Fanconi anemia is a rare disorder that affects approximately 1 in 160,000 births worldwide. It is more common in certain populations, such as Ashkenazi Jews and individuals of Spanish descent. Fanconi anemia can be inherited in an autosomal recessive pattern, meaning that a child must inherit two copies of the mutated gene (one from each parent) to develop the disorder.

Overall, Fanconi anemia is a complex and rare genetic disorder that requires specialized medical care and ongoing research to better understand its causes and develop effective treatments. With appropriate management and supportive therapies, individuals with Fanconi anemia can lead fulfilling lives despite the challenges associated with the disorder.

The symptoms of HUS include:

* Diarrhea
* Vomiting
* Abdominal pain
* Fatigue
* Weakness
* Shortness of breath
* Pale or yellowish skin
* Easy bruising or bleeding

If you suspect that someone has HUS, it is important to seek medical attention immediately. A healthcare provider will perform a physical examination and order blood tests to diagnose the condition. Treatment for HUS typically involves addressing the underlying cause of the condition, such as stopping certain medications or treating an infection. In some cases, hospitalization may be necessary to manage complications such as kidney failure.

Preventative measures to reduce the risk of developing HUS include:

* Practicing good hygiene, especially during outbreaks of diarrheal illnesses
* Avoiding certain medications that are known to increase the risk of HUS
* Maintaining a healthy diet and staying hydrated
* Managing any underlying medical conditions such as high blood pressure or diabetes.

In hypochromic anemia, the RBCs are smaller than normal and have a lower concentration of hemoglobin. This can lead to a decrease in the amount of oxygen being carried to the body's tissues, which can cause fatigue, weakness, and shortness of breath.

There are several possible causes of hypochromic anemia, including:

1. Iron deficiency: Iron is essential for the production of hemoglobin, so a lack of iron can lead to a decrease in hemoglobin levels and the development of hypochromic anemia.
2. Vitamin deficiency: Vitamins such as vitamin B12 and folate are important for the production of red blood cells, so a deficiency in these vitamins can lead to hypochromic anemia.
3. Chronic disease: Certain chronic diseases, such as kidney disease, rheumatoid arthritis, and cancer, can lead to hypochromic anemia.
4. Inherited disorders: Certain inherited disorders, such as thalassemia and sickle cell anemia, can cause hypochromic anemia.
5. Autoimmune disorders: Autoimmune disorders, such as autoimmune hemolytic anemia, can cause hypochromic anemia by destroying red blood cells.

Hypochromic anemia is typically diagnosed through a combination of physical examination, medical history, and laboratory tests such as complete blood counts (CBCs) and serum iron studies. Treatment depends on the underlying cause of the anemia and may include dietary changes, supplements, medication, or blood transfusions.

Symptoms of macrocytic anemia may include fatigue, weakness, pale skin, and shortness of breath. Diagnosis is typically made through a complete blood count (CBC) test that shows an elevated mean corpuscular volume (MCV) and reticulocyte count. Treatment depends on the underlying cause, but may include vitamin supplements, changes in medication, or addressing any underlying medical conditions.

In summary, macrocytic anemia is a type of anemia characterized by large red blood cells that are prone to breakdown and can be caused by various factors. It can cause symptoms such as fatigue, weakness, and shortness of breath, and diagnosis is made through a CBC test. Treatment depends on the underlying cause.

Note: The information provided above is a general definition of the medical condition 'Anemia, Pernicious'. It is not meant to be a substitute for professional medical advice or treatment. If you have any concerns about this condition, you should consult a qualified healthcare professional for proper evaluation and care.

Sickle cell anemia is caused by mutations in the HBB gene that codes for hemoglobin. The most common mutation is a point mutation at position 6, which replaces the glutamic acid amino acid with a valine (Glu6Val). This substitution causes the hemoglobin molecule to be unstable and prone to forming sickle-shaped cells.

The hallmark symptom of sickle cell anemia is anemia, which is a low number of healthy red blood cells. People with the condition may also experience fatigue, weakness, jaundice (yellowing of the skin and eyes), infections, and episodes of severe pain. Sickle cell anemia can also increase the risk of stroke, heart disease, and other complications.

Sickle cell anemia is diagnosed through blood tests that measure hemoglobin levels and the presence of sickle cells. Treatment typically involves managing symptoms and preventing complications with medications, blood transfusions, and antibiotics. In some cases, bone marrow transplantation may be recommended.

Prevention of sickle cell anemia primarily involves avoiding the genetic mutations that cause the condition. This can be done through genetic counseling and testing for individuals who have a family history of the condition or are at risk of inheriting it. Prenatal testing is also available for pregnant women who may be carriers of the condition.

Overall, sickle cell anemia is a serious genetic disorder that can significantly impact quality of life and life expectancy if left untreated. However, with proper management and care, individuals with the condition can lead fulfilling lives and manage their symptoms effectively.

The symptoms of sideroblastic anemia can vary depending on the severity of the condition, but may include fatigue, weakness, pale skin, shortness of breath, and a rapid heart rate. Treatment options for sideroblastic anemia typically involve addressing the underlying genetic cause of the condition, such as through gene therapy or enzyme replacement therapy, and managing symptoms with medication and lifestyle modifications.

In summary, sideroblastic anemia is a rare inherited disorder characterized by abnormalities in iron metabolism that can lead to impaired red blood cell production and various other symptoms. It is important for individuals with this condition to receive timely and appropriate medical attention to manage their symptoms and prevent complications.

Symptoms of megaloblastic anemia may include fatigue, weakness, shortness of breath, pale skin, and weight loss. The condition is typically diagnosed through a physical examination, blood tests (including a complete blood count and blood chemistry tests), and possibly a bone marrow biopsy.

Treatment for megaloblastic anemia usually involves addressing the underlying cause of the condition, such as vitamin B12 or folate supplements. In some cases, medications to stimulate the production of red blood cells may be prescribed. If left untreated, megaloblastic anemia can lead to complications such as heart problems and increased risk of infections.

There are several subtypes of refractory anemia, including:

1. Refractory anemia with excess blasts (RAEB): This type of anemia is characterized by a high number of immature red blood cells in the bone marrow.
2. Refractory anemia with ringed sideroblasts (RARS): This type of anemia is characterized by the presence of abnormal red blood cells that have a "ring-like" appearance under a microscope.
3. Refractory anemia with multilineage dysplasia (RARMD): This type of anemia is characterized by abnormal cell development in the bone marrow, including immature red blood cells, white blood cells, and platelets.

Refractory anemia can be caused by a variety of factors, including genetic mutations, exposure to certain chemicals or toxins, and certain medical conditions such as chronic kidney disease or rheumatoid arthritis. Treatment for refractory anemia typically involves blood transfusions and supportive care, such as folic acid supplements and antibiotics to prevent infection. In some cases, bone marrow transplantation may be recommended.

The symptoms of EIA can vary in severity and may include fever, loss of appetite, weight loss, depression, and anemia. In severe cases, the disease can lead to death. There is no cure for EIA, but it can be managed with antiretroviral medications and supportive care.

EIA is a significant concern in the equine industry, as infected animals can transmit the disease to other horses and can be a risk to human health. Testing for EIA is done through a blood test, and infected animals are typically euthanized to prevent the spread of the disease.

The condition is caused by sensitization of the mother's immune system to the Rh factor, which can occur when the mother's blood comes into contact with the fetus's blood during pregnancy or childbirth. The antibodies produced by the mother's immune system can attack the red blood cells of the fetus, leading to hemolytic anemia and potentially causing stillbirth or death in the newborn.

Erythroblastosis fetalis is diagnosed through blood tests that measure the levels of antibodies against the Rh factor. Treatment typically involves the administration of Rh immune globulin, which can help to prevent the mother's immune system from producing more antibodies against the Rh factor and reduce the risk of complications for the fetus. In severe cases, a blood transfusion may be necessary to increase the newborn's red blood cell count.

Erythroblastosis fetalis is a serious condition that requires close monitoring and proper medical management to prevent complications and ensure the best possible outcome for both the mother and the baby.

Also known as: Hereditary spherocytosis (HSS)

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Source: Genetic Home Reference: NIH

1. Iron deficiency anemia: This is the most common hematologic complication of pregnancy, caused by the increased demand for iron and the potential for poor dietary intake or gastrointestinal blood loss.
2. Thrombocytopenia: A decrease in platelet count, which can be mild and resolve spontaneously or severe and require treatment.
3. Leukemia: Rare but potentially serious, leukemia can occur during pregnancy and may require prompt intervention to ensure the health of both the mother and the fetus.
4. Thrombosis: The formation of a blood clot in a blood vessel, which can be life-threatening for both the mother and the baby if left untreated.
5. Hemorrhage: Excessive bleeding during pregnancy, which can be caused by various factors such as placenta previa or abruption.
6. Preeclampsia: A condition characterized by high blood pressure and damage to organs such as the kidneys and liver, which can increase the risk of hemorrhage and other complications.
7. Ectopic pregnancy: A pregnancy that develops outside of the uterus, often in the fallopian tube, which can cause severe bleeding and be life-threatening if left untreated.

A condition where newborn babies have a lower than normal number of red blood cells or low levels of hemoglobin in their blood. The condition can be caused by various factors such as premature birth, low birth weight, infections, and genetic disorders. Symptoms may include jaundice, fatigue, and difficulty breathing. Treatment options may vary depending on the underlying cause but may include blood transfusions and iron supplements.

Example usage: "Neonatal anemia is a common condition in newborn babies that can be caused by various factors such as premature birth or low birth weight."

The condition is inherited in an X-linked recessive pattern, meaning that the gene for G6PD deficiency is located on the X chromosome and affects males more frequently than females. Females may also be affected but typically have milder symptoms or may be carriers of the condition without experiencing any symptoms themselves.

G6PD deficiency can be caused by mutations in the G6PD gene, which can lead to a reduction in the amount of functional enzyme produced. The severity of the condition depends on the specific nature of the mutation and the degree to which it reduces the activity of the enzyme.

Symptoms of G6PD deficiency may include jaundice (yellowing of the skin and eyes), fatigue, weakness, and shortness of breath. In severe cases, the condition can lead to hemolytic anemia, which is characterized by the premature destruction of red blood cells. This can be triggered by certain drugs, infections, or foods that contain high levels of oxalic acid or other oxidizing agents.

Diagnosis of G6PD deficiency typically involves a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment is focused on managing symptoms and preventing complications through dietary modifications, medications, and avoidance of triggers such as certain drugs or infections.

Overall, G6PD deficiency is a relatively common genetic disorder that can have significant health implications if left untreated. Understanding the causes, symptoms, and treatment options for this condition is important for ensuring appropriate care and management for individuals affected by it.

The term "refractory" refers to the fact that this type of anemia does not respond well to standard treatments, such as blood transfusions or medications. The term "excess blasts" refers to the presence of a large number of immature cells in the bone marrow.

RAEB is a serious and potentially life-threatening condition that can develop into acute myeloid leukemia (AML), a type of cancer that affects the blood and bone marrow. AML is characterized by the rapid growth of abnormal white blood cells, which can crowd out normal cells in the bone marrow and lead to a variety of symptoms, including fatigue, fever, night sweats, and weight loss.

RAEB is usually diagnosed in adults over the age of 60, although it can occur at any age. The condition is often associated with other health problems, such as myelodysplastic syndrome (MDS), a group of disorders that affect the bone marrow and blood cells.

Treatment for RAEB typically involves chemotherapy and/or bone marrow transplantation. The goal of treatment is to slow the progression of the disease, reduce symptoms, and improve quality of life. In some cases, RAEB may be managed with supportive care, such as blood transfusions and antibiotics, to help manage symptoms and prevent complications.

Overall, refractory anemia with excess blasts is a serious and complex condition that requires careful management by a healthcare team of hematologists, oncologists, and other specialists. With appropriate treatment, many people with RAEB are able to achieve long-term remission and improve their quality of life.

Pallor is often used as an indicator of underlying disease, particularly in conditions where there is a decrease in the amount of hemoglobin in the blood, such as anemia or blood loss. It can also be a sign of other diseases such as liver cirrhosis, kidney failure, and some types of cancer.

There are different types of pallor, including:

1. Anemic pallor: This is the most common type of pallor and is caused by a decrease in the number of red blood cells or hemoglobin in the blood. It can be seen in conditions such as iron deficiency anemia, vitamin deficiency anemia, and sickle cell anemia.
2. Post-inflammatory pallor: This type of pallor is caused by inflammation that leads to a decrease in blood flow to the skin. It can be seen in conditions such as erythema migrans (Lyme disease), and other inflammatory conditions.
3. Cirrhotic pallor: This type of pallor is caused by liver cirrhosis and is characterized by a pale, washed-out appearance of the skin.
4. Renal pallor: This type of pallor is caused by kidney failure and is characterized by a pale, washed-out appearance of the skin.
5. Cancer pallor: This type of pallor is caused by certain types of cancer, such as carcinomas and lymphomas, and is characterized by a pale, washed-out appearance of the skin.

In summary, pallor is a term used to describe an abnormal paleness or whiteness of the skin that can be caused by a variety of underlying medical conditions. It is often used as an indicator of illness and can be seen in a wide range of conditions, including anemia, inflammation, liver cirrhosis, kidney failure, and certain types of cancer.

Blood group incompatibility can occur in various ways, including:

1. ABO incompatibility: This is the most common type of blood group incompatibility and occurs when the patient's blood type (A or B) is different from the donor's blood type.
2. Rh incompatibility: This occurs when the patient's Rh factor is different from the donor's Rh factor.
3. Other antigens: In addition to ABO and Rh, there are other antigens on red blood cells that can cause incompatibility, such as Kell, Duffy, and Xg.

Blood group incompatibility can be diagnosed through blood typing and cross-matching tests. These tests determine the patient's and donor's blood types and identify any incompatible antigens that may cause an immune response.

Treatment of blood group incompatibility usually involves finding a compatible donor or using specialized medications to reduce the risk of a negative reaction. In some cases, plasmapheresis, also known as plasma exchange, may be used to remove the incompatible antibodies from the patient's blood.

Prevention of blood group incompatibility is important, and this can be achieved by ensuring that patients receive only compatible blood products during transfusions. Blood banks maintain a database of donor blood types and perform thorough testing before releasing blood for transfusion to ensure compatibility. Additionally, healthcare providers should carefully review the patient's medical history and current medications to identify any potential allergies or sensitivities that may affect blood compatibility.

The term splenomegaly is used to describe any condition that results in an increase in the size of the spleen, regardless of the underlying cause. This can be caused by a variety of factors, such as infection, inflammation, cancer, or genetic disorders.

Splenomegaly can be diagnosed through a physical examination, where the doctor may feel the enlarged spleen during an abdominal palpation. Imaging tests, such as ultrasound, computed tomography (CT) scans, or magnetic resonance imaging (MRI), may also be used to confirm the diagnosis and evaluate the extent of the splenomegaly.

Treatment for splenomegaly depends on the underlying cause. For example, infections such as malaria or mononucleosis are treated with antibiotics, while cancerous conditions may require surgical intervention or chemotherapy. In some cases, the spleen may need to be removed, a procedure known as splenectomy.

In conclusion, splenomegaly is an abnormal enlargement of the spleen that can be caused by various factors and requires prompt medical attention for proper diagnosis and treatment.

The two main types of TMAs are:

1. Thrombotic thrombocytopenic purpura (TTP): This is a rare autoimmune disorder caused by the formation of antibodies against ADAMTS13, an enzyme involved in platelet function. TTP patients have low levels of ADAMTS13 and abnormal platelets that are prone to clotting.
2. Hemolytic uremic syndrome (HUS): This is a condition that occurs when red blood cells are destroyed and removed from the circulation, leading to anemia, low platelet count, and kidney failure. HUS can be caused by various factors, such as infections, certain medications, or genetic mutations.

Both TTP and HUS can lead to TMAs, which can cause severe morbidity and mortality if left untreated. Treatment options for TMAs include plasmapheresis, corticosteroids, and immunosuppressive drugs, as well as dialysis in cases of acute kidney injury. Early diagnosis and aggressive treatment are essential to prevent long-term complications and improve patient outcomes.

The disorder is caused by mutations in the HBB gene that codes for the beta-globin subunit of hemoglobin. These mutations result in the production of abnormal hemoglobins that are unstable and prone to breakdown, leading to the release of free hemoglobin into the urine.

HP is classified into two types based on the severity of symptoms:

1. Type 1 HP: This is the most common form of the disorder and is characterized by mild to moderate anemia, occasional hemoglobinuria, and a normal life expectancy.
2. Type 2 HP: This is a more severe form of the disorder and is characterized by severe anemia, recurrent hemoglobinuria, and a shorter life expectancy.

There is no cure for HP, but treatment options are available to manage symptoms and prevent complications. These may include blood transfusions, folic acid supplements, and medications to reduce the frequency and severity of hemoglobinuria episodes.

Isoimmunization is a condition that occurs when an individual has antibodies against their own red blood cell antigens, specifically the Rh antigen. This can happen due to various reasons such as:

1. Incompatibility between the mother's and father's Rh antigens, leading to the development of antibodies in the mother during pregnancy or childbirth.
2. Blood transfusions from an incompatible donor.
3. Certain medical conditions like autoimmune hemolytic anemia or bone marrow transplantation.

Rh isoimmunization can lead to a range of complications, including:

1. Hemolytic disease of the newborn: This is a condition where the baby's red blood cells are destroyed by the mother's antibodies, leading to anemia, jaundice, and other serious complications.
2. Rh hemolytic crisis: This is a severe and potentially life-threatening complication that can occur during pregnancy or childbirth.
3. Chronic hemolytic anemia: This is a condition where the red blood cells are continuously destroyed, leading to anemia and other complications.

Rh isoimmunization can be diagnosed through blood tests such as the direct antiglobulin test (DAT) or the indirect Coombs test (ICT). Treatment typically involves managing any underlying conditions and monitoring for complications. In severe cases, a bone marrow transplant may be necessary. Prevention is key, and women who are Rh-negative should receive an injection of Rh immune globulin during pregnancy to prevent the development of antibodies against the Rh antigen.

There are several possible causes of thrombocytopenia, including:

1. Immune-mediated disorders such as idiopathic thrombocytopenic purpura (ITP) or systemic lupus erythematosus (SLE).
2. Bone marrow disorders such as aplastic anemia or leukemia.
3. Viral infections such as HIV or hepatitis C.
4. Medications such as chemotherapy or non-steroidal anti-inflammatory drugs (NSAIDs).
5. Vitamin deficiencies, especially vitamin B12 and folate.
6. Genetic disorders such as Bernard-Soulier syndrome.
7. Sepsis or other severe infections.
8. Disseminated intravascular coagulation (DIC), a condition where blood clots form throughout the body.
9. Postpartum thrombocytopenia, which can occur in some women after childbirth.

Symptoms of thrombocytopenia may include easy bruising, petechiae (small red or purple spots on the skin), and prolonged bleeding from injuries or surgical sites. Treatment options depend on the underlying cause but may include platelet transfusions, steroids, immunosuppressive drugs, and in severe cases, surgery.

In summary, thrombocytopenia is a condition characterized by low platelet counts that can increase the risk of bleeding and bruising. It can be caused by various factors, and treatment options vary depending on the underlying cause.

There are two main types of thalassemia: alpha-thalassemia and beta-thalassemia. Alpha-thalassemia is caused by abnormalities in the production of the alpha-globin chain, which is one of the two chains that make up hemoglobin. Beta-thalassemia is caused by abnormalities in the production of the beta-globin chain.

Thalassemia can cause a range of symptoms, including anemia, fatigue, pale skin, and shortness of breath. In severe cases, it can lead to life-threatening complications such as heart failure, liver failure, and bone deformities. Thalassemia is usually diagnosed through blood tests that measure the levels of hemoglobin and other proteins in the blood.

There is no cure for thalassemia, but treatment can help manage the symptoms and prevent complications. Treatment may include blood transfusions, folic acid supplements, and medications to reduce the severity of anemia. In some cases, bone marrow transplantation may be recommended.

Preventive measures for thalassemia include genetic counseling and testing for individuals who are at risk of inheriting the disorder. Prenatal testing is also available for pregnant women who are carriers of the disorder. In addition, individuals with thalassemia should avoid marriage within their own family or community to reduce the risk of passing on the disorder to their children.

Overall, thalassemia is a serious and inherited blood disorder that can have significant health implications if left untreated. However, with proper treatment and management, individuals with thalassemia can lead fulfilling lives and minimize the risk of complications.

There are two main types of beta-thalassemia:

1. Beta-thalassemia major (also known as Cooley's anemia): This is the most severe form of the condition, and it can cause serious health problems and a shortened lifespan if left untreated. Children with this condition are typically diagnosed at birth or in early childhood, and they may require regular blood transfusions and other medical interventions to manage their symptoms and prevent complications.
2. Beta-thalassemia minor (also known as thalassemia trait): This is a milder form of the condition, and it may not cause any noticeable symptoms. People with beta-thalassemia minor have one mutated copy of the HBB gene and one healthy copy, which allows them to produce some normal hemoglobin. However, they may still be at risk for complications such as anemia, fatigue, and a higher risk of infections.

The symptoms of beta-thalassemia can vary depending on the severity of the condition and the age of onset. Common symptoms include:

* Fatigue
* Weakness
* Pale skin
* Shortness of breath
* Frequent infections
* Yellowing of the skin and eyes (jaundice)
* Enlarged spleen

Beta-thalassemia is most commonly found in people of Mediterranean, African, and Southeast Asian ancestry. It is caused by mutations in the HBB gene, which is inherited from one's parents. There is no cure for beta-thalassemia, but it can be managed with blood transfusions, chelation therapy, and other medical interventions. Bone marrow transplantation may also be a viable option for some patients.

In conclusion, beta-thalassemia is a genetic disorder that affects the production of hemoglobin, leading to anemia, fatigue, and other complications. While there is no cure for the condition, it can be managed with medical interventions and bone marrow transplantation may be a viable option for some patients. Early diagnosis and management are crucial in preventing or minimizing the complications of beta-thalassemia.

Here are some common types of E. coli infections:

1. Urinary tract infections (UTIs): E. coli is a leading cause of UTIs, which occur when bacteria enter the urinary tract and cause inflammation. Symptoms include frequent urination, burning during urination, and cloudy or strong-smelling urine.
2. Diarrheal infections: E. coli can cause diarrhea, abdominal cramps, and fever if consumed through contaminated food or water. In severe cases, this type of infection can lead to dehydration and even death, particularly in young children and the elderly.
3. Septicemia (bloodstream infections): If E. coli bacteria enter the bloodstream, they can cause septicemia, a life-threatening condition that requires immediate medical attention. Symptoms include fever, chills, rapid heart rate, and low blood pressure.
4. Meningitis: In rare cases, E. coli infections can spread to the meninges, the protective membranes covering the brain and spinal cord, causing meningitis. This is a serious condition that requires prompt treatment with antibiotics and supportive care.
5. Hemolytic-uremic syndrome (HUS): E. coli infections can sometimes cause HUS, a condition where the bacteria destroy red blood cells, leading to anemia, kidney failure, and other complications. HUS is most common in young children and can be fatal if not treated promptly.

Preventing E. coli infections primarily involves practicing good hygiene, such as washing hands regularly, especially after using the bathroom or before handling food. It's also essential to cook meat thoroughly, especially ground beef, to avoid cross-contamination with other foods. Avoiding unpasteurized dairy products and drinking contaminated water can also help prevent E. coli infections.

If you suspect an E. coli infection, seek medical attention immediately. Your healthcare provider may perform a urine test or a stool culture to confirm the diagnosis and determine the appropriate treatment. In mild cases, symptoms may resolve on their own within a few days, but antibiotics may be necessary for more severe infections. It's essential to stay hydrated and follow your healthcare provider's recommendations to ensure a full recovery.

The most common types of hemoglobinopathies include:

1. Sickle cell disease: This is caused by a point mutation in the HBB gene that codes for the beta-globin subunit of hemoglobin. It results in the production of sickle-shaped red blood cells, which can cause anemia, infections, and other complications.
2. Thalassemia: This is a group of genetic disorders that affect the production of hemoglobin and can result in anemia, fatigue, and other complications.
3. Hemophilia A: This is caused by a defect in the F8 gene that codes for coagulation factor VIII, which is essential for blood clotting. It can cause bleeding episodes, especially in males.
4. Glucose-6-phosphate dehydrogenase (G6PD) deficiency: This is caused by a point mutation in the G6PD gene that codes for an enzyme involved in red blood cell production. It can cause hemolytic anemia, especially in individuals who consume certain foods or medications.
5. Hereditary spherocytosis: This is caused by point mutations in the ANK1 or SPTA1 genes that code for proteins involved in red blood cell membrane structure. It can cause hemolytic anemia and other complications.

Hemoglobinopathies can be diagnosed through genetic testing, such as DNA sequencing or molecular genetic analysis. Treatment options vary depending on the specific disorder but may include blood transfusions, medications, and in some cases, bone marrow transplantation.

Favism is characterized by a sudden and severe anemia, often triggered by exposure to certain foods or medications that contain a chemical called quinine. Quinine is found in the bark of the cinchona tree, which is used to make antimalarial drugs. In individuals with favism, quinine can cause red blood cells to rupture and die prematurely, leading to anemia and other complications.

Symptoms of favism usually begin within 24 hours of exposure to quinine and may include fatigue, jaundice, dark urine, and a low platelet count. In severe cases, favism can lead to life-threatening complications such as kidney failure and cardiac arrest.

Favism is most commonly found in individuals of Mediterranean or African descent, particularly those from Greece, Italy, Turkey, and the Middle East. It is estimated that approximately 10% of these populations carry the G6PD deficiency that causes favism.

There is no cure for favism, but certain medications and dietary changes can help manage symptoms and prevent complications. Individuals with favism are advised to avoid consuming foods or medications containing quinine, and may require regular monitoring of their red blood cell count and other clinical parameters.

In conclusion, favism is a rare genetic disorder that affects the metabolism of hemoglobin and can cause sudden and severe anemia in certain populations. It is important to be aware of this condition and take necessary precautions to prevent complications, particularly when consuming certain foods or medications containing quinine.

Hemoglobinuria can be caused by a variety of factors, including:

1. Blood disorders such as sickle cell disease, thalassemia, and von Willebrand disease.
2. Inherited genetic disorders such as hemophilia.
3. Autoimmune disorders such as autoimmune hemolytic anemia.
4. Infections such as septicemia or meningococcemia.
5. Toxins such as lead, which can damage red blood cells and cause hemoglobinuria.
6. Certain medications such as antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs).
7. Kidney disease or failure.
8. Transfusion-related acute lung injury (TRALI), which can occur after blood transfusions.
9. Hemolytic uremic syndrome (HUS), a condition that occurs when red blood cells are damaged and broken down, leading to kidney failure.

The symptoms of hemoglobinuria may include:

1. Red or brown-colored urine
2. Frequent urination
3. Pale or yellowish skin
4. Fatigue
5. Shortness of breath
6. Nausea and vomiting
7. Headache
8. Dizziness or lightheadedness
9. Confusion or loss of consciousness in severe cases.

Diagnosis of hemoglobinuria is typically made through urine testing, such as a urinalysis, which can detect the presence of hemoglobin in the urine. Additional tests may be ordered to determine the underlying cause of hemoglobinuria, such as blood tests, imaging studies, or biopsies.

Treatment of hemoglobinuria depends on the underlying cause and severity of the condition. In some cases, treatment may involve addressing the underlying condition that is causing the hemoglobinuria, such as managing an infection or stopping certain medications. Other treatments may include:

1. Fluid and electrolyte replacement to prevent dehydration and maintain proper fluid balance.
2. Medications to help remove excess iron from the body.
3. Blood transfusions to increase the number of red blood cells in the body and improve oxygen delivery.
4. Dialysis to filter waste products from the blood when the kidneys are unable to do so.
5. Supportive care, such as oxygen therapy and pain management.

In severe cases of hemoglobinuria, complications can include:

1. Kidney damage or failure
2. Septicemia (blood infection)
3. Respiratory failure
4. Heart problems
5. Increased risk of infections and other complications.

Prevention of hemoglobinuria involves managing any underlying medical conditions, such as diabetes or infections, and avoiding certain medications that can cause the condition. It is also important to seek medical attention if symptoms of hemoglobinuria develop, as early treatment can help prevent complications and improve outcomes.

There are two main forms of alpha-Thalassemia:

1. Alpha-thalassemia major (also known as Hemoglobin Bart's hydrops fetalis): This is a severe form of the disorder that can cause severe anemia, enlarged spleen, and death in infancy. It is caused by a complete absence of one or both of the HBA1 or HBA2 genes.
2. Alpha-thalassemia minor (also known as Hemoglobin carrier state): This form of the disorder is milder and may not cause any symptoms at all. It is caused by a partial deletion of one or both of the HBA1 or HBA2 genes.

People with alpha-thalassemia minor may have slightly lower levels of hemoglobin and may be more susceptible to anemia, but they do not typically experience any severe symptoms. Those with alpha-thalassemia major, on the other hand, are at risk for serious complications such as anemia, infections, and organ failure.

There is no cure for alpha-thalassemia, but treatment options include blood transfusions, iron chelation therapy, and management of associated complications. Screening for alpha-thalassemia is recommended for individuals who are carriers of the disorder, as well as for those who have a family history of the condition.

Examples of hematologic diseases include:

1. Anemia - a condition where there are not enough red blood cells or hemoglobin in the body.
2. Leukemia - a type of cancer that affects the bone marrow and blood, causing an overproduction of immature white blood cells.
3. Lymphoma - a type of cancer that affects the lymphatic system, including the bone marrow, spleen, and lymph nodes.
4. Thalassemia - a genetic disorder that affects the production of hemoglobin, leading to anemia and other complications.
5. Sickle cell disease - a genetic disorder that affects the production of hemoglobin, causing red blood cells to become sickle-shaped and prone to breaking down.
6. Polycythemia vera - a rare disorder where there is an overproduction of red blood cells.
7. Myelodysplastic syndrome - a condition where the bone marrow produces abnormal blood cells that do not mature properly.
8. Myeloproliferative neoplasms - a group of conditions where the bone marrow produces excessive amounts of blood cells, including polycythemia vera, essential thrombocythemia, and primary myelofibrosis.
9. Deep vein thrombosis - a condition where a blood clot forms in a deep vein, often in the leg or arm.
10. Pulmonary embolism - a condition where a blood clot travels to the lungs and blocks a blood vessel, causing shortness of breath, chest pain, and other symptoms.

These are just a few examples of hematologic diseases, but there are many others that can affect the blood and bone marrow. Treatment options for these diseases can range from watchful waiting and medication to surgery, chemotherapy, and stem cell transplantation. It is important to seek medical attention if you experience any symptoms of hematologic disease, as early diagnosis and treatment can improve outcomes.

Causes:

* Dietary deficiency due to a lack of animal products in the diet
* Malabsorption due to gastrointestinal disorders such as Crohn's disease or celiac disease
* Pernicious anemia, an autoimmune condition that affects the absorption of vitamin B12 in the gut.
* Surgical removal of part of the small intestine
* Certain medications such as metformin and proton pump inhibitors

Symptoms:

* Fatigue, weakness, and shortness of breath
* Pale skin and mouth sores
* Difficulty walking or balance problems
* Numbness or tingling sensations in the hands and feet
* Memory loss and depression
* Poor appetite and weight loss

Diagnosis:

* Blood tests to measure vitamin B12 levels and other related markers such as homocysteine
* Physical examination and medical history to identify risk factors or signs of deficiency

Treatment:

* Dietary changes to include more animal products such as meat, fish, eggs, and dairy products.
* Vitamin B12 supplements in the form of tablets, lozenges, or injections.
* Addressing underlying conditions that may be contributing to the deficiency such as gastrointestinal disorders.

Prevention:

* Consuming animal products as part of a balanced diet
* Avoiding medications that can interfere with vitamin B12 absorption.

There are several different types of malaria, including:

1. Plasmodium falciparum: This is the most severe form of malaria, and it can be fatal if left untreated. It is found in many parts of the world, including Africa, Asia, and Latin America.
2. Plasmodium vivax: This type of malaria is less severe than P. falciparum, but it can still cause serious complications if left untreated. It is found in many parts of the world, including Africa, Asia, and Latin America.
3. Plasmodium ovale: This type of malaria is similar to P. vivax, but it can cause more severe symptoms in some people. It is found primarily in West Africa.
4. Plasmodium malariae: This type of malaria is less common than the other three types, and it tends to cause milder symptoms. It is found primarily in parts of Africa and Asia.

The symptoms of malaria can vary depending on the type of parasite that is causing the infection, but they typically include:

1. Fever
2. Chills
3. Headache
4. Muscle and joint pain
5. Fatigue
6. Nausea and vomiting
7. Diarrhea
8. Anemia (low red blood cell count)

If malaria is not treated promptly, it can lead to more severe complications, such as:

1. Seizures
2. Coma
3. Respiratory failure
4. Kidney failure
5. Liver failure
6. Anemia (low red blood cell count)

Malaria is typically diagnosed through a combination of physical examination, medical history, and laboratory tests, such as blood smears or polymerase chain reaction (PCR) tests. Treatment for malaria typically involves the use of antimalarial drugs, such as chloroquine or artemisinin-based combination therapies. In severe cases, hospitalization may be necessary to manage complications and provide supportive care.

Prevention is an important aspect of managing malaria, and this can include:

1. Using insecticide-treated bed nets
2. Wearing protective clothing and applying insect repellent when outdoors
3. Eliminating standing water around homes and communities to reduce the number of mosquito breeding sites
4. Using indoor residual spraying (IRS) or insecticide-treated wall lining to kill mosquitoes
5. Implementing malaria control measures in areas where malaria is common, such as distribution of long-lasting insecticidal nets (LLINs) and indoor residual spraying (IRS)
6. Improving access to healthcare services, particularly in rural and remote areas
7. Providing education and awareness about malaria prevention and control
8. Encouraging the use of preventive medications, such as intermittent preventive treatment (IPT) for pregnant women and children under the age of five.

Early diagnosis and prompt treatment are critical in preventing the progression of malaria and reducing the risk of complications and death. In areas where malaria is common, it is essential to have access to reliable diagnostic tools and effective antimalarial drugs.

The term "reticulocytosis" is derived from the Latin words "reticulum," meaning net-like, and "cytosis," meaning the condition of cells. This refers to the characteristic net-like appearance of reticulocytes under a microscope.

There are several possible causes of reticulocytosis, including:

1. Inherited disorders such as hereditary elliptocytosis, hereditary spherocytosis, and pyruvate kinase (PK) deficiency.
2. Acquired disorders such as hemolytic anemia, thalassemia, and sickle cell disease.
3. Infections such as malaria, dengue fever, and babesiosis.
4. Medications such as antibiotics, chemotherapy drugs, and anti-inflammatory medications.
5. Other conditions such as chronic kidney disease, liver disease, and autoimmune disorders.

Reticulocytosis can be diagnosed through a blood test called a complete blood count (CBC) or a reticulocyte count. Treatment depends on the underlying cause of the condition. In some cases, no treatment may be necessary, while in other cases, medication or blood transfusions may be required.

Symptoms of pancytopenia may include fatigue, weakness, shortness of breath, and increased risk of bleeding or infection. Treatment depends on the underlying cause, but may include blood transfusions, antibiotics, or immunosuppressive medications. In severe cases, pancytopenia can lead to anemia, infections, or bleeding complications that can be life-threatening.

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Symptoms of iron overload can include fatigue, weakness, joint pain, and abdominal discomfort. Treatment for iron overload usually involves reducing iron intake and undergoing regular phlebotomy (blood removal) to remove excess iron from the body. In severe cases, iron chelation therapy may be recommended to help remove excess iron from tissues and organs.

In addition to these medical definitions and treatments, there are also some key points to keep in mind when it comes to iron overload:

1. Iron is essential for human health, but too much of it can be harmful. The body needs a certain amount of iron to produce hemoglobin, the protein in red blood cells that carries oxygen throughout the body. However, excessive iron levels can damage organs and tissues.
2. Hereditary hemochromatosis is the most common cause of iron overload. This genetic disorder causes the body to absorb too much iron from food, leading to its accumulation in organs and tissues.
3. Iron overload can increase the risk of certain diseases, such as liver cirrhosis, diabetes, and heart disease. It can also lead to a condition called hemosiderosis, which is characterized by the deposition of iron in tissues and organs.
4. Phlebotomy is a safe and effective treatment for iron overload. Regular blood removal can help reduce excess iron levels and prevent complications such as liver damage, heart failure, and anemia.
5. Iron chelation therapy may be recommended in severe cases of iron overload. This involves using drugs to remove excess iron from tissues and organs, but it is not always necessary and can have potential side effects.

The symptoms of RCPA can vary depending on the severity of the condition and may include:

* Severe anemia
* Fatigue
* Pale skin
* Shortness of breath
* Increased risk of bleeding

Diagnosis of RCPA typically involves a combination of physical examination, medical history, and laboratory tests, including blood counts, genetic analysis, and bone marrow aspiration. Treatment for RCPA may involve blood transfusions, iron chelation therapy, and in some cases, hematopoietic stem cell transplantation.

The prognosis for RCPA is generally poor, with a high risk of bleeding and death in early childhood if left untreated. However, with timely diagnosis and appropriate treatment, patients with RCPA can have a good quality of life and a normal lifespan.

The main symptoms of PTI include:

* Purple spots or bruises (purpura) on the skin, which may be caused by minor trauma or injury.
* Thrombocytopenia (low platelet count), typically less than 50,000 platelets/mm3.
* Mild anemia and reticulocytosis (increased immature red blood cells).
* Elevated levels of autoantibodies against platelet membrane glycoproteins (GP) and other platelet proteins.
* No evidence of other causes of thrombocytopenia, such as bone marrow disorders or infections.

The exact cause of PTI is unknown, but it is believed to involve an immune-mediated response triggered by a genetic predisposition. Treatment options for PTI include corticosteroids, intravenous immunoglobulin (IVIG), and splenectomy in severe cases. The prognosis for PTI is generally good, with most patients experiencing resolution of symptoms and normalization of platelet counts within a few months to a year after treatment. However, some individuals may experience recurrent episodes of thrombocytopenia and purpura throughout their lives.

1. Anemia: Folic acid plays a critical role in the production of red blood cells, so a deficiency can lead to anemia, which can cause fatigue, weakness, and shortness of breath.
2. Birth defects: Folic acid is crucial for fetal development during pregnancy, and a deficiency can increase the risk of birth defects such as spina bifida and cleft palate.
3. Heart disease: Folic acid helps to regulate homocysteine levels in the blood, which are associated with an increased risk of heart disease and stroke.
4. Neurological problems: Folic acid is important for the health of the nervous system, and a deficiency can lead to neurological problems such as cognitive impairment, mood disturbances, and seizures.
5. Poor wound healing: Folic acid is necessary for the production of collagen, which is important for wound healing. A deficiency can lead to slow or poor wound healing.
6. Increased risk of cancer: Some studies suggest that a folic acid deficiency may increase the risk of certain types of cancer, such as colon cancer.
7. Hair loss: Folic acid is important for hair growth, and a deficiency can lead to hair loss.
8. Skin problems: Folic acid is important for skin health, and a deficiency can lead to skin problems such as dry, flaky skin and mouth sores.
9. Mood changes: Folic acid plays a role in the production of neurotransmitters, which are chemicals that regulate mood. A deficiency can lead to mood changes such as depression and anxiety.
10. Fatigue: Folic acid is important for energy metabolism, and a deficiency can lead to fatigue and weakness.

Folic acid deficiency can be caused by a number of factors, including:

1. Poor diet: A diet that is low in folate-rich foods can lead to a deficiency.
2. Malabsorption: Certain medical conditions such as celiac disease and Crohn's disease can lead to malabsorption of folic acid.
3. Pregnancy and lactation: Women who are pregnant or breastfeeding have a higher need for folic acid, and may be at risk for deficiency if they do not consume enough.
4. Alcoholism: Heavy alcohol consumption can interfere with the absorption of folic acid.
5. Certain medications: Some medications, such as antacids and proton pump inhibitors, can interfere with the absorption of folic acid.

To diagnose a folic acid deficiency, a healthcare provider may perform a physical exam, take a medical history, and order blood tests to measure folic acid levels. Treatment for a folic acid deficiency typically involves dietary changes and supplements. Dietary changes may include consuming more folate-rich foods, such as leafy green vegetables, legumes, and whole grains. Supplements may include folic acid tablets or liquid supplements. In severe cases of deficiency, injections of folic acid may be necessary. It is important to seek medical attention if you suspect a folic acid deficiency, as untreated deficiencies can lead to serious health problems.

A condition in which the kidneys gradually lose their function over time, leading to the accumulation of waste products in the body. Also known as chronic kidney disease (CKD).

Prevalence:

Chronic kidney failure affects approximately 20 million people worldwide and is a major public health concern. In the United States, it is estimated that 1 in 5 adults has CKD, with African Americans being disproportionately affected.

Causes:

The causes of chronic kidney failure are numerous and include:

1. Diabetes: High blood sugar levels can damage the kidneys over time.
2. Hypertension: Uncontrolled high blood pressure can cause damage to the blood vessels in the kidneys.
3. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste and excess fluids from the blood.
4. Interstitial nephritis: Inflammation of the tissue between the kidney tubules.
5. Pyelonephritis: Infection of the kidneys, usually caused by bacteria or viruses.
6. Polycystic kidney disease: A genetic disorder that causes cysts to grow on the kidneys.
7. Obesity: Excess weight can increase blood pressure and strain on the kidneys.
8. Family history: A family history of kidney disease increases the risk of developing chronic kidney failure.

Symptoms:

Early stages of chronic kidney failure may not cause any symptoms, but as the disease progresses, symptoms can include:

1. Fatigue: Feeling tired or weak.
2. Swelling: In the legs, ankles, and feet.
3. Nausea and vomiting: Due to the buildup of waste products in the body.
4. Poor appetite: Loss of interest in food.
5. Difficulty concentrating: Cognitive impairment due to the buildup of waste products in the brain.
6. Shortness of breath: Due to fluid buildup in the lungs.
7. Pain: In the back, flank, or abdomen.
8. Urination changes: Decreased urine production, dark-colored urine, or blood in the urine.
9. Heart problems: Chronic kidney failure can increase the risk of heart disease and heart attack.

Diagnosis:

Chronic kidney failure is typically diagnosed based on a combination of physical examination findings, medical history, laboratory tests, and imaging studies. Laboratory tests may include:

1. Blood urea nitrogen (BUN) and creatinine: Waste products in the blood that increase with decreased kidney function.
2. Electrolyte levels: Imbalances in electrolytes such as sodium, potassium, and phosphorus can indicate kidney dysfunction.
3. Kidney function tests: Measurement of glomerular filtration rate (GFR) to determine the level of kidney function.
4. Urinalysis: Examination of urine for protein, blood, or white blood cells.

Imaging studies may include:

1. Ultrasound: To assess the size and shape of the kidneys, detect any blockages, and identify any other abnormalities.
2. Computed tomography (CT) scan: To provide detailed images of the kidneys and detect any obstructions or abscesses.
3. Magnetic resonance imaging (MRI): To evaluate the kidneys and detect any damage or scarring.

Treatment:

Treatment for chronic kidney failure depends on the underlying cause and the severity of the disease. The goals of treatment are to slow progression of the disease, manage symptoms, and improve quality of life. Treatment may include:

1. Medications: To control high blood pressure, lower cholesterol levels, reduce proteinuria, and manage anemia.
2. Diet: A healthy diet that limits protein intake, controls salt and water intake, and emphasizes low-fat dairy products, fruits, and vegetables.
3. Fluid management: Monitoring and control of fluid intake to prevent fluid buildup in the body.
4. Dialysis: A machine that filters waste products from the blood when the kidneys are no longer able to do so.
5. Transplantation: A kidney transplant may be considered for some patients with advanced chronic kidney failure.

Complications:

Chronic kidney failure can lead to several complications, including:

1. Heart disease: High blood pressure and anemia can increase the risk of heart disease.
2. Anemia: A decrease in red blood cells can cause fatigue, weakness, and shortness of breath.
3. Bone disease: A disorder that can lead to bone pain, weakness, and an increased risk of fractures.
4. Electrolyte imbalance: Imbalances of electrolytes such as potassium, phosphorus, and sodium can cause muscle weakness, heart arrhythmias, and other complications.
5. Infections: A decrease in immune function can increase the risk of infections.
6. Nutritional deficiencies: Poor appetite, nausea, and vomiting can lead to malnutrition and nutrient deficiencies.
7. Cardiovascular disease: High blood pressure, anemia, and other complications can increase the risk of cardiovascular disease.
8. Pain: Chronic kidney failure can cause pain, particularly in the back, flank, and abdomen.
9. Sleep disorders: Insomnia, sleep apnea, and restless leg syndrome are common complications.
10. Depression and anxiety: The emotional burden of chronic kidney failure can lead to depression and anxiety.

The most common parvoviridae infection in animals is feline panleukopenia (FPV) or canine parvovirus (CPV), which affects dogs and cats. These infections are highly contagious and can cause a range of symptoms, including fever, vomiting, diarrhea, lethargy, and loss of appetite. In severe cases, they can lead to life-threatening complications such as anemia, bone marrow failure, and death.

There is no specific treatment for parvoviridae infections, but supportive care such as fluid therapy, antibiotics, and anti-inflammatory medication can help manage symptoms and prevent complications. Vaccination is the most effective way to prevent parvoviridae infections, and vaccines are available for dogs, cats, and other animals.

In humans, parvoviridae infections are rare but can occur through contact with infected animals or contaminated feces. The most common human parvoviridae infection is erythema infectiosum (Fifth disease), which causes a rash, fever, and mild symptoms. Pregnant women who contract parvoviridae infections may experience complications such as miscarriage or preterm labor. There is no specific treatment for human parvoviridae infections, but supportive care can help manage symptoms.

The main symptoms of hereditary elliptocytosis are mild anemia, fatigue, jaundice, and splenomegaly (enlargement of the spleen). The disorder can also cause recurrent infections, including bacterial infections such as pneumonia and urinary tract infections. In severe cases, hereditary elliptocytosis can lead to a condition called hemolytic anemia, which is characterized by the premature destruction of RBCs.

Hereditary elliptocytosis is diagnosed through a combination of physical examination, medical history, and laboratory tests, including blood smears and genetic analysis. Treatment for the disorder is generally focused on managing symptoms and preventing complications. This may include blood transfusions, antibiotics to treat infections, and splenectomy (removal of the spleen) in severe cases.

The prognosis for hereditary elliptocytosis is generally good, with most individuals leading normal lives with proper management and care. However, the disorder can be inherited by children of affected parents, and genetic counseling may be helpful for families who have a history of the condition.

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.

What is a Chronic Disease?

A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:

1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke

Impact of Chronic Diseases

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.

Addressing Chronic Diseases

Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:

1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.

Conclusion

Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.

The term "hydrops" refers to the excessive accumulation of fluid in the body, and "fetalis" indicates that the condition occurs during fetal development. The condition is often diagnosed during the second or third trimester of pregnancy, and it can be associated with other congenital anomalies or genetic disorders.

The symptoms of hydrops fetalis can vary depending on the underlying cause, but they may include:

* Enlargement of the fetus
* Increased amniotic fluid levels
* Poor fetal growth
* Abnormalities in the ultrasound examination
* Premature birth or stillbirth

Hydrops fetalis is a serious condition that requires close monitoring and management by a multidisciplinary team of healthcare providers, including obstetricians, maternal-fetal medicine specialists, and perinatologists. Treatment options may include:

* Close monitoring of the pregnancy to detect any complications early
* Medications to help manage symptoms such as high blood pressure or heart failure
* Surgical interventions, such as amnioreduction or fetoscopy, to reduce fluid accumulation and improve fetal growth
* In some cases, delivery of the baby may be necessary, either through cesarean section or vaginal delivery.

The prognosis for hydrops fetalis is generally poor, with high rates of stillbirth and neonatal mortality. However, with early diagnosis and appropriate management, the outcome can be improved. It is important for pregnant women to seek medical attention immediately if they experience any symptoms or abnormalities that may indicate hydrops fetalis.

Sources:

1. Dictionary of Medical Microbiology, Second Edition. Edited by A. S. Chakrabarti and S. K. Das. Springer, 2012.
2. Medical Microbiology, Fourth Edition. Edited by P. R. Murray, K. S. N air, and M. J. Laurence. Mosby, 2014.

There are several types of diarrhea, including:

1. Acute diarrhea: This type of diarrhea is short-term and usually resolves on its own within a few days. It can be caused by a viral or bacterial infection, food poisoning, or medication side effects.
2. Chronic diarrhea: This type of diarrhea persists for more than 4 weeks and can be caused by a variety of conditions, such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), or celiac disease.
3. Diarrhea-predominant IBS: This type of diarrhea is characterized by frequent, loose stools and abdominal pain or discomfort. It can be caused by a variety of factors, including stress, hormonal changes, and certain foods.
4. Infectious diarrhea: This type of diarrhea is caused by a bacterial, viral, or parasitic infection and can be spread through contaminated food and water, close contact with an infected person, or by consuming contaminated food.

Symptoms of diarrhea may include:

* Frequent, loose, and watery stools
* Abdominal cramps and pain
* Bloating and gas
* Nausea and vomiting
* Fever and chills
* Headache
* Fatigue and weakness

Diagnosis of diarrhea is typically made through a physical examination, medical history, and laboratory tests to rule out other potential causes of the symptoms. Treatment for diarrhea depends on the underlying cause and may include antibiotics, anti-diarrheal medications, fluid replacement, and dietary changes. In severe cases, hospitalization may be necessary to monitor and treat any complications.

Prevention of diarrhea includes:

* Practicing good hygiene, such as washing hands frequently and thoroughly, especially after using the bathroom or before preparing food
* Avoiding close contact with people who are sick
* Properly storing and cooking food to prevent contamination
* Drinking safe water and avoiding contaminated water sources
* Avoiding raw or undercooked meat, poultry, and seafood
* Getting vaccinated against infections that can cause diarrhea

Complications of diarrhea can include:

* Dehydration: Diarrhea can lead to a loss of fluids and electrolytes, which can cause dehydration. Severe dehydration can be life-threatening and requires immediate medical attention.
* Electrolyte imbalance: Diarrhea can also cause an imbalance of electrolytes in the body, which can lead to serious complications.
* Inflammation of the intestines: Prolonged diarrhea can cause inflammation of the intestines, which can lead to abdominal pain and other complications.
* Infections: Diarrhea can be a symptom of an infection, such as a bacterial or viral infection. If left untreated, these infections can lead to serious complications.
* Malnutrition: Prolonged diarrhea can lead to malnutrition and weight loss, which can have long-term effects on health and development.

Treatment of diarrhea will depend on the underlying cause, but may include:

* Fluid replacement: Drinking plenty of fluids to prevent dehydration and replace lost electrolytes.
* Anti-diarrheal medications: Over-the-counter or prescription medications to slow down bowel movements and reduce diarrhea.
* Antibiotics: If the diarrhea is caused by a bacterial infection, antibiotics may be prescribed to treat the infection.
* Rest: Getting plenty of rest to allow the body to recover from the illness.
* Dietary changes: Avoiding certain foods or making dietary changes to help manage symptoms and prevent future episodes of diarrhea.

It is important to seek medical attention if you experience any of the following:

* Severe diarrhea that lasts for more than 3 days
* Diarrhea that is accompanied by fever, blood in the stool, or abdominal pain
* Diarrhea that is severe enough to cause dehydration or electrolyte imbalances
* Diarrhea that is not responding to treatment

Prevention of diarrhea includes:

* Good hand hygiene: Washing your hands frequently, especially after using the bathroom or before preparing food.
* Safe food handling: Cooking and storing food properly to prevent contamination.
* Avoiding close contact with people who are sick.
* Getting vaccinated against infections that can cause diarrhea, such as rotavirus.

Overall, while diarrhea can be uncomfortable and disruptive, it is usually a minor illness that can be treated at home with over-the-counter medications and plenty of fluids. However, if you experience severe or persistent diarrhea, it is important to seek medical attention to rule out any underlying conditions that may require more formal treatment.

Sickle cell trait is relatively common in certain populations, such as people of African, Mediterranean, or Middle Eastern descent. It is estimated that about 1 in 12 African Americans carry the sickle cell gene, and 1 in 500 are homozygous for the trait (meaning they have two copies of the sickle cell gene).

Although people with sickle cell trait do not develop sickle cell anemia, they can experience certain complications related to the trait. For example, they may experience episodes of hemolytic crisis, which is a condition in which red blood cells are destroyed faster than they can be replaced. This can occur under certain conditions, such as dehydration or infection.

There are several ways that sickle cell trait can affect an individual's life. For example, some people with the trait may experience discrimination or stigma based on their genetic status. Additionally, individuals with sickle cell trait may be more likely to experience certain health problems, such as kidney disease or eye damage, although these risks are generally low.

There is no cure for sickle cell trait, but it can be managed through proper medical care and self-care. Individuals with the trait should work closely with their healthcare provider to monitor their health and address any complications that arise.

Overall, sickle cell trait is a relatively common genetic condition that can have significant implications for an individual's life. It is important for individuals with the trait to understand their risk factors and take steps to manage their health and well-being.

1. Types of Hookworms: There are two main types of hookworms that can infect humans: Ancylostoma duodenale and Necator americanus. A. duodenale is more common in temperate climates, while N. americanus is found in tropical and subtropical regions.
2. Transmission: Hookworms are typically spread through contact with contaminated feces or soil. This can happen when someone ingests food or water that has been contaminated with hookworm eggs or larvae. In rare cases, hookworms can also be transmitted through blood transfusions or organ transplants.
3. Symptoms: The symptoms of hookworm infections can vary depending on the severity of the infection and the number of worms present. Common symptoms include diarrhea, abdominal pain, fatigue, weight loss, and anemia. In severe cases, hookworms can cause inflammation of the intestines, which can lead to complications such as bowel obstruction or perforation.
4. Diagnosis: Hookworm infections are typically diagnosed through a stool sample or blood test. A doctor may also perform a physical examination and take a medical history to help determine the presence of hookworms.
5. Treatment: Hookworm infections can be treated with antiparasitic medications, such as albendazole or mebendazole. These medications work by killing the worms in the intestines, which helps to relieve symptoms and prevent complications. In some cases, treatment may also involve addressing any underlying conditions that have been exacerbated by the hookworm infection, such as anemia or malnutrition.
6. Prevention: The best way to prevent hookworm infections is to practice good hygiene and avoid contact with contaminated feces or soil. This includes washing your hands frequently, especially after using the bathroom or before handling food. Additionally, wearing shoes when outdoors can help reduce the risk of contracting a hookworm infection through contact with contaminated soil.


Hemoglobin C disease is characterized by the presence of both normal hemoglobin (HbA) and abnormal hemoglobin (HbC) in red blood cells, which leads to a variety of symptoms and complications. The severity of the disease can range from mild to severe, depending on the specific mutations present and the percentage of HbC in the blood.

Symptoms of Hemoglobin C Disease:

The symptoms of hemoglobin C disease can vary in severity and may include:

1. Anemia: People with HbC disease often have lower than normal levels of red blood cells, which can lead to fatigue, weakness, and shortness of breath.
2. Jaundice: Yellowing of the skin and eyes due to high bilirubin levels can occur in severe cases of HbC disease.
3. Enlarged spleen: The spleen may become enlarged due to the accumulation of abnormal red blood cells.
4. Gallstones: People with HbC disease are at increased risk of developing gallstones.
5. Pain: Pain in the abdomen, joints, and other parts of the body can occur due to the abnormal hemoglobin.
6. Increased risk of infections: People with HbC disease may be more susceptible to infections due to their anemia and weakened immune system.
7. Delayed development: Children with HbC disease may experience delayed development and growth.

Complications of Hemoglobin C Disease:

Hemoglobin C disease can lead to a number of complications, including:

1. Stroke: People with HbC disease are at increased risk of stroke due to the abnormal hemoglobin.
2. Heart failure: The heart may become enlarged and fail to pump blood effectively due to the strain placed on it by the abnormal red blood cells.
3. Kidney damage: The kidneys may be damaged due to the accumulation of abnormal red blood cells.
4. Anemia: People with HbC disease may develop anemia, which can lead to fatigue, weakness, and shortness of breath.
5. Blood transfusions: Regular blood transfusions may be necessary to maintain healthy red blood cell levels.
6. Iron overload: The frequent blood transfusions can lead to iron overload, which can cause liver damage and other complications.
7. Increased risk of cancer: People with HbC disease may be at increased risk of developing certain types of cancer, such as leukemia.
8. Increased risk of thrombosis: The abnormal hemoglobin can increase the risk of blood clots and thrombosis.
9. Shortened lifespan: People with HbC disease may have a shorter lifespan compared to those without the condition.
10. Reduced quality of life: HbC disease can significantly impact an individual's quality of life, leading to fatigue, pain, and other symptoms that can affect daily activities and relationships.

It is important to note that these complications can be managed with proper medical care and attention. Regular monitoring and follow-up with a healthcare provider are crucial for managing the disease and preventing or minimizing these complications.

Falciparum malaria can cause a range of symptoms, including fever, chills, headache, muscle and joint pain, fatigue, nausea, and vomiting. In severe cases, the disease can lead to anemia, organ failure, and death.

Diagnosis of falciparum malaria typically involves a physical examination, medical history, and laboratory tests to detect the presence of parasites in the blood or other bodily fluids. Treatment usually involves the use of antimalarial drugs, such as artemisinin-based combination therapies (ACTs) or quinine, which can effectively cure the disease if administered promptly.

Prevention of falciparum malaria is critical to reducing the risk of infection, and this includes the use of insecticide-treated bed nets, indoor residual spraying (IRS), and preventive medications for travelers to high-risk areas. Eliminating standing water around homes and communities can also help reduce the number of mosquitoes and the spread of the disease.

In summary, falciparum malaria is a severe and life-threatening form of malaria caused by the Plasmodium falciparum parasite, which is responsible for the majority of malaria-related deaths worldwide. Prompt diagnosis and treatment are essential to prevent complications and death from this disease. Prevention measures include the use of bed nets, indoor spraying, and preventive medications, as well as reducing standing water around homes and communities.

There are several possible causes of methemoglobinemia, including:

1. Exposure to certain medications or chemicals, such as nitrates or aniline dyes.
2. Genetic disorders that affect the production or function of hemoglobin.
3. Infections, such as bacterial infections of the blood or respiratory tract.
4. Poor nutrition or malnutrition.
5. Certain chronic medical conditions, such as sickle cell anemia or thalassemia.

Methemoglobinemia can be diagnosed through a variety of tests, including:

1. Complete blood count (CBC) to measure the levels of methemoglobin in the blood.
2. Blood gas analysis to measure the partial pressure of oxygen and carbon dioxide in the blood.
3. Co-oximetry to measure the levels of methemoglobin and other forms of hemoglobin.
4. Urine tests to check for the presence of abnormal hemoglobin.
5. Genetic testing to identify inherited disorders that may be causing the condition.

Treatment of methemoglobinemia depends on the underlying cause and may include:

1. Administration of oxygen therapy to increase the amount of oxygen in the blood.
2. Use of medications to reduce the levels of methemoglobin and increase the levels of normal hemoglobin.
3. Transfusions of red blood cells to replace abnormal hemoglobin with normal hemoglobin.
4. Management of underlying medical conditions, such as infections or genetic disorders.
5. Dietary changes to address any nutritional deficiencies that may be contributing to the condition.

In severe cases of methemoglobinemia, hospitalization may be necessary to provide oxygen therapy and other treatments. In some cases, patients with methemoglobinemia may require long-term management and follow-up care to prevent complications and manage the underlying cause of the condition.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Types of Kidney Diseases:

1. Acute Kidney Injury (AKI): A sudden and reversible loss of kidney function that can be caused by a variety of factors, such as injury, infection, or medication.
2. Chronic Kidney Disease (CKD): A gradual and irreversible loss of kidney function that can lead to end-stage renal disease (ESRD).
3. End-Stage Renal Disease (ESRD): A severe and irreversible form of CKD that requires dialysis or a kidney transplant.
4. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste products.
5. Interstitial Nephritis: An inflammation of the tissue between the tubules and blood vessels in the kidneys.
6. Kidney Stone Disease: A condition where small, hard mineral deposits form in the kidneys and can cause pain, bleeding, and other complications.
7. Pyelonephritis: An infection of the kidneys that can cause inflammation, damage to the tissues, and scarring.
8. Renal Cell Carcinoma: A type of cancer that originates in the cells of the kidney.
9. Hemolytic Uremic Syndrome (HUS): A condition where the immune system attacks the platelets and red blood cells, leading to anemia, low platelet count, and damage to the kidneys.

Symptoms of Kidney Diseases:

1. Blood in urine or hematuria
2. Proteinuria (excess protein in urine)
3. Reduced kidney function or renal insufficiency
4. Swelling in the legs, ankles, and feet (edema)
5. Fatigue and weakness
6. Nausea and vomiting
7. Abdominal pain
8. Frequent urination or polyuria
9. Increased thirst and drinking (polydipsia)
10. Weight loss

Diagnosis of Kidney Diseases:

1. Physical examination
2. Medical history
3. Urinalysis (test of urine)
4. Blood tests (e.g., creatinine, urea, electrolytes)
5. Imaging studies (e.g., X-rays, CT scans, ultrasound)
6. Kidney biopsy
7. Other specialized tests (e.g., 24-hour urinary protein collection, kidney function tests)

Treatment of Kidney Diseases:

1. Medications (e.g., diuretics, blood pressure medication, antibiotics)
2. Diet and lifestyle changes (e.g., low salt intake, increased water intake, physical activity)
3. Dialysis (filtering waste products from the blood when the kidneys are not functioning properly)
4. Kidney transplantation ( replacing a diseased kidney with a healthy one)
5. Other specialized treatments (e.g., plasmapheresis, hemodialysis)

Prevention of Kidney Diseases:

1. Maintaining a healthy diet and lifestyle
2. Monitoring blood pressure and blood sugar levels
3. Avoiding harmful substances (e.g., tobacco, excessive alcohol consumption)
4. Managing underlying medical conditions (e.g., diabetes, high blood pressure)
5. Getting regular check-ups and screenings

Early detection and treatment of kidney diseases can help prevent or slow the progression of the disease, reducing the risk of complications and improving quality of life. It is important to be aware of the signs and symptoms of kidney diseases and seek medical attention if they are present.

Examples of pregnancy complications, parasitic include:

1. Toxoplasmosis: This is a condition caused by the Toxoplasma gondii parasite, which can infect the mother and/or the fetus during pregnancy. Symptoms include fever, headache, and fatigue. In severe cases, toxoplasmosis can cause birth defects, such as intellectual disability, blindness, and deafness.
2. Malaria: This is a condition caused by the Plasmodium spp. parasite, which can be transmitted to the mother and/or the fetus during pregnancy. Symptoms include fever, chills, and flu-like symptoms. In severe cases, malaria can cause anemia, organ failure, and death.
3. Schistosomiasis: This is a condition caused by the Schistosoma spp. parasite, which can infect the mother and/or the fetus during pregnancy. Symptoms include abdominal pain, diarrhea, and fatigue. In severe cases, schistosomiasis can cause organ damage and infertility.

Pregnancy complications, parasitic can be diagnosed through blood tests, imaging studies, and other medical procedures. Treatment depends on the type of parasite and the severity of the infection. In some cases, treatment may involve antibiotics, antimalarial drugs, or anti-parasitic medications.

Preventive measures for pregnancy complications, parasitic include:

1. Avoiding contact with cat feces, as Toxoplasma gondii can be transmitted through contaminated soil and food.
2. Avoiding travel to areas where malaria and other parasitic infections are common.
3. Taking antimalarial medications before and during pregnancy if living in an area where malaria is common.
4. Using insecticide-treated bed nets and wearing protective clothing to prevent mosquito bites.
5. Practicing good hygiene, such as washing hands regularly, especially after handling food or coming into contact with cats.
6. Avoiding drinking unpasteurized dairy products and undercooked meat, as these can increase the risk of infection.
7. Ensuring that any water used for cooking or drinking is safe and free from parasites.

Preventive measures for pregnancy complications, parasitic are important for women who are pregnant or planning to become pregnant, as well as for their partners and healthcare providers. By taking these preventive measures, the risk of infection and complications can be significantly reduced.

In conclusion, pregnancy complications, parasitic are a serious issue that can have severe consequences for both the mother and the fetus. However, by understanding the causes, risk factors, symptoms, diagnosis, treatment, and preventive measures, women can take steps to protect themselves and their unborn babies from these infections. It is important for healthcare providers to be aware of these issues and provide appropriate education and care to pregnant women to reduce the risk of complications.

FAQs
1. What are some common parasitic infections that can occur during pregnancy?
Ans: Some common parasitic infections that can occur during pregnancy include malaria, toxoplasmosis, and cytomegalovirus (CMV).
2. How do parasitic infections during pregnancy affect the baby?
Ans: Parasitic infections during pregnancy can have serious consequences for the developing fetus, including birth defects, growth restriction, and stillbirth.
3. Can parasitic infections during pregnancy be treated?
Ans: Yes, parasitic infections during pregnancy can be treated with antibiotics and other medications. Early detection and treatment are important to prevent complications.
4. How can I prevent parasitic infections during pregnancy?
Ans: Preventive measures include avoiding areas where parasites are common, using insect repellents, wearing protective clothing, and practicing good hygiene. Pregnant women should also avoid undercooked meat and unpasteurized dairy products.
5. Do all pregnant women need to be tested for parasitic infections?
Ans: No, not all pregnant women need to be tested for parasitic infections. However, certain groups of women, such as those who live in areas where parasites are common or have a history of previous parasitic infections, may need to be tested and monitored more closely.
6. Can I prevent my baby from getting a parasitic infection during pregnancy?
Ans: Yes, there are several steps you can take to reduce the risk of your baby getting a parasitic infection during pregnancy, such as avoiding certain foods and taking antibiotics if necessary. Your healthcare provider can provide guidance on how to prevent and treat parasitic infections during pregnancy.
7. How are parasitic infections diagnosed during pregnancy?
Ans: Parasitic infections can be diagnosed through blood tests, stool samples, or imaging tests such as ultrasound or MRI. Your healthcare provider may also perform a physical exam and take a medical history to determine the likelihood of a parasitic infection.
8. Can parasitic infections cause long-term health problems for my baby?
Ans: Yes, some parasitic infections can cause long-term health problems for your baby, such as developmental delays or learning disabilities. In rare cases, parasitic infections can also lead to more serious complications, such as organ damage or death.
9. How are parasitic infections treated during pregnancy?
Ans: Treatment for parasitic infections during pregnancy may involve antibiotics, antiparasitic medications, or other supportive care. Your healthcare provider will determine the best course of treatment based on the severity and type of infection, as well as your individual circumstances.
10. Can I take steps to prevent parasitic infections during pregnancy?
Ans: Yes, there are several steps you can take to prevent parasitic infections during pregnancy, such as avoiding undercooked meat and fish, washing fruits and vegetables thoroughly, and practicing good hygiene. Additionally, if you have a higher risk of parasitic infections due to travel or other factors, your healthcare provider may recommend preventative medications or screening tests.
11. I'm pregnant and have been exposed to a parasitic infection. What should I do?
Ans: If you suspect that you have been exposed to a parasitic infection during pregnancy, it is important to seek medical attention immediately. Your healthcare provider can perform tests to determine if you have an infection and provide appropriate treatment to prevent any potential complications for your baby.
12. Can I breastfeed while taking medication for a parasitic infection?
Ans: It may be safe to breastfeed while taking medication for a parasitic infection, but it is important to consult with your healthcare provider before doing so. Some medications may not be safe for your baby and could potentially be passed through your milk. Your healthcare provider can provide guidance on the safest treatment options for you and your baby.
13. What are some common complications of parasitic infections during pregnancy?
Ans: Complications of parasitic infections during pregnancy can include miscarriage, preterm labor, low birth weight, and congenital anomalies. In rare cases, parasitic infections can also be transmitted to the baby during pregnancy or childbirth, which can lead to serious health problems for the baby.
14. Can I get a parasitic infection from my pet?
Ans: Yes, it is possible to get a parasitic infection from your pet if you come into contact with their feces or other bodily fluids. For example, toxoplasmosis can be transmitted through contact with cat feces, while hookworm infections can be spread through contact with contaminated soil or feces. It is important to practice good hygiene and take precautions when handling pets or coming into contact with potentially contaminated areas.
15. How can I prevent parasitic infections?
Ans: Preventing parasitic infections involves taking steps to avoid exposure to parasites and their vectors, as well as practicing good hygiene and taking precautions when traveling or engaging in activities that may put you at risk. Some ways to prevent parasitic infections include:
* Avoiding undercooked meat, especially pork and wild game
* Avoiding raw or unpasteurized dairy products
* Avoiding contaminated water and food
* Washing your hands frequently, especially after using the bathroom or before handling food
* Avoiding contact with cat feces, as toxoplasmosis can be transmitted through contact with cat feces
* Using protective clothing and insect repellent when outdoors in areas where parasites are common
* Keeping your home clean and free of clutter to reduce the risk of parasite infestations
* Avoiding touching or eating wild animals or plants that may be contaminated with parasites
16. What are some common misconceptions about parasitic infections?
Ans: There are several common misconceptions about parasitic infections, including:
* All parasites are the same and have similar symptoms
* Parasitic infections are only a problem for people who live in developing countries or have poor hygiene
* Only certain groups of people, such as children or pregnant women, are at risk for parasitic infections
* Parasitic infections are rare in developed countries
* All parasites can be treated with antibiotics
* Parasitic infections are not serious and do not require medical attention
17. How can I diagnose a parasitic infection?
Ans: Diagnosing a parasitic infection typically involves a combination of physical examination, medical history, and laboratory tests. Some common methods for diagnosing parasitic infections include:
* Physical examination to look for signs such as skin lesions or abdominal pain
* Blood tests to check for the presence of parasites or their waste products
* Stool tests to detect the presence of parasite eggs or larvae
* Imaging tests, such as X-rays or CT scans, to look for signs of parasite infection in internal organs
* Endoscopy, which involves inserting a flexible tube with a camera into the body to visualize the inside of the digestive tract and other organs.
18. How are parasitic infections treated?
Ans: Treatment for parasitic infections depends on the type of parasite and the severity of the infection. Some common methods for treating parasitic infections include:
* Antiparasitic drugs, such as antibiotics or antimalarials, to kill the parasites
* Supportive care, such as fluids and electrolytes, to manage symptoms and prevent complications
* Surgery to remove parasites or repair damaged tissues
* Antibiotics to treat secondary bacterial infections that may have developed as a result of the parasitic infection.
It is important to seek medical attention if you suspect that you have a parasitic infection, as untreated infections can lead to serious complications and can be difficult to diagnose.
19. How can I prevent parasitic infections?
Ans: Preventing parasitic infections involves taking steps to avoid contact with parasites and their vectors, as well as maintaining good hygiene practices. Some ways to prevent parasitic infections include:
* Avoiding undercooked meat and unpasteurized dairy products, which can contain harmful parasites such as Trichinella spiralis and Toxoplasma gondii
* Washing your hands frequently, especially after using the bathroom or before eating
* Avoiding contact with contaminated water or soil, which can harbor parasites such as Giardia and Cryptosporidium
* Using insecticides and repellents to prevent mosquito bites, which can transmit diseases such as malaria and dengue fever
* Wearing protective clothing and applying insect repellent when outdoors in areas where ticks and other vectors are common
* Avoiding contact with animals that may carry parasites, such as dogs and cats that can transmit Toxoplasma gondii
* Using clean water and proper sanitation to prevent the spread of parasitic infections in communities and developing countries.
It is also important to be aware of the risks of parasitic infections when traveling to areas where they are common, and to take appropriate precautions such as avoiding undercooked meat and unpasteurized dairy products, and using insecticides and repellents to prevent mosquito bites.
20. What is the prognosis for parasitic infections?
Ans: The prognosis for parasitic infections varies depending on the specific type of infection and the severity of symptoms. Some parasitic infections can be easily treated with antiparasitic medications, while others may require more extensive treatment and management.
In general, the prognosis for parasitic infections is good if the infection is detected early and properly treated. However, some parasitic infections can cause long-term health problems or death if left untreated. It is important to seek medical attention if symptoms persist or worsen over time.
It is also important to note that some parasitic infections can be prevented through public health measures such as using clean water and proper sanitation, and controlling the spread of insect vectors. Prevention is key to avoiding the negative outcomes associated with these types of infections.
21. What are some common complications of parasitic infections?
Ans: Some common complications of parasitic infections include:
* Anemia and other blood disorders, such as thrombocytopenia and leukopenia
* Allergic reactions to parasite antigens
* Inflammation and damage to organs and tissues, such as the liver, kidneys, and brain
* Increased risk of infections with other microorganisms, such as bacteria and viruses
* Malnutrition and deficiencies in essential nutrients
* Organ failure and death.
22. Can parasitic infections be prevented? If so, how?
Ans: Yes, some parasitic infections can be prevented through public health measures such as:
* Using clean water and proper sanitation to reduce the risk of ingesting infected parasites.
* Avoiding contact with insect vectors, such as mosquitoes and ticks, by using repellents, wearing protective clothing, and staying indoors during peak biting hours.
* Properly cooking and storing food to kill parasites that may be present.
* Avoiding consuming undercooked or raw meat, especially pork and wild game.
* Practicing safe sex to prevent the transmission of parasitic infections through sexual contact.
* Keeping children away from areas where they may come into contact with contaminated soil or water.
* Using antiparasitic drugs and other treatments as recommended by healthcare providers.
* Implementing control measures for insect vectors, such as spraying insecticides and removing breeding sites.
30. Can parasitic infections be treated with antibiotics? If so, which ones and why?
Ans: No, antibiotics are not effective against parasitic infections caused by protozoa, such as giardiasis and amoebiasis, because these organisms are not bacteria. However, antibiotics may be used to treat secondary bacterial infections that can develop as a complication of parasitic infections.
32. What is the difference between a parasite and a pathogen?
Ans: A parasite is an organism that lives on or in another organism, called the host, and feeds on the host's tissues or fluids without providing any benefits. A pathogen, on the other hand, is an organism that causes disease. While all parasites are pathogens, not all pathogens are parasites. For example, bacteria and viruses can cause diseases but are not considered parasites because they do not live within the host's body.

People with pica may eat these items in secret and experience a sense of relief or satisfaction after consuming them. The condition is more common in children and adolescents, but it can also affect adults. Pica can lead to nutritional deficiencies, gastrointestinal problems, and other health issues if the eaten items are not digestible or contain harmful substances.

Treatment for pica usually involves addressing any underlying mental health issues and providing education on nutrition and healthy eating habits. In some cases, medication may be prescribed to help manage symptoms. It is important to seek medical attention if you or someone you know is experiencing symptoms of pica, as early intervention can help prevent complications and improve overall health.

There are several possible causes of hyperbilirubinemia, including:

1. Hemolytic anemia: This is a condition where red blood cells are broken down faster than they can be replaced, leading to an accumulation of bilirubin in the blood.
2. Liver dysfunction: The liver plays a crucial role in processing and eliminating bilirubin from the body. If the liver is not functioning properly, bilirubin levels can become elevated.
3. Sepsis: This is a systemic infection that can cause inflammation throughout the body, including the liver, which can disrupt the normal processing of bilirubin.
4. Neonatal jaundice: This is a condition that affects newborn babies and is caused by an immature liver that is unable to process bilirubin quickly enough.

Symptoms of hyperbilirubinemia can include yellowing of the skin and whites of the eyes (jaundice), dark urine, pale or clay-colored stools, and fatigue. In severe cases, hyperbilirubinemia can lead to kernicterus, a condition that can cause brain damage and hearing loss.

Diagnosis of hyperbilirubinemia is typically made through blood tests that measure the level of bilirubin in the blood. Treatment depends on the underlying cause of the condition and may include blood transfusions, liver function tests, and phototherapy (exposure to light) to help break down bilirubin. In severe cases, hospitalization may be necessary to monitor and treat the condition.

Examples of autoimmune diseases include:

1. Rheumatoid arthritis (RA): A condition where the immune system attacks the joints, leading to inflammation, pain, and joint damage.
2. Lupus: A condition where the immune system attacks various body parts, including the skin, joints, and organs.
3. Hashimoto's thyroiditis: A condition where the immune system attacks the thyroid gland, leading to hypothyroidism.
4. Multiple sclerosis (MS): A condition where the immune system attacks the protective covering of nerve fibers in the central nervous system, leading to communication problems between the brain and the rest of the body.
5. Type 1 diabetes: A condition where the immune system attacks the insulin-producing cells in the pancreas, leading to high blood sugar levels.
6. Guillain-Barré syndrome: A condition where the immune system attacks the nerves, leading to muscle weakness and paralysis.
7. Psoriasis: A condition where the immune system attacks the skin, leading to red, scaly patches.
8. Crohn's disease and ulcerative colitis: Conditions where the immune system attacks the digestive tract, leading to inflammation and damage to the gut.
9. Sjögren's syndrome: A condition where the immune system attacks the glands that produce tears and saliva, leading to dry eyes and mouth.
10. Vasculitis: A condition where the immune system attacks the blood vessels, leading to inflammation and damage to the blood vessels.

The symptoms of autoimmune diseases vary depending on the specific disease and the organs or tissues affected. Common symptoms include fatigue, fever, joint pain, skin rashes, and swollen lymph nodes. Treatment for autoimmune diseases typically involves medication to suppress the immune system and reduce inflammation, as well as lifestyle changes such as dietary changes and stress management techniques.

Some common types of fish diseases include:

1. Bacterial infections: These are caused by bacteria such as Aeromonas, Pseudomonas, and Mycobacterium. Symptoms can include fin and tail rot, body slime, and ulcers.
2. Viral infections: These are caused by viruses such as viral hemorrhagic septicemia (VHS) and infectious hematopoietic necrosis (IHN). Symptoms can include lethargy, loss of appetite, and rapid death.
3. Protozoan infections: These are caused by protozoa such as Cryptocaryon and Ichthyophonus. Symptoms can include flashing, rapid breathing, and white spots on the body.
4. Fungal infections: These are caused by fungi such as Saprolegnia and Achlya. Symptoms can include fuzzy growths on the body and fins, and sluggish behavior.
5. Parasitic infections: These are caused by parasites such as Ichthyophonus and Cryptocaryon. Symptoms can include flashing, rapid breathing, and white spots on the body.

Diagnosis of fish diseases is typically made through a combination of physical examination, laboratory tests, and observation of the fish's behavior and environment. Treatment options vary depending on the type of disease and the severity of symptoms, and can include antibiotics, antifungals, and medicated baths. Prevention is key in managing fish diseases, and this includes maintaining good water quality, providing a balanced diet, and keeping the fish in a healthy environment.

Note: The information provided is a general overview of common fish diseases and their symptoms, and should not be considered as professional medical advice. If you suspect your fish has a disease, it is recommended that you consult with a veterinarian or a qualified aquarium expert for proper diagnosis and treatment.

Examples of syndromes include:

1. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21 that affects intellectual and physical development.
2. Turner syndrome: A genetic disorder caused by a missing or partially deleted X chromosome that affects physical growth and development in females.
3. Marfan syndrome: A genetic disorder affecting the body's connective tissue, causing tall stature, long limbs, and cardiovascular problems.
4. Alzheimer's disease: A neurodegenerative disorder characterized by memory loss, confusion, and changes in personality and behavior.
5. Parkinson's disease: A neurological disorder characterized by tremors, rigidity, and difficulty with movement.
6. Klinefelter syndrome: A genetic disorder caused by an extra X chromosome in males, leading to infertility and other physical characteristics.
7. Williams syndrome: A rare genetic disorder caused by a deletion of genetic material on chromosome 7, characterized by cardiovascular problems, developmental delays, and a distinctive facial appearance.
8. Fragile X syndrome: The most common form of inherited intellectual disability, caused by an expansion of a specific gene on the X chromosome.
9. Prader-Willi syndrome: A genetic disorder caused by a defect in the hypothalamus, leading to problems with appetite regulation and obesity.
10. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dry eyes and mouth.

Syndromes can be diagnosed through a combination of physical examination, medical history, laboratory tests, and imaging studies. Treatment for a syndrome depends on the underlying cause and the specific symptoms and signs presented by the patient.

1. Parvovirus (Parvo): A highly contagious viral disease that affects dogs of all ages and breeds, causing symptoms such as vomiting, diarrhea, and severe dehydration.
2. Distemper: A serious viral disease that can affect dogs of all ages and breeds, causing symptoms such as fever, coughing, and seizures.
3. Rabies: A deadly viral disease that affects dogs and other animals, transmitted through the saliva of infected animals, and causing symptoms such as aggression, confusion, and paralysis.
4. Heartworms: A common condition caused by a parasitic worm that infects the heart and lungs of dogs, leading to symptoms such as coughing, fatigue, and difficulty breathing.
5. Ticks and fleas: These external parasites can cause skin irritation, infection, and disease in dogs, including Lyme disease and tick-borne encephalitis.
6. Canine hip dysplasia (CHD): A genetic condition that affects the hip joint of dogs, causing symptoms such as arthritis, pain, and mobility issues.
7. Osteosarcoma: A type of bone cancer that affects dogs, often diagnosed in older dogs and causing symptoms such as lameness, swelling, and pain.
8. Allergies: Dog allergies can cause skin irritation, ear infections, and other health issues, and may be triggered by environmental factors or specific ingredients in their diet.
9. Gastric dilatation-volvulus (GDV): A life-threatening condition that occurs when a dog's stomach twists and fills with gas, causing symptoms such as vomiting, pain, and difficulty breathing.
10. Cruciate ligament injuries: Common in active dogs, these injuries can cause joint instability, pain, and mobility issues.

It is important to monitor your dog's health regularly and seek veterinary care if you notice any changes or abnormalities in their behavior, appetite, or physical condition.

Examples of acute diseases include:

1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.

Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.

1. Protein-energy malnutrition (PEM): This type of malnutrition is caused by a lack of protein and energy in the diet. It is common in developing countries and can lead to weight loss, weakness, and stunted growth in children.
2. Iron deficiency anemia: This type of malnutrition is caused by a lack of iron in the diet, which is necessary for the production of hemoglobin in red blood cells. Symptoms include fatigue, weakness, and shortness of breath.
3. Vitamin and mineral deficiencies: Malnutrition can also be caused by a lack of essential vitamins and minerals such as vitamin A, vitamin D, calcium, and iodine. Symptoms vary depending on the specific deficiency but can include skin problems, impaired immune function, and poor wound healing.
4. Obesity: This type of malnutrition is caused by consuming too many calories and not enough nutrients. It can lead to a range of health problems including diabetes, high blood pressure, and heart disease.

Signs and symptoms of malnutrition can include:

* Weight loss or weight gain
* Fatigue or weakness
* Poor wound healing
* Hair loss
* Skin problems
* Increased infections
* Poor appetite or overeating
* Digestive problems such as diarrhea or constipation
* Impaired immune function

Treatment for malnutrition depends on the underlying cause and may include:

* Dietary changes: Eating a balanced diet that includes a variety of nutrient-rich foods can help to correct nutrient deficiencies.
* Nutritional supplements: In some cases, nutritional supplements such as vitamins or minerals may be recommended to help address specific deficiencies.
* Medical treatment: Certain medical conditions that contribute to malnutrition, such as digestive disorders or infections, may require treatment with medication or other interventions.

Prevention is key, and there are several steps you can take to help prevent malnutrition:

* Eat a balanced diet that includes a variety of nutrient-rich foods.
* Avoid restrictive diets or fad diets that limit specific food groups.
* Stay hydrated by drinking plenty of water.
* Avoid excessive alcohol consumption, which can interfere with nutrient absorption and lead to malnutrition.
* Maintain a healthy weight through a combination of a balanced diet and regular exercise.

It is important to note that malnutrition can be subtle and may not always be easily recognizable. If you suspect you or someone you know may be experiencing malnutrition, it is important to seek medical attention to receive an accurate diagnosis and appropriate treatment.

Jaundice is typically diagnosed through physical examination and laboratory tests such as blood tests to measure bilirubin levels. Treatment depends on the underlying cause, but may include medications to reduce bilirubin production or increase its excretion, or surgery to remove blockages in the bile ducts.

Here are some of the synonyms for Jaundice:

1. Yellow fever
2. Yellow jaundice
3. Hepatitis
4. Gallstones
5. Cholestasis
6. Obstruction of the bile ducts
7. Biliary tract disease
8. Hemochromatosis
9. Sickle cell anemia
10. Crigler-Najjar syndrome

Here are some of the antonyms for Jaundice:

1. Pinkness
2. Normal skin color
3. Healthy liver function
4. Bilirubin levels within normal range
5. No signs of liver disease or obstruction of bile ducts.

There are two main types of Renal Insufficiency:

1. Acute Kidney Injury (AKI): This is a sudden and reversible decrease in kidney function, often caused by injury, sepsis, or medication toxicity. AKI can resolve with appropriate treatment and supportive care.
2. Chronic Renal Insufficiency (CRI): This is a long-standing and irreversible decline in kidney function, often caused by diabetes, high blood pressure, or chronic kidney disease. CRI can lead to ESRD if left untreated.

Signs and symptoms of Renal Insufficiency may include:

* Decreased urine output
* Swelling in the legs and ankles (edema)
* Fatigue
* Nausea and vomiting
* Shortness of breath (dyspnea)
* Pain in the back, flank, or abdomen

Diagnosis of Renal Insufficiency is typically made through a combination of physical examination, medical history, laboratory tests, and imaging studies. Laboratory tests may include urinalysis, blood urea nitrogen (BUN) and creatinine levels, and a 24-hour urine protein collection. Imaging studies, such as ultrasound or CT scans, may be used to evaluate the kidneys and rule out other possible causes of the patient's symptoms.

Treatment of Renal Insufficiency depends on the underlying cause and the severity of the condition. Treatment may include medications to control blood pressure, manage fluid balance, and reduce proteinuria (excess protein in the urine). In some cases, dialysis or a kidney transplant may be necessary.

Prevention of Renal Insufficiency includes managing underlying conditions such as diabetes and hypertension, avoiding nephrotoxic medications and substances, and maintaining a healthy diet and lifestyle. Early detection and treatment of acute kidney injury can also help prevent the development of chronic renal insufficiency.

In conclusion, Renal Insufficiency is a common condition that can have significant consequences if left untreated. It is important for healthcare providers to be aware of the causes, symptoms, and diagnosis of Renal Insufficiency, as well as the treatment and prevention strategies available. With appropriate management, many patients with Renal Insufficiency can recover and maintain their kidney function over time.

1. Leukemia: A type of cancer that affects the blood and bone marrow, characterized by an overproduction of immature white blood cells.
2. Lymphoma: A type of cancer that affects the immune system, often involving the lymph nodes and other lymphoid tissues.
3. Multiple myeloma: A type of cancer that affects the plasma cells in the bone marrow, leading to an overproduction of abnormal plasma cells.
4. Myelodysplastic syndrome (MDS): A group of disorders characterized by the impaired development of blood cells in the bone marrow.
5. Osteopetrosis: A rare genetic disorder that causes an overgrowth of bone, leading to a thickened bone marrow.
6. Bone marrow failure: A condition where the bone marrow is unable to produce enough blood cells, leading to anemia, infection, and other complications.
7. Myelofibrosis: A condition characterized by the scarring of the bone marrow, which can lead to an overproduction of blood cells and an increased risk of bleeding and infection.
8. Polycythemia vera: A rare blood disorder that causes an overproduction of red blood cells, leading to an increased risk of blood clots and other complications.
9. Essential thrombocythemia: A rare blood disorder that causes an overproduction of platelets, leading to an increased risk of blood clots and other complications.
10. Myeloproliferative neoplasms (MPNs): A group of rare blood disorders that are characterized by the overproduction of blood cells and an increased risk of bleeding and infection.

These are just a few examples of bone marrow diseases. There are many other conditions that can affect the bone marrow, and each one can have a significant impact on a person's quality of life. If you suspect that you or someone you know may have a bone marrow disease, it is important to seek medical attention as soon as possible. A healthcare professional can perform tests and provide a proper diagnosis and treatment plan.

Some common types of streptococcal infections include:

1. Strep throat (pharyngitis): an infection of the throat and tonsils that can cause fever, sore throat, and swollen lymph nodes.
2. Sinusitis: an infection of the sinuses (air-filled cavities in the skull) that can cause headache, facial pain, and nasal congestion.
3. Pneumonia: an infection of the lungs that can cause cough, fever, chills, and shortness of breath.
4. Cellulitis: an infection of the skin and underlying tissue that can cause redness, swelling, and warmth over the affected area.
5. Endocarditis: an infection of the heart valves, which can cause fever, fatigue, and swelling in the legs and abdomen.
6. Meningitis: an infection of the membranes covering the brain and spinal cord that can cause fever, headache, stiff neck, and confusion.
7. Septicemia (blood poisoning): an infection of the bloodstream that can cause fever, chills, rapid heart rate, and low blood pressure.

Streptococcal infections are usually treated with antibiotics, which can help clear the infection and prevent complications. In some cases, hospitalization may be necessary to monitor and treat the infection.

Prevention measures for streptococcal infections include:

1. Good hygiene practices, such as washing hands frequently, especially after contact with someone who is sick.
2. Avoiding close contact with people who have streptococcal infections.
3. Keeping wounds and cuts clean and covered to prevent bacterial entry.
4. Practicing safe sex to prevent the spread of streptococcal infections through sexual contact.
5. Getting vaccinated against streptococcus pneumoniae, which can help prevent pneumonia and other infections caused by this bacterium.

It is important to seek medical attention if you suspect you or someone else may have a streptococcal infection, as early diagnosis and treatment can help prevent complications and improve outcomes.

The symptoms of hypoproteinemia can vary depending on the underlying cause and severity of the condition. Some common symptoms include:

1. Weakness and fatigue
2. Loss of appetite
3. Nausea and vomiting
4. Diarrhea or constipation
5. Skin, hair, and nail problems
6. Increased risk of infections
7. Muscle wasting and loss of muscle mass
8. Poor wound healing
9. Hair loss
10. Edema (swelling)

If you suspect that you or someone you know may have hypoproteinemia, it is important to consult a healthcare professional for proper diagnosis and treatment. A healthcare provider will typically perform a physical examination, take a medical history, and order blood tests to determine the levels of protein and other essential nutrients in the body.

Treatment of hypoproteinemia depends on the underlying cause of the condition. In cases where the condition is caused by malnutrition or dietary deficiencies, dietary modifications and supplements may be recommended. For example, a patient with hypoproteinemia due to malnutrition may need to consume more protein-rich foods, such as meat, poultry, fish, eggs, dairy products, legumes, and nuts. In cases where the condition is caused by an underlying medical condition, such as liver or kidney disease, treatment may involve managing the underlying condition.

It is important to note that hypoproteinemia can lead to serious complications if left untreated, such as muscle wasting, poor wound healing, and increased risk of infections. Therefore, it is crucial to seek medical attention if you suspect that you or someone you know may have hypoproteinemia.

In summary, hypoproteinemia is a condition characterized by low levels of protein in the blood. It can be caused by various factors, such as malnutrition, liver or kidney disease, and other medical conditions. Treatment options depend on the underlying cause of the condition, and early diagnosis and treatment are crucial to prevent complications. If you suspect that you or someone you know may have hypoproteinemia, it is essential to consult a healthcare professional for proper diagnosis and treatment.

In healthy individuals, the normal platelet count ranges from 150,000 to 450,000 platelets per microliter of blood. In thrombocytosis, the platelet count is significantly higher than this range, often above 600,000 platelets/μL.

Thrombocytosis can be caused by a variety of factors, including:

1. Bone marrow disorders: Disorders such as essential thrombocythemia, polycythemia vera, and myelofibrosis can lead to an overproduction of platelets in the bone marrow.
2. Infection: Sepsis and other infections can cause a temporary increase in platelet production.
3. Inflammation: Certain inflammatory conditions, such as appendicitis and pancreatitis, can also lead to thrombocytosis.
4. Cancer: Some types of cancer, such as leukemia and lymphoma, can cause an overproduction of platelets.
5. Medications: Certain medications, such as estrogens and corticosteroids, can increase platelet production.

Thrombocytosis can lead to a range of complications, including:

1. Blood clots: The excessive number of platelets in the blood can increase the risk of blood clots forming in the veins and arteries.
2. Pulmonary embolism: If a blood clot forms in the lungs, it can cause a pulmonary embolism, which can be life-threatening.
3. Stroke: Thrombocytosis can increase the risk of stroke, especially if there are existing risk factors such as high blood pressure or a history of cardiovascular disease.
4. Heart attack and heart failure: Excessive platelet activity can increase the risk of heart attack and heart failure.
5. Gastrointestinal bleeding: The increased number of platelets in the blood can make it more difficult to control bleeding, especially in the gastrointestinal tract.

Thrombocytosis is typically diagnosed through a combination of physical examination, medical history, and laboratory tests, such as:

1. Complete blood count (CBC): This test measures the number of platelets in the blood, as well as other components such as red and white blood cells.
2. Blood smear: A sample of blood is examined under a microscope to assess the shape and size of the platelets.
3. Bone marrow aspiration and biopsy: These tests involve removing a small sample of bone marrow tissue to examine the number and type of cells present.
4. Imaging studies: Imaging tests such as ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) may be used to look for evidence of blood clots or other complications.

Treatment for thrombocytosis depends on the underlying cause and the severity of the condition. Some common treatments include:

1. Medications: Drugs such as aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners may be used to reduce the risk of blood clots and other complications.
2. Plateletpheresis: This is a procedure in which the patient's blood is removed and the platelets are separated from the rest of the blood components. The remaining blood is then returned to the body.
3. Splenectomy: In some cases, surgical removal of the spleen may be necessary to treat thrombocytosis.
4. Chemotherapy: This is a treatment that uses drugs to kill cancer cells, which can cause thrombocytosis in some cases.

Overall, it is important to seek medical attention if you experience any symptoms of thrombocytosis, as early diagnosis and treatment can help prevent complications and improve outcomes.

The definition of AKI has evolved over time, and it is now defined as a syndrome characterized by an abrupt or rapid decrease in kidney function, with or without oliguria (decreased urine production), and with evidence of tubular injury. The RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria are commonly used to diagnose and stage AKI based on serum creatinine levels, urine output, and other markers of kidney damage.

There are three stages of AKI, with stage 1 representing mild injury and stage 3 representing severe and potentially life-threatening injury. Treatment of AKI typically involves addressing the underlying cause, correcting fluid and electrolyte imbalances, and providing supportive care to maintain blood pressure and oxygenation. In some cases, dialysis may be necessary to remove waste products from the blood.

Early detection and treatment of AKI are crucial to prevent long-term damage to the kidneys and improve outcomes for patients.

There are two main types of PTP:

1. Type 1: This is the most common form of PTP, and it is caused by a defect in the ADAMTS13 gene. This gene helps to regulate the activity of platelets and is essential for their proper function.
2. Type 2: This type of PTP is less common and is caused by mutations in other genes that are involved in platelet formation and function.

PTP can be diagnosed with a combination of physical examination, medical history, and laboratory tests. Treatment options for the condition include platelet transfusions, medications to increase platelet production, and surgery to remove any abnormal platelets from the bloodstream. In severe cases, bone marrow transplantation may be necessary.

While there is no cure for PTP, with proper treatment, people with this condition can lead relatively normal lives and reduce their risk of complications. It is important for individuals with PTP to avoid activities that could cause injury or trauma, take precautions to prevent bleeding, and seek medical attention promptly if they experience any signs of bleeding or bruising.

Neonatal jaundice can be caused by a variety of factors, including:

* Immaturity of the liver and biliary system, which can lead to an inability to process bilirubin properly
* Infection or sepsis
* Breastfeeding difficulties or poor milk intake
* Blood type incompatibility between the baby and mother
* Genetic disorders such as Crigler-Najjar syndrome
* Other medical conditions such as hypothyroidism or anemia

Symptoms of neonatal jaundice may include:

* Yellowing of the skin and whites of the eyes
* Dark-colored urine
* Pale or clay-colored stools
* Lack of appetite or poor feeding
* Lethargy or irritability

Treatment for neonatal jaundice may include:

* Phototherapy, which involves exposure to blue light to help break down bilirubin in the blood
* Exchange transfusion, which involves replacing some of the baby's blood with fresh blood to lower bilirubin levels
* Medication to stimulate bowel movements and increase the elimination of bilirubin
* Intravenous fluids to prevent dehydration

In some cases, neonatal jaundice may be a sign of a more serious underlying condition, such as a liver or gallbladder disorder. It is important for parents to seek medical attention if they notice any signs of jaundice in their newborn baby, particularly if the baby is feeding poorly or appears lethargic or irritable.

White blood cells are an important part of the immune system, and they help to fight off infections and diseases. A low number of white blood cells can make a person more susceptible to infections and other health problems.

There are several different types of leukopenia, including:

* Severe congenital neutropenia: This is a rare genetic disorder that causes a severe decrease in the number of neutrophils, a type of white blood cell.
* Chronic granulomatous disease: This is a genetic disorder that affects the production of white blood cells and can cause recurring infections.
* Autoimmune disorders: These are conditions where the immune system mistakenly attacks its own cells, including white blood cells. Examples include lupus and rheumatoid arthritis.
* Bone marrow failure: This is a condition where the bone marrow does not produce enough white blood cells, red blood cells, or platelets.

Symptoms of leukopenia can include recurring infections, fever, fatigue, and weight loss. Treatment depends on the underlying cause of the condition and may include antibiotics, immunoglobulin replacement therapy, or bone marrow transplantation.

Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.

In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.

1. Feline Leukemia Virus (FeLV): This is a highly contagious virus that weakens the immune system, making cats more susceptible to other infections and cancer.
2. Feline Immunodeficiency Virus (FIV): Similar to HIV in humans, this virus attacks the immune system and can lead to a range of secondary infections and diseases.
3. Feline Infectious Peritonitis (FIP): A viral disease that causes fluid accumulation in the abdomen and chest, leading to difficulty breathing and abdominal pain.
4. Feline Lower Urinary Tract Disease (FLUTD): A group of conditions that affect the bladder and urethra, including urinary tract infections and kidney stones.
5. Feline Diabetes: Cats can develop diabetes, which can lead to a range of complications if left untreated, including urinary tract infections, kidney disease, and blindness.
6. Feline Hyperthyroidism: An overactive thyroid gland that can cause weight loss, anxiety, and heart problems if left untreated.
7. Feline Cancer: Cats can develop various types of cancer, including lymphoma, leukemia, and skin cancer.
8. Dental disease: Cats are prone to dental problems, such as tartar buildup, gum disease, and tooth resorption.
9. Obesity: A common problem in cats, obesity can lead to a range of health issues, including diabetes, arthritis, and heart disease.
10. Behavioral disorders: Cats can develop behavioral disorders such as anxiety, stress, and aggression, which can impact their quality of life and relationships with humans.

It's important to note that many of these diseases can be prevented or managed with proper care, including regular veterinary check-ups, vaccinations, parasite control, a balanced diet, exercise, and mental stimulation. Additionally, early detection and treatment can significantly improve the outcome for cats with health issues.

The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.

There are several subtypes of LES, including:

1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.

There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.

It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.

Hellp Syndrome is a medical emergency that requires immediate attention. Treatment typically involves providing supportive care, such as oxygen therapy, mechanical ventilation, and fluid and electrolyte replacement, as well as addressing the underlying cause of the syndrome, such as preeclampsia or eclampsia. In severe cases, delivery of the baby may be necessary to prevent further complications.

AIHA can be classified as warm autoimmune hemolytic anemia or cold autoimmune hemolytic anemia, which includes cold agglutinin ... Autoimmune hemolytic anemia, Acquired hemolytic anemia, Autoimmune diseases, Transfusion medicine). ... The National Cancer Institute considers "immunohemolytic anemia", "autoimmune hemolytic anemia", and "immune complex hemolytic ... and hemolytic anemias so produced are autoimmune hemolytic anemias. In general, AIHA in children has a good prognosis and is ...
... (MAIHA) is a type of autoimmune hemolytic anemia which combines the features of cold ... "Orphanet: Autoimmune hemolytic anemia, warm type". Orphanet. 2019-02-14. Retrieved 2019-02-15. Das, SudiptaSekhar; Chakrabarty ... Berentsen, Sigbjørn; Sundic, Tatjana (2015-01-29). "Red Blood Cell Destruction in Autoimmune Hemolytic Anemia: Role of ... Berentsen, Sigbjørn; Sundic, Tatjana (2015-01-29). "Red Blood Cell Destruction in Autoimmune Hemolytic Anemia: Role of ...
AIHA can be classified as warm autoimmune hemolytic anemia or cold autoimmune hemolytic anemia, which includes cold agglutinin ... Cold autoimmune hemolytic anemia, Acquired hemolytic anemia, Autoimmune diseases, Transfusion medicine). ... Autoimmune hemolytic anemia Warm-antibody type Primary Secondary (lymphoproliferative disorders, autoimmune disorders) : 259 ... autoimmune disorders) Drug-induced immune hemolytic anemia : 259 Autoimmune type Drug absorption type Neoantigen type Cold ...
... is a form of hemolytic anemia. In some cases, a drug can cause the immune system to ... It is known that more than 150 drugs can cause this type of hemolytic anemia. The list includes : Cephalosporins (a class of ... MedlinePlus Encyclopedia: Drug-induced immune hemolytic anemia Stroncek, David; Procter, Jo L.; Johnson, Judy (2000). "Drug- ... Cefotetan-dependent hemolytic anemia mimicking an acute intravascular immune transfusion reaction". American Journal of ...
... (WAIHA) is the most common form of autoimmune haemolytic anemia. About half of the ... Contrary to cold autoimmune hemolytic anemia (e.g., cold agglutinin disease and paroxysmal cold hemoglobinuria) which happens ... 2001 Nowak-Wegrzyn A, King KE, Shirey RS, Chen AR, McDonough C, Lederman HM (May 2001). "Fatal warm autoimmune hemolytic anemia ... ISBN 0-7216-0187-1. AUTOIMMUNE HEMOLYTIC ANEMIA (AIHA) Archived 2009-10-07 at the Wayback Machine By J.L. Jenkins. The Regional ...
Autoimmune diseases, Cold autoimmune hemolytic anemia, Acquired hemolytic anemia, Transfusion medicine). ... induced hemolytic response inside vessels leading to anemia and, thus, a cold antibody autoimmune hemolytic anemias (CAAHA). In ... For example, there was a case study reporting that autoimmune hemolytic anemia where an IgA Donath-Landsteiner denoted as [D-L ... Göttsche, B; Salama, A; Mueller-Eckhardt, C (1990). "Donath-Landsteiner autoimmune hemolytic anemia in children. A study of 22 ...
"Autoimmune hemolytic anemia , Genetic and Rare Diseases Information Center (GARD) - an NCATS Program". rarediseases.info.nih. ... autoimmune hemolytic anemia). Hypothyroidism and chronic kidney disease Parasitic infestations: some examples are hookworm or ... conditions such as iron-deficiency anemia or anemia as a result of an infection). The causes of anemia during pregnancy can be ... The majority of women presenting with postpartum anemia have pre-delivery iron deficiency anemia or iron deficiency anemia ...
... or permanent factors as in autoimmune diseases like autoimmune hemolytic anemia (itself more common in diseases such as ... Hemolytic anemia or haemolytic anaemia is a form of anemia due to hemolysis, the abnormal breakdown of red blood cells (RBCs), ... Low-grade hemolytic anemia occurs in 70% of prosthetic heart valve recipients, and severe hemolytic anemia occurs in 3%. In ... In cold hemolytic anemia there is advantage in transfusing warmed blood. In severe immune-related hemolytic anemia, steroid ...
... autoimmune hemolytic anemia, hemolysis secondary to drug toxicity, thalassemia minor, and congenital dyserythropoietic anemias ... Brodsky RA (August 2019). "Warm Autoimmune Hemolytic Anemia". The New England Journal of Medicine. 381 (7): 647-654. doi: ... Autoimmune hemolytic anemia (AIHA), in which autoantibodies react with self red blood cells and cause their destruction. This ... If chronic hemolytic jaundice is diagnosed in a newborn, development of anemia and bilirubin cholelithiasis should be monitored ...
Acquired Autoimmune Hemolytic Anemia Allgood, JW; Chaplin, H Jr (1967). "Idiopathic acquired autoimmune hemolytic anemia. A ... Berentsen, Sigbjørn; Sundic, Tatjana (2015-01-29). "Red Blood Cell Destruction in Autoimmune Hemolytic Anemia: Role of ... Barcellini, W (2015), "Pitfalls in the diagnosis of autoimmune haemolytic anaemia.", Blood Transfusion = Trasfusione del Sangue ... "Type-specific cold auto-antibodies as a cause of acquired hemolytic anemia and hemolytic transfusion reactions: biologic test ...
Autoimmune diseases, Acquired hemolytic anemia, Cold autoimmune hemolytic anemia). ... hemolytic anemia List of hematologic conditions Paroxysmal cold hemoglobinuria Warm antibody autoimmune hemolytic anemia "Cold ... It is a form of autoimmune hemolytic anemia, specifically one in which antibodies bind red blood cells only at low body ... Dacie, J. (1992). "Auto-immune haemolytic anaemia (AIHA): Cold antibody syndromes I: Idiopathic types: Clinical presentation ...
"Autoimmune hemolytic anemia: current knowledge and perspectives". Immunity & Ageing. 17 (1): 38. doi:10.1186/s12979-020-00208-7 ... leading to anemia. Rarely, individuals have the i antigen on their red blood cells into adulthood, known as the adult i ... may have developed as an evolutionary mechanism to prevent ABO hemolytic disease of the fetus and newborn. Enhanced expression ...
... abnormalities Antibody-mediated Warm autoimmune hemolytic anemia is caused by autoimmune attack against red blood cells, ... Causes include: Acute blood loss Anemia of chronic disease Aplastic anemia (bone marrow failure) Hemolytic anemia A dimorphic ... ISBN 978-0-7216-0187-8. "Autoimmune Hemolytic Anemia (AIHA)" By J.L. Jenkins. The Regional Cancer Center. 2001 Archived October ... The causes of anemia may be classified as impaired red blood cell (RBC) production, increased RBC destruction (hemolytic anemia ...
In autoimmune hemolytic anemia, concentrations of HbA1 is undetectable. Administration of prednisolone will allow the HbA1 to ... "Undetectable Glycosolated Hemoglobin in Autoimmune Hemolytic Anemia" (PDF). repository.oai.yamaguchi-u.ac.jp. Retrieved 2009-08 ... hemolytic anemia, or genetic differences in the hemoglobin molecule (hemoglobinopathy) such as sickle-cell disease and other ... Results can be unreliable in many circumstances, for example after blood loss, after surgery, blood transfusions, anemia, or ...
"Autoimmune Hemolytic Anemia and Red Blood Cell Autoantibodies". Archives of Pathology & Laboratory Medicine. 139 (11): 1455-8. ... When a person produces antibodies against their own red blood cells, as in cold agglutinin disease and other autoimmune ...
Autoimmune hemolytic anemia is an autoimmune blood disorder. Sebaceous adenitis is an autoimmune skin disorder believed to be ... Day, M.J (1999). "Antigen specificity in canine autoimmune haemolytic anaemia". Veterinary Immunology and Immunopathology. 69 ( ... Hypothyroidism, also known as autoimmune hypothyroidism, is an autoimmune disease that affects the thyroid gland. Other ... Many autoimmune diseases are known to occur in the Akita, including: Vogt-Koyanagi-Harada syndrome, also known as uveo- ...
Rare patients with MBL may present with the autoimmune disease-induced cytopenias of hemolytic anemia (reduced circulating red ... autoimmune hemolytic anemia and immune thrombocytopenic purpura; 3) unexplained kidney disease as manifested by chronic kidney ... cases of CLL/SLL MBL associated with an autoimmune disease were diagnosed as CLL/SLL. However, patients with these autoimmune ... are best diagnosed as CLL/SLL MBL with autoimmune cytopenia rather than CLL/SLL. Monoclonal CLL/SLL phenotype B cells have been ...
Quist, Erin; Koepsell, Scott (2015). "Autoimmune Hemolytic Anemia and Red Blood Cell Autoantibodies". Archives of Pathology & ... 13 and warm autoimmune hemolytic anemia.: 88 In cases of red cell agglutination, the direct antiglobulin test can be used to ... a type of autoimmune hemolytic anemia in which people produce antibodies (termed cold agglutinins) that bind to their red blood ... People with warm autoimmune hemolytic anemia may exhibit red cell agglutination that does not resolve on warming.: 88 Bain, BJ ...
June 1998). "Severe autoimmune hemolytic anemia in eight patients treated with fludarabine". Hematology and Cell Therapy. 40 (3 ... Fludarabine is associated with the development of severe autoimmune hemolytic anemia in a proportion of patients. Difficulties ... Fludarabine causes anemia, thrombocytopenia and neutropenia, requiring regular blood count monitoring. Some patients require ...
These include autoimmune hemolytic anemia, autoimmune neutropenia, and autoimmune thrombocytopenia. Other autoimmune ... The most common autoimmune presentations include autoimmune cytopenias, which can be mild to very severe and intermittent or ... Another sign is autoimmune cytopenias and polyclonal hypergammaglobulinemia and a family history of ALPS or non-malignant ... No longer considered a subtype of ALPS but distinct disease Treatment is most commonly directed at autoimmune disease and may ...
Its overall phenotype resembles a combination of autoimmune hemolytic anemia and immune thrombocytopenic purpura. Autoimmune ... Liu H, Shao Z, Jing L (2001). "[The effectiveness of cyclosporin A in the treatment of autoimmune hemolytic anemia and Evans ... Cai JR, Yu QZ, Zhang FQ (1989). "[Autoimmune hemolytic anemia: clinical analysis of 100 cases]". Zhonghua Nei Ke Za Zhi (in ... It has been variously reported that between 7.8% and 23% of patients who have autoimmune hemolytic anemia, will also have ...
One patient with severe autoimmune hemolytic anemia responded well to rituximab. Blocking IL-6 activation with tocilizumab in ... Hematologic autoimmunity is most prevalent including autoimmune hemolytic anemia, neutropenia, and/or thrombocytopenia. Others ... Of the two patients treated by HCT, one patient died and the other was cured of autoimmune symptoms and improved growth. Larger ... Germline gain-of-function (GOF) mutations in the gene STAT3 causes this early-onset autoimmune disease characterized by ...
... this mouse has a high incidence of spontaneous autoimmune hemolytic anemia. They looked at the inheritance of autoimmune ... In 1963, Autoimmune Diseases: Pathogenesis, Chemistry and Therapy, which he authored with Ian Mackay, was published. He also ... The last project he worked on at the Institute was a study with assistant Margaret Holmes of autoimmune disease in the New ... His theory predicted almost all of the key features of the immune system as we understand it today, including autoimmune ...
AIHA can be classified as warm autoimmune hemolytic anemia or cold autoimmune hemolytic anemia, which includes cold agglutinin ... Autoimmune hemolytic anemia Warm-antibody type Primary Secondary (lymphoproliferative disorders, autoimmune disorders): 259 ... autoimmune disorders) Drug-induced immune hemolytic anemia: 259 Autoimmune type Drug absorption type Neoantigen type Acute PCH ... On excluding warm autoimmune hemolytic anemia (WAIHA), the cold agglutinin titer should be examined for cold agglutinin disease ...
Warm autoimmune hemolytic anemia Cold autoimmune hemolytic anemia/paroxysmal cold hemoglobinuria Acute and delayed hemolytic ... Spherocytes are found in all hemolytic anemias to some degree. Hereditary spherocytosis and autoimmune hemolytic anemia are ... Spherocytes are found in immunologically-mediated hemolytic anemias and in hereditary spherocytosis, but the former would have ... Anemia Blood Blood diseases Red blood cells Hereditary diseases Robert S. Hillman; Kenneth A. Ault; Henry M. Rinder (2005). ...
It has not been associated with autoimmune hemolytic anemia of the fetus. However, it does cause difficulty in the blood bank ...
The multiple inflammatory developments include nonspecific lymphadenopathy, hepatosplenomegaly, and autoimmune hemolytic anemia ... in 2010 and titled Joint contractures, Muscular Atrophy, Microcytic anemia, and Panniculitis-induced Lipodystrophy (JMP) ... microcytic anemia, and panniculitis-associated lipodystrophy". The Journal of Clinical Endocrinology and Metabolism. Endocrine ...
One case of autoimmune hemolytic anemia involving auto-anti-Lan has been described. Serologic reagents and molecular assays for ... It has been associated with severe transfusion reactions and mild cases of hemolytic disease of the newborn, but in some cases ... and have also been implicated in mild cases of hemolytic disease of the newborn. However, the clinical significance of the ... when a Dutch patient suffered a severe hemolytic transfusion reaction.: 220 : 489 The patient was found to produce an antibody ...
... autoimmune haemolytic anaemia. These associations are not completely specific and should not be relied upon solely for ... PBC is seen primarily in middle-aged women, and in those afflicted with other autoimmune diseases. Several of the antigens ... the autoimmune disease primary biliary cirrhosis (PBC; also known as primary biliary cholangitis). PBC causes scarring of liver ... autoimmune hepatitis; M1 - syphilis; M3 - drug-induced lupus erythematosus; M6 - drug-induced hepatitis; M7 - cardiomyopathy, ...
"Autoimmune Hemolytic Anemia". The Merck Manuals: Online Medical Library. Merck Sharp and Dohme. Retrieved 25 March 2011. " ... "Anemia of prematurity". Retrieved 2010-05-31. Aplastic anemia at Mount Sinai Hospital [1] at Mount Sinai Hospital "Hemolytic ... "Spur-cell hemolytic anemia in severe alcoholic cirrhosis". Blood. The American Society of Hematology. 101 (1): 3-4. January 1, ... Reviewed by Vorvick, Linda J.; Chen, Yi-Bin (31 January 2010). "Hemolytic anemia". Pub Med Health. National Center for ...
Brodsky RA (November 2015). "Complement in hemolytic anemia". Blood. 126 (22): 2459-65. doi:10.1182/blood-2015-06-640995. PMID ... CHAPLE syndrome is characterized by complement-mediated autoimmune hemolysis and paroxysmal nocturnal hemoglobinuria. The ...
... some autoimmune disorders (e.g., autoimmune haemolytic anaemia, drug-induced hemolytic anemia, atypical hemolytic uremic ... Low-grade hemolytic anemia occurs in 70% of prosthetic heart valve recipients, and severe hemolytic anemia occurs in 3%. ... or permanent factors as in autoimmune diseases like autoimmune hemolytic anemia (itself more common in diseases such as ... Lead poisoning or poisoning by arsine or stibine causes non-immune hemolytic anemia. Runners can develop hemolytic anemia due ...
... hemolytic anemias 283.0 Autoimmune hemolytic anemias Warm autoimmune hemolytic anemia 283.1 Non-autoimmune hemolytic anemias ... anemia 285.1 Acute posthemorrhagic anemia 285.2 Anemia in chronic illness 285.21 Anemia in chronic kidney disease 285.22 Anemia ... 280 Iron deficiency anemias 280.0 Iron deficiency anemia secondary to blood loss (chronic) 280.1 Iron deficiency anemia ... Anemia of other chronic illness 285.3 Antineoplastic chemotherapy induced anemia 285.8 Other specified anemias 285.9 Anemia ...
... which is abnormal and can occur in conditions like autoimmune hemolytic anemia, hemolytic disease of the newborn and ... Serological tests may be performed to diagnose infections and autoimmune illnesses, to check if a person has immunity to ... Serologic tests can help to diagnose autoimmune disorders by identifying abnormal antibodies directed against a person's own ... in instances of autoimmune disease). In either case, the procedure is simple.[citation needed] Serological tests are diagnostic ...
... warm autoimmune hemolytic anemia in 10-15% of patients, and bone marrow failure. Chronic lymphocytic leukemia may also develop ... Enlargement of the spleen and low red blood cells (anemia) may also occur. It typically worsens gradually over years. Risk ... anemia, or thrombocytopenia Stage II: characterized by absolute lymphocytosis with either hepatomegaly or splenomegaly with or ... anemia, or thrombocytopenia Stage I: characterized by absolute lymphocytosis with lymphadenopathy without hepatosplenomegaly, ...
Ice Hockey Association American Industrial Hygiene Association Austrian Ice Hockey Association Autoimmune haemolytic anaemia ...
Gelen SA, Kara B, Şimsek IE, Güngör M, Zengin E, Sarper N (2021-11-02). "Autoimmune Hemolytic Anemia Due to ... hemolytic anemia, and hypothyroidism. This subset of symptoms affects the central nervous system. These include ataxia, muscle ... This subset of symptoms primarily affects the immune system (immunodeficiency) and also causes autoimmune diseases, which ... causing autoimmune diseases and resulting in the disruption of other systems such as the hematological one), the neurological ...
The cause of hemolytic crises in this disease is unknown (mainly due to intravascular haemolysis). There is rapid and massive ... Within a few days of onset there are chills, with rigor, high fever, jaundice, vomiting, rapidly progressive anemia, and dark ... The most probable explanation for blackwater fever is an autoimmune reaction apparently caused by the interaction of the ...
This can occur in hemolytic anemia and idiopathic thrombocytopenic purpura A normal eosinophil count is considered to be less ... Some are autoimmune, but many are neoplastic. Another way to categorize disorders of white blood cells is qualitatively. There ... It is occasionally abnormal, when it is neoplastic or autoimmune in origin. A decrease below the lower limit is called ... aplastic anemia Infectious diseases - viral (AIDS, SARS, West Nile encephalitis, hepatitis, herpes, measles, others), bacterial ...
... autoimmune hemolytic anemia and food allergy. IPEX syndrome is inherited in males via an x-linked recessive manner, as the ... Autoimmune polyendocrine syndrome FOXP3 Autoimmune polyendocrine syndrome type 2 "Orphanet: Immune dysregulation ... The disorder is one of the autoimmune polyendocrine syndromes and manifests with autoimmune enteropathy, psoriasiform or ... autoimmune anemia and decreased number of FOXP3 Treg cells. Genetic testing: single-gene testing and multigene panel. In terms ...
SEC23B Anemia, hemolytic, due to UMPH1 deficiency; 266120; NT5C3 Anemia, hemolytic, Rh-null, regulator type; 268150; RHAG ... CASP10 Autoimmune lymphoproliferative syndrome, type IIB; 607271; CASP8 Autoimmune polyendocrinopathy syndrome, type I, with or ... SLC40A1 Hemolytic anemia due to adenylate kinase deficiency; 612631; AK1 Hemolytic anemia due to gamma-glutamylcysteine ... GCLC Hemolytic anemia due to glutathione synthetase deficiency; 231900; GSS Hemolytic anemia due to hexokinase deficiency; ...
While there may be a link between hydroxychloroquine and hemolytic anemia in those with glucose-6-phosphate dehydrogenase ... Fox R (June 1996). "Anti-malarial drugs: possible mechanisms of action in autoimmune disease and prospects for drug development ... "Examination of Hydroxychloroquine Use and Hemolytic Anemia in G6PDH-Deficient Patients". Arthritis Care & Research. 70 (3): 481 ... Chloroquine and hydroxychloroquine are anti-malarial medications also used against some auto-immune diseases. Chloroquine, ...
... hemolytic anemia Donath-Landsteiner syndrome: an autoimmune hemolytic anemia featured by complement-mediated ...
Hematology: acquired (autoimmune) hemolytic anemia, idiopathic thrombocytopenic purpura, secondary thrombocytopenia, ... erythroblastopenia, leukemia, lymphoma and congenital (erythroid) hypoplastic anemia. Pulmonary: aspiration pneumonitis, ...
... hemolytic anemia, limbic encephalopathy, myocarditis, nephrotic syndrome, panhypopituitarism, pernicious anemia, polymyositis, ... Additional associated autoimmune conditions include thymoma-associated multiorgan autoimmunity, pure red cell aplasia and Good ... One-third of patients have their tumors discovered because they have an associated autoimmune disorder. As mentioned earlier, ... "Thymoma associated with autoimmune diseases: 85 cases and literature review". Autoimmunity Reviews. 15 (1): 82-92. doi:10.1016/ ...
Mycoplasma atypical pneumonia can be complicated by Stevens-Johnson syndrome, autoimmune hemolytic anemia, cardiovascular ...
Arrhythmias Skin pigmentation Glycosuria Hypoglycaemia Paralytic ileus Agranulocytosis Haemolytic anaemia Aplastic anaemia A-V ... An autoimmune condition in of which the body's defences attack the neuromuscular junction - the gap between muscle and nerve ... high blood pressure A dangerous skin reaction An autoimmune reaction A potentially fatal collection of symptoms (i.e. syndrome ...
... as well as the mechanism by which penicillin-class drugs cause autoimmune hemolytic anemia. Other haptens that are commonly ... Some haptens can induce autoimmune disease. An example is hydralazine, a blood pressure-lowering drug that occasionally can ... Toxin Antigen Erkes, Dan; Selvan, Senthamil (2014). "Hapten-Induced Contact Hypersensitivity, Autoimmune Reactions, and Tumor ... to induce autoimmune-like responses. The concept of haptens emerged from the work of Austrian immunologist Karl Landsteiner, ...
... hemolytic anemia, thrombosis, hepatitis, anaphylaxis, backache, aseptic meningitis, acute kidney injury, hypokalemic ... The results add to the understanding of how immunoglobulin may affect inflammation of the central nervous system in autoimmune ... August 2008). "Hemolytic transfusion reactions after administration of intravenous immune (gamma) globulin: a case series ... Immunoglobulin therapy is also used for a number of other conditions, including in many autoimmune disorders such as ...
... suggests hemolytic jaundice as the underlying disease process. Urobilinogen will be greater than 2 units, as hemolytic anemia ... autoimmune etiology, or less commonly, due to inheritable genetic diseases. The following is a partial list of hepatic causes ... Thalassemia Pyruvate kinase deficiency Glucose-6-phosphate dehydrogenase deficiency Microangiopathic hemolytic anemia Hemolytic ... "What causes jaundice in hemolytic anemia?". www.medscape.com. Retrieved 26 April 2022. "What Is Sickle Cell Disease?". National ...
Blood-hematologic disorder-hemolytic anemia (low red blood cell count), leukopenia (white blood cell count. 3.0.CO;2-F. PMID ... SLE is regarded as a prototype disease due to the significant overlap in its symptoms with other autoimmune diseases. Drug- ... Anemia is common in children with SLE and develops in about 50% of cases. Low platelet count and white blood cell count may be ... Fatigue in SLE is probably multifactorial and has been related to not only disease activity or complications such as anemia or ...
... had been reported in a few cases to effectively treat acne, but the risk of hemolytic anemia kept it from being widely ... Liang SE, Hoffmann R, Peterson E, Soter NA (2019). "Use of Dapsone in the Treatment of Chronic Idiopathic and Autoimmune ... It may lead to hemolytic anemia and methemoglobinemia. The side-effect is more common and severe in those with glucose-6- ... Sanders SW, Zone JJ, Foltz RL, Tolman KG, Rollins DE (April 1982). "Hemolytic anemia induced by dapsone transmitted through ...
In past there have been reports showing that in patients with sickle cell disease, spherocytosis, autoimmune hemolytic anemia, ... A low Hx level is one of the diagnostic features of an intravascular hemolytic anemia. Hx has been implicated in cardiovascular ... "Bilirubin and hemolytic anemia". eClinpath. Retrieved 2019-05-08. Online Mendelian Inheritance in Man (OMIM): Orthosatic ... and underlies the rationale for exogenous Hp and Hx as therapeutic proteins in hemolytic or hemorrhagic conditions. Hemopexin ...
Antibodies directed against red blood cell surface antigens in immune mediated hemolytic anemia are detected with the Coombs ... autoimmune hepatitis and cirrhosis. Autoimmune disorders can often be traced to antibodies that bind the body's own epitopes; ... Urbaniak SJ, Greiss MA (March 2000). "RhD haemolytic disease of the fetus and the newborn". Blood Reviews. 14 (1): 44-61. doi: ... Dean L (2005). "Chapter 4: Hemolytic disease of the newborn". Blood Groups and Red Cell Antigens. NCBI Bethesda (MD): National ...
... autoimmune hemolytic anemia, enlargements of liver and/or spleen and lymphadenopathy) plus symptoms of multiple myelomas. ... autoimmune hemolytic anemia) require treatments used in chronic lymphocytic leukemia. Some patients who lack appreciable ... and cold-induced hemolytic anemia. IgM, IgG, and to lesser extents κ and λ free light chain myeloma proteins can cause Immune ... In this study the only factor predictive of a more rapid progress was a finding of anemia (hemoglobin level 0.5 grams and/or ...
Atypical hemolytic uremic syndrome Austrian syndrome Autoimmune disease Autoimmune lymphoproliferative syndrome Autoimmune ... lysis syndrome Tumor necrosis factor receptor associated periodic syndrome Turner syndrome Twiddler's syndrome Twin Anemia- ... polyendocrine syndrome type 1 Autoimmune polyendocrine syndrome type 2 Autoimmune polyendocrine syndrome type 3 Autoimmune ... Hemihyperplasia-multiple lipomatosis syndrome Hemimegalencephaly Hemispatial neglect Hemoglobin Lepore syndrome Hemolytic- ...
Autoimmune hemolytic anemia (AIHA) is a heterogeneous disease mainly due to autoantibody-mediated destruction of erythrocytes ... Current and emerging treatment options for autoimmune hemolytic anemia Expert Rev Clin Immunol. 2018 Oct;14(10):857-872. doi: ... Autoimmune hemolytic anemia (AIHA) is a heterogeneous disease mainly due to autoantibody-mediated destruction of erythrocytes ...
Despite its widespread use, dydrogesterone-induced hepatotoxicity and dydrogesterone-induced hemolytic anemia have, to the best ... A case of autoimmune hepatitis and autoimmune hemolytic anemia following hepatitis A infection. Urganci N, Akyildiz B, ... Dydrogesterone-induced hepatitis and autoimmune hemolytic anemia Engin Altintaş 1 , Dilek Oğuz, Sabite Kaçar, Yasemin Ozderin, ... Dydrogesterone-induced hepatitis and autoimmune hemolytic anemia Engin Altintaş et al. Turk J Gastroenterol. 2004 Mar. ...
Common Variable Immunodeficiency, Autoimmune Hemolytic Anemia, and Pancytopenia Associated With a Defect in IKAROS Ebru Yilmaz ... Common Variable Immunodeficiency, Autoimmune Hemolytic Anemia, and Pancytopenia Associated With a Defect in IKAROS Ebru Yilmaz ... autoimmune hemolytic anemia (AIHA), and malignancies. In this study, we aimed to assess the DNA-binding ability and ... autoimmune diseases, and hematologic malignancies. Diverse clinical phenotypes resulting from IKZF1 mutations include pulmonary ...
Learn about Autoimmune Hemolytic Anemia and which treatments are most effective in stopping your body from attacking its own ... Autoimmune Hemolytic Anemia When the body fights its own red blood cells. Autoimmune Hemolytic Anemia (AIHA) is a blood disease ... This results in anemia.. The body will try to make up for this loss by increasing the red blood cell production in the bone ... The anemia can be a long-standing problem for many.. Antibody production against red blood cells is also associated with ...
Data Registry of Auto Immune Hemolytic Anemia A Study of INCB050465 in Participants With Autoimmune Hemolytic Anemia ... ALXN1830 in Patients With Warm Autoimmune Hemolytic Anemia Efficacy and Safety of M281 in Adults With Warm Autoimmune Hemolytic ... A Study of Obexelimab in Patients With Warm Autoimmune Hemolytic Anemia (SApHiAre) Ibrutinib for the Treatment of AIHA in ... A Study of Efficacy and Safety of Ianalumab in Previously Treated Patients With Warm Autoimmune Hemolytic Anemia Efficacy of ...
CONCLUSION: Autoimmune hemolytic anemia is an uncommon cause of hemolytic anemia in children. Tubercular infection is an ... Autoimmune hemolytic anemia. Indian Journal of Pediatrics. 2008 May; 75(5): 451-4. ... Twelve children were diagnosed with auto immune hemolytic anemia over a period of four years. Direct antiglobulin test was ... To study the clinico-hematological profile and treatment outcome in children suffering from auto immune hemolytic anemia (AIHA ...
AIHA can be classified as warm autoimmune hemolytic anemia or cold autoimmune hemolytic anemia, which includes cold agglutinin ... The National Cancer Institute considers "immunohemolytic anemia", "autoimmune hemolytic anemia", and "immune complex hemolytic ... and hemolytic anemias so produced are autoimmune hemolytic anemias. In children. In general, AIHA in children has a good ... Although MeSH uses the term "autoimmune hemolytic anemia", some sources prefer the term "immunohemolytic anemia" so drug ...
Autoimmune hemolytic anaemia (AIHA) has traditionally been classified based on the temperature sensitivity of the ... Clinical Profile and Severity of Hemolysis in Adult Patients of Primary Autoimmune Hemolytic Anemia and Their Response to ... Laboratory investigations were performed to establish haemolytic anaemia and to assess severity of haemolysis. ... Clinical Profile and Severity of Hemolysis in Adult Patients of Primary Autoimmune Hemolyt ...
Autoimmune hemolytic anemia typically produces an anemia of rapid onset that may be life-threatening. Patients complain of ... Warm autoimmune hemolytic anemia is an acquired disorder in which an IgG autoantibody is formed that binds to a red blood cell ... Damon LE, Andreadis C. Damon L.E., & Andreadis C Damon, Lloyd E., and Charalambos Babis Andreadis.Autoimmune Hemolytic Anemia. ... Damon LE, Andreadis C. Damon L.E., & Andreadis C Damon, Lloyd E., and Charalambos Babis Andreadis. "Autoimmune Hemolytic Anemia ...
Hemolytic anemia occurs when your red blood cells are destroyed faster than they can be replaced. Learn about its causes, ... How is hemolytic anemia treated?. Treatment. If you have mild hemolytic anemia, you may not have any symptoms or need treatment ... What is hemolytic anemia?. What it is. Hemolytic anemia is a blood condition that occurs when your red blood cells are ... How is hemolytic anemia diagnosed?. Diagnosis. To diagnose hemolytic anemia, your doctor will do a physical exam and order ...
Michel M. Autoimmune and intravascular hemolytic anemias. In: Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 26th ed. ... Your health care provider may recommend this test if you have signs or symptoms of anemia or jaundice (yellowing of the skin or ... Blood disease in newborns called erythroblastosis fetalis (also called hemolytic disease of the newborn) ... These antibodies sometimes destroy red blood cells and cause anemia. ...
Warm antibody hemolytic anemia is the most common form of autoimmune hemolytic anemia. When therapy is needed, corticosteroids ... The role of rituximab in adults with warm antibody autoimmune hemolytic anemia.. Daan Dierickx, Alain Kentos, André Delannoy. ... If this finding is confirmed, rituximab will emerge as a major component of the management of warm antibody hemolytic anemia ... In some major European centers, rituximab is now the preferred second-line therapy of warm antibody hemolytic anemia in adults ...
Autoimmune disease * Autoimmune cytopenias such as hemolytic anemia and immune thrombocytopenia (ITP) ...
... hemolytic anemia; pure red cell aplasia; Diamond-Blackfan anemia. ... autoimmune) ...
Uncontrolled autoimmune hemolytic anemia -Inability to swallow oral medications, or disease involve that significantly limits ...
Autoimmune hemolytic anemia].. Karasawa M. Nihon Rinsho; 2008 Mar; 66(3):520-3. PubMed ID: 18326320. [TBL] ... 8. Mixed-type autoimmune haemolytic anaemia: unusual cases and a case associated with splenic T-cell angioimmunoblastic non- ... 5. [Anti-CD20 monoclonal antibody for the treatment of refractory autoimmune hemolytic anemia].. Wang L; Xu W; Li JY; Xie XY; ... Efficacy and safety of rituximab in auto-immune hemolytic anemia: A meta-analysis of 21 studies.. Reynaud Q; Durieu I; Dutertre ...
Pernicious anemia with autoimmune hemolytic anemia: a case report and literature review. Case Rep Hematol 2016;2016:7231503. ... To evaluate for autoimmune hemolytic anemia, we ordered a direct Coomb test, which was negative. This result, combined with a ... Direct Coomb tests have a sensitivity of 90%-95% and specificity of 99% in diagnosing autoimmune hemolytic anemia.1 We chose to ... allowed us to conclude that a diagnosis of autoimmune hemolytic anemia was unlikely. ...
Anemia happens when there arent enough healthy red blood cells in the body. It can be caused by many things, including dietary ... Anemias from when red blood cells get broken down too fast, called hemolytic anemias. They include: *autoimmune hemolytic ... Anemia. What Is Anemia?. Anemia is when the number of red blood cells in the body gets too low. Red blood cells carry ... There are many different kinds of anemia, so treatments vary.. What Are the Different Kinds of Anemia?. The types of anemia are ...
Hemolytic anemia due to G6PD deficiency; Idiopathic autoimmune hemolytic anemia; Immune hemolytic anemia; Cancers Leukemia; ...
The hematology-oncology team diagnosed him with autoimmune hemolytic anemia. They had started him on immunoglobulins and high- ... The low hemoglobin meant he had anemia, and the high unconjugated bilirubin meant his red blood cells were destroyed. ... and poor oxygen-carrying capacity of his blood due to the anemia was too much for his brain to handle. ...
We study patients with a spectrum of poorly characterized, inherited immunodeficiencies and autoimmune diseases, who lack ... including hemolytic anemia and idiopathic thrombocytopenic purpura. By carefully investigating these "experiments of nature" we ... We study patients with poorly characterized, inherited immunodeficiencies and autoimmune diseases, often lacking molecular ...
Autoimmune hemolytic anemia,. Idiopathic thrombocytopenic purpura,. Lymphadenopathy.. Respiratory, thoracic and mediastinal ...
Immune-mediated hemolytic anemia and thrombocytopenia in the dog: A retrospective study of 55 cases diagnosed from 1969 to 1983 ... There are theoretical reasons to suspect that vaccination could induce clinical autoimmune disease, such as IMHA or ITP, by a ... Risk of immune hemolytic anemia in children following immunization. Vaccine. 2009; Dec. 9;27(52):7394-7. ... Immune-mediated hemolytic anemia: 70 cases (1988-1996). J Am Anim Hosp Assoc. 1999; 35:384-391 ...
... autoimmune disorders (eg, hemolytic anemia), thrombocytopenia, and thyroid disease. Further controlled trials are needed to ... Avoidance of calcineurin may be considered in patients with a primary etiology of atypical hemolytic uremic syndrome or other ... Postrenal transplant hemolytic uremic syndrome/thrombotic microangiopathy: Ahmedabad experience. Transplant Proc. 2008 May. 40( ... Adverse effects associated with mTOR inhibitors are hyperlipidemia, thrombocytopenia, anemia, pneumonitis, oral ulcers, and ...
Hematological: Autoimmune hemolytic anemia, immune thrombocytopenic purpura. Musculoskeletal: Myositis, rhabdomyolysis. ... Hematologic/immune effects may include hemolytic anemia, aplastic anemia, hemophagocytic lymphohistiocytosis, systemic ... autoimmune neuropathy, and Vogt-Koyanagi- Harada syndrome ...
The minimum criteria for the diagnosis of TTP are thrombocytopenia and microangiopathic hemolytic anemia without an apparent ... Autoimmune Thrombocytopenias. Immune thrombocytopenia. Immune thrombocytopenia (ITP) is one of the most common autoimmune ... Hemolytic-uremic syndrome. Patients with hemolytic-uremic syndrome (HUS) have vascular lesions indistinguishable from those ... Thus, the pathophysiology of this disease is similar to that of the hemolytic disease of newborns. Unlike hemolytic disease, ...
  • Autoimmune hemolytic anemia (AIHA) is a heterogeneous disease mainly due to autoantibody-mediated destruction of erythrocytes but also involves complement activation, dysregulation of cellular and innate immunity, and defective bone marrow compensatory response. (nih.gov)
  • Autoimmune Hemolytic Anemia (AIHA) is a blood disease in which a person produces substances that cause their own body to destroy red blood cells (RBCs), resulting in anemia (low hemoglobin). (ihtc.org)
  • A blood transfusion does not correct the underlying cause of the AIHA, but it prevents serious complications from severe anemia. (ihtc.org)
  • OBJECTIVE: To study the clinico-hematological profile and treatment outcome in children suffering from auto immune hemolytic anemia (AIHA). (who.int)
  • Autoimmune hemolytic anemia ( AIHA ) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to an insufficient number of oxygen-carrying red blood cells in the circulation. (findzebra.com)
  • The most common causes of secondary warm-type AIHA include lymphoproliferative disorders (e.g., chronic lymphocytic leukemia, lymphoma) and other autoimmune disorders (e.g., systemic lupus erythematosus, rheumatoid arthritis, scleroderma, Crohn's disease, ulcerative colitis). (findzebra.com)
  • Autoimmune hemolytic anaemia (AIHA) has traditionally been classified based on the temperature sensitivity of the autoagglutinins as warm (WAIHA), cold (CAIHA) and mixed type. (bvsalud.org)
  • 9. B-cell depletion with rituximab as treatment for immune hemolytic anemia and chronic thrombocytopenia. (nih.gov)
  • 18. Alemtuzumab to treat refractory autoimmune hemolytic anemia or thrombocytopenia in chronic lymphocytic leukemia. (nih.gov)
  • Human immunodeficiency virus (HIV) infection not only leads to a compromised immune system, but also disrupts normal haematopoiesis, resulting in the frequent manifestation of cytopenias (anaemia, thrombocytopenia and neutropenia). (who.int)
  • In this review, we describe the frequencies of anaemia, thrombocytopenia and neutropenia reported for HIV-infected, treatment-naïve cohorts studied in eastern and southern sub-Saharan African countries. (who.int)
  • It is sometimes claimed that vaccination can induce autoimmune diseases, such as immune-mediated thrombocytopenia (ITP) and immune-mediated hemolytic anemia (IMHA) in companion animals. (veterinarypracticenews.com)
  • While recovering from acute liver failure, the patient became delirious and developed acute renal failure, acute pancreatitis, pronounced thrombocytopenia, microangiopathic hemolytic anemia, epistaxis, and petechial hemorrhage. (erowid.org)
  • Acquired (autoimmune) hemolytic anemia, congenital (erythroid) hypoplastic anemia (Diamond-Blackfan anemia), idiopathic thrombocytopenic purpura in adults, pure red cell aplasia, and selected cases of secondary thrombocytopenia. (nih.gov)
  • Other causes of hemolytic anemia like thalassemia syndromes, hereditary spherocytosis, G6PD deficiency were excluded by appropriate tests. (who.int)
  • METHODS: Twelve children were diagnosed with auto immune hemolytic anemia over a period of four years. (who.int)
  • 10. Efficacy and safety of rituximab in auto-immune hemolytic anemia: A meta-analysis of 21 studies. (nih.gov)
  • The National Cancer Institute considers "immunohemolytic anemia", "autoimmune hemolytic anemia", and "immune complex hemolytic anemia" to all be synonyms. (findzebra.com)
  • There were no other complications of tial diagnosis of immune hemolytic anemia with negative babesiosis, such as splenic infarction, acute respira- results for antiglobulin tests. (cdc.gov)
  • For dogs with autoimmune hemolytic anemia, corticosteroids are given to suppress the unwanted activity of the dog s immune system. (safehounds.com)
  • such as autoimmune diseases where your dogs body attacks its own red blood cells (called immune-mediated hemolytic anemia - INHA), an under active thyroid, and cancer. (dog-health-guide.org)
  • This type of anemia is primarily caused by either blood loss or a condition called hemolysis or immune-mediated hemolytic anemia (IMHA) which refers to cases where red blood cells are created, but destroyed prematurely by the immune system. (dog-health-guide.org)
  • An autoimmune disease is one in which the body's immune system-its normal defense against harmful invaders including viruses and bacteria-turns its attack against the body's own organs, tissues, and cells. (nih.gov)
  • Erythroid precursor cells may predominate secondary to hemorrhage or erythrocyte destruction (i.e., hemolytic anemia or autoimmune-mediated anemia), whereas myeloid precursor cells may predominate secondary to inflammatory, neoplastic, or immune-mediated conditions. (nih.gov)
  • Autoimmune hemolysis might be a precursor of later onset systemic lupus erythematosus. (findzebra.com)
  • Clinical Profile and Severity of Hemolysis in Adult Patients of Primary Autoimmune Hemolytic Anemia and Their Response to Steroid: A Prospective Cohort Study from Single Institution. (bvsalud.org)
  • Hemolytic anemia occurs when you have a low number of red blood cells due to too much hemolysis in the body. (nih.gov)
  • Mutations in IKZF1, which encodes Ikaros family zinc finger 1 (IKAROS) transcription factor, are associated with recurrent infections, cytopenia, autoimmune diseases, and hematologic malignancies. (nih.gov)
  • We study patients with poorly characterized, inherited immunodeficiencies and autoimmune diseases, often lacking molecular diagnoses. (nih.gov)
  • The destruction of red blood cells caused by autoimmune diseases and other diseases would as well result to anemia. (safehounds.com)
  • Anemia of Inflammatory Disease: diseases such as chronic kidney disease, which affects older dogs can cause anemia. (dog-health-guide.org)
  • The ACE network of biomedical research centers will foster collaborations among basic and clinical scientists and facilitate cooperative clinical trials in autoimmune diseases. (nih.gov)
  • Systemic lupus erythematosus (SLE, or lupus) is one of more than 80 known autoimmune diseases. (nih.gov)
  • In some autoimmune diseases, the target of the attack is limited to a particular part of the body-the blood vessels, moisture-producing glands of the eyes and mouth, or insulin-producing cells of the pancreas, for example. (nih.gov)
  • The most heterogeneous of the autoimmune diseases, lupus is also one of the most difficult to understand and treat. (nih.gov)
  • Those results confirmed the diagnosis as a B. microti in- College School of Basic Medicine, Beijing (H. Wang, C. Wei) fection causing severe intravascular hemolytic anemia. (cdc.gov)
  • 12. Diagnosis and treatment of autoimmune haemolytic anaemias in adults: a clinical review. (nih.gov)
  • This result, combined with a normal total complement test, allowed us to conclude that a diagnosis of autoimmune hemolytic anemia was unlikely. (cmaj.ca)
  • Anemia can be treated but a diagnosis will be necessary to before a treatment plan can be made. (safehounds.com)
  • A common occurrence, dog anemia is a symptom, not a diagnosis. (dog-health-guide.org)
  • Michel M. Autoimmune and intravascular hemolytic anemias. (medlineplus.gov)
  • Disseminated intravascular coagulation, hemo-chromatosis, Wilson disease, and infectious and autoimmune hepatitis were excluded. (erowid.org)
  • We describe a case of hepatitis and warm antibody hemolytic anemia due to dydrogesterone. (nih.gov)
  • The role of rituximab in adults with warm antibody autoimmune hemolytic anemia. (qxmd.com)
  • Warm antibody hemolytic anemia is the most common form of autoimmune hemolytic anemia. (qxmd.com)
  • In some major European centers, rituximab is now the preferred second-line therapy of warm antibody hemolytic anemia in adults, although no prospective study convincingly supports this attitude. (qxmd.com)
  • If this finding is confirmed, rituximab will emerge as a major component of the management of warm antibody hemolytic anemia not only after relapse but as soon as treatment is needed. (qxmd.com)
  • 5. [Anti-CD20 monoclonal antibody for the treatment of refractory autoimmune hemolytic anemia]. (nih.gov)
  • 7. Success of anti-CD20 monoclonal antibody treatment for severe autoimmune hemolytic anemia caused by warm-reactive immunoglobulin A, immunoglobulin G, and immunoglobulin M autoantibodies in a child: a case report. (nih.gov)
  • 2. Alemtuzumab induced complete remission of autoimmune hemolytic anemia refractory to corticosteroids, splenectomy and rituximab. (nih.gov)
  • and/or 3) autoimmunity, including hemolytic anemia and idiopathic thrombocytopenic purpura. (nih.gov)
  • Less commonly, it can be caused by concomitant autoimmune disorders. (findzebra.com)
  • The long-term goal of my translational research is to develop new diagnostic methods, improve diagnostic criteria, and advance our understanding of the pathogenesis of neuromuscular disorders, with particular focus on autoimmune and autophagic myopathies. (ucsf.edu)
  • People with Wiskott-Aldrich syndrome are at greater risk of developing autoimmune disorders, such as rheumatoid arthritis , vasculitis, or hemolytic anemia. (nih.gov)
  • Chronic Endocrine disorders: Hypothyroidism and Addison's disease can trigger anemia. (dog-health-guide.org)
  • 16. Use of rituximab for refractory cytopenias associated with autoimmune lymphoproliferative syndrome (ALPS). (nih.gov)
  • Anaemia which manifests clinical y as cytopenias. (who.int)
  • This corrects the severe anemia which could be life threatening. (ihtc.org)
  • Severe anemia will cause the dog to collapse. (safehounds.com)
  • Severe parasite infestation is also one of the possible causes of anemia. (safehounds.com)
  • A dog with severe anemia may require blood transfusions. (safehounds.com)
  • 15. Rituximab-based immunosuppression for autoimmune haemolytic anaemia in infants. (nih.gov)
  • 11. Successful treatment of refractory autoimmune hemolytic anemia with monthly rituximab following nonmyeloablative stem cell transplantation for sickle cell disease. (nih.gov)
  • SCA, i.e. vaso-occlusive crisis and haemo- quently used in sickle-cell anaemia (SCA) lytic crisis [4,10]. (who.int)
  • What are the symptoms of hemolytic anemia? (nih.gov)
  • If you have mild hemolytic anemia, you may not have any symptoms or need treatment . (nih.gov)
  • Your health care provider may recommend this test if you have signs or symptoms of anemia or jaundice (yellowing of the skin or eyes). (medlineplus.gov)
  • Some children with anemia don't have any symptoms. (kidshealth.org)
  • Both microangiopathic anemia and cobalamin (vitamin B 12 ) deficiency should be considered. (cmaj.ca)
  • To assess for underlying microangiopathic hemolytic anemia, we requested a peripheral blood smear, which showed polychromatophilia, macro-ovalocytes, hypersegmented neutrophils and large platelets ( Figures 1 and 2 ). (cmaj.ca)
  • 1. Successful induction and maintenance of long-term remission in a child with chronic relapsing autoimmune hemolytic anemia using rituximab. (nih.gov)
  • The antibodies and anemia tend to go away after the infections are completely resolved. (ihtc.org)
  • Despite the profusion of hypothetical mechanisms, and the widespread belief vaccines might be a risk factor for autoimmune disease, it has been very difficult to find compelling evidence that this is a real and significant problem. (veterinarypracticenews.com)
  • Billions of humans have been vaccinated over the past century, yet reports of clear associations between vaccination and autoimmune disease are scarce. (veterinarypracticenews.com)
  • A blood disease called autoimmune hemolytic anemia happens when antibodies destroy your own red blood cells faster than your body can make them. (webmd.com)
  • Babies with yellowish skin and eyes may have hemolytic disease of the newborn (HDN). (webmd.com)
  • Anemia is not a disease in itself but a symptom of another disease. (safehounds.com)
  • If a dog is not able to product red book cells the disease is characterized as non-regenerative anemia. (dog-health-guide.org)
  • In the case of anemia related kidney disease there is a treatment that uses darbepoetin, a synthetic form of erythropoietin that is tolerated well by dogs. (dog-health-guide.org)
  • Two health problems in Shih Tzus are related to the blood: blood-clotting disease (von Willebrand's) and autoimmune hemolytic anemia. (yourpurebredpuppy.com)
  • Although MeSH uses the term "autoimmune hemolytic anemia", some sources prefer the term "immunohemolytic anemia" so drug reactions can be included in this category. (findzebra.com)
  • Zinc contamination and other infectious agents can trigger hemolytic anemia. (safehounds.com)
  • These antibodies sometimes destroy red blood cells and cause anemia . (medlineplus.gov)
  • 13. Monoclonal antibodies: new therapeutic agents for autoimmune hemolytic anemia? (nih.gov)
  • Acute hepatitis, autoimmune hemolytic anemia, and erythroblastocytopenia induced by ceftriaxone. (nih.gov)
  • Drug-induced hepatitis, drug-induced autoimmunity or classical autoimmune hepatitis: how can we differentiate? (nih.gov)
  • It must be distinguished from drug-induced hemolytic anemia. (mhmedical.com)
  • 3. Sustained response to rituximab of autoimmune hemolytic anemia associated with antiphospholipid syndrome. (nih.gov)
  • 4. [Successful treatment with rituximab in a patient with refractory mixed-type autoimmune hemolytic anemia]. (nih.gov)
  • 6. Successful treatment with rituximab of an infant with refractory autoimmune hemolytic anemia. (nih.gov)
  • 14. Two cases of refractory warm autoimmune hemolytic anemia treated with rituximab. (nih.gov)
  • 17. Rituximab: a very efficient therapy in cold agglutinins and refractory autoimmune haemolytic anaemia associated with CD20-positive, low-grade non-Hodgkin's lymphoma. (nih.gov)
  • 20. Addition of rituximab to standard therapy improves response rate and progression-free survival in relapsed or refractory thrombotic thrombocytopenic purpura and autoimmune haemolytic anaemia. (nih.gov)
  • 8. Mixed-type autoimmune haemolytic anaemia: unusual cases and a case associated with splenic T-cell angioimmunoblastic non-Hodgkin's lymphoma. (nih.gov)
  • A case of autoimmune hepatitis and autoimmune hemolytic anemia following hepatitis A infection. (nih.gov)
  • Tubercular infection is an underlying pathology in cases of secondary autoimmune hemolytic anemia. (who.int)
  • The most common Grade 3 or 4 adverse reactions (≥2%) were anemia, increased transaminases, urinary tract infection, fatigue/asthenia, and diarrhea. (biospace.com)
  • A veterinarian will first confirm that the anemia is present, the severity of the condition and if the bone marrow is functioning normally. (dog-health-guide.org)
  • This type of anemia is characterized by blood loss that can threaten the life of the dog while at the same time, the dog is capable of producing red blood cells, it means that the bone marrow is still functioning in a normal range. (dog-health-guide.org)
  • Warm autoimmune hemolytic anemia is an acquired disorder in which an IgG autoantibody is formed that binds to a red blood cell membrane protein and does so most avidly at body temperature (ie, a "warm" autoantibody). (mhmedical.com)
  • Hemolytic anemia is a blood condition that occurs when your red blood cells are destroyed faster than they can be replaced. (nih.gov)
  • These are signs that the body is destroying red blood cells, and anemia will result. (ihtc.org)
  • Direct complement lysis of cells is rare, but the presence of C3b on the surface of red blood cells allows Kupffer cells in the liver to participate in the hemolytic process via C3b receptors. (mhmedical.com)
  • To diagnose hemolytic anemia, your doctor will do a physical exam and order blood tests. (nih.gov)
  • Anemia is when the number of red blood cells in the body gets too low. (kidshealth.org)
  • Anemias from when red blood cells get broken down too fast , called hemolytic anemias . (kidshealth.org)
  • The low hemoglobin meant he had anemia, and the high unconjugated bilirubin meant his red blood cells were destroyed. (kevinmd.com)
  • However, a combination of low blood pressure, losing heart function for some minutes, and poor oxygen-carrying capacity of his blood due to the anemia was too much for his brain to handle. (kevinmd.com)
  • The dog may be suffering from anemia, a condition that is primarily characterized by pale gums and lips resulting from the inadequate number of red blood cells. (safehounds.com)
  • Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS . (nih.gov)
  • Dog anemia is a decreased number of red blood cells or iron in the blood (hemoglobin) or both. (dog-health-guide.org)
  • Anemia is also caused by the body using red blood cells faster than normal such as when their is a bleeding condition. (dog-health-guide.org)
  • Spherocytes are found in immunologically-mediated hemolytic anemias. (findzebra.com)
  • Autoimmune hemolytic anemia typically produces an anemia of rapid onset that may be life-threatening. (mhmedical.com)
  • The prognosis is better in dogs with anemia that gradually worsens vs. those that have a sudden onset of anemia. (dog-health-guide.org)
  • If your hemolytic anemia is caused by medicines or another health condition, your doctor may change your treatment to manage or stop hemolytic anemia. (nih.gov)
  • People who have mild hemolytic anemia may not need treatment. (nih.gov)
  • Treatment for anemia depends on the cause. (kidshealth.org)
  • If your dog has very pale gums and lips does this mean that he is suffering from anemia? (safehounds.com)
  • Home / Blog / If your dog has very pale gums and lips does this mean that he is suffering from anemia? (safehounds.com)
  • Apart from the pale gums and lips, a dog with anemia will be weak. (safehounds.com)
  • Autoimmune hemolytic anemia is as well characterized by pale gums. (safehounds.com)
  • Laboratory investigations were performed to establish haemolytic anaemia and to assess severity of haemolysis . (bvsalud.org)
  • Hemolytic anemia can develop quickly or slowly, and it can be mild or serious. (nih.gov)
  • Often this form of anemia is mild and does not cause clinical signs. (dog-health-guide.org)