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AnemiaAnemia, HemolyticAnemia, Hemolytic, AutoimmuneAnemia, Hemolytic, CongenitalHemolysisAnemia, AplasticHemolytic AgentsFanconi AnemiaAnemia, Hemolytic, Congenital NonspherocyticHemolytic-Uremic SyndromeAnemia, HypochromicAnemia, MacrocyticAnemia, PerniciousAnemia, Sickle CellHemolysin ProteinsSecurity MeasuresErythrocytesCoombs TestAnemia, MegaloblasticInfectious Anemia Virus, EquineAnemia, RefractoryComplement Hemolytic Activity AssayErythropoietinHemolytic Plaque TechniqueEquine Infectious AnemiaErythroblastosis, FetalPhenylhydrazinesChicken anemia virusSpherocytosis, HereditaryAnemia, Dyserythropoietic, CongenitalIronHeinz BodiesErythrocyte CountAnemia, Diamond-BlackfanFanconi Anemia Complementation Group ProteinsPregnancy Complications, HematologicReticulocyte CountHematocritErythrocyte AgingOsmotic FragilityErythropoiesisErythrocytes, AbnormalAnemia, NeonatalBlood TransfusionGlucosephosphate Dehydrogenase DeficiencyHematinicsAnemia, Refractory, with Excess of BlastsErythrocyte IndicesErythrocyte MembraneFanconi Anemia Complementation Group C ProteinRh-Hr Blood-Group SystemFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group A ProteinHemoglobinometryComplement System ProteinsStreptolysinsFerritinsPallorErythrocyte TransfusionComplement Factor HShiga ToxinBlood Group IncompatibilityHemoglobins, AbnormalSplenectomyAntimicrobial Cationic PeptidesSplenomegalyThrombotic MicroangiopathiesMolecular Sequence DataHemoglobinuria, ParoxysmalReticulocytesComplement ActivationRh IsoimmunizationBacterial ToxinsFanconi Anemia Complementation Group G ProteinThrombocytopeniaHorsesPlasma ExchangeThalassemiaSheepSea CucumbersChromium Isotopesbeta-ThalassemiaBone MarrowMethemoglobinPyruvate KinaseSpherocytesIron, DietaryEscherichia coli InfectionsHemoglobinopathiesBlood Transfusion, IntrauterineWater MovementsAmino Acid SequenceEscherichia coli O157Blood Cell CountSuppression, GeneticHepcidinsFavismAutoantibodiesTreatment OutcomePrimaquineFetal HemoglobinHemoglobinuriaRecombinant ProteinsComplement C3Spectrinalpha-ThalassemiaGlucosephosphate DehydrogenasePrevalenceErythroblastsInfant, NewbornPregnancyHemoglobin, SickleShiga Toxin 2Hematologic DiseasesComplement Factor IVitamin B 12 DeficiencyComplement C5MalariaSpleenReticulocytosisShiga Toxin 1Base SequenceEscherichia coliRisk FactorsComplement Pathway, AlternativeIsavirusTime FactorsPancytopeniaRabbitsIron OverloadBlood Grouping and CrossmatchingDapsoneRetrospective StudiesMitomycinShiga-Toxigenic Escherichia coliFanconi Anemia Complementation Group F ProteinRed-Cell Aplasia, PureBacterial ProteinsFanconi Anemia Complementation Group E ProteinComplement C4Purpura, Thrombocytopenic, IdiopathicVirulenceHemolysin FactorsIsoantibodiesParvovirus B19, HumanFolic Acid DeficiencyKidney Failure, ChronicParvoviridae InfectionsErythrocyte DeformabilityPsoroptidaeHomozygoteImmunoglobulin GElliptocytosis, HereditaryVitamin B 12Chronic DiseaseBilirubinMethyldopaComplement C3b Inactivator ProteinsFish VenomsTrihexosylceramidesHaptoglobinsHydrops FetalisPedigreeBlood Group AntigensBlood ProteinsImmunosuppressive AgentsHemagglutinationMelittenAnion Exchange Protein 1, ErythrocyteAntilymphocyte SerumCucumariaPhenotypeParasitemiaFerrous CompoundsHematologyDiarrheaSickle Cell TraitHookworm InfectionsReceptors, TransferrinToxins, BiologicalAnti-Bacterial AgentsRenal DialysisStreptococcusAeromonasFatal OutcomeHemoglobin C DiseasePhenacetinComplement C8Malaria, FalciparumMethemoglobinemiaSeverity of Illness IndexErythrocyte VolumeBone Marrow TransplantationCnidarian VenomsProspective StudiesIntrinsic FactorAntigens, CD46Complement C3bComplement Inactivator ProteinsFollow-Up StudiesDisease Models, Animal
Anemia: A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN.Anemia, Hemolytic: A condition of inadequate circulating red blood cells (ANEMIA) or insufficient HEMOGLOBIN due to premature destruction of red blood cells (ERYTHROCYTES).Anemia, Hemolytic, Autoimmune: Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.Anemia, Hemolytic, Congenital: Hemolytic anemia due to various intrinsic defects of the erythrocyte.Hemolysis: The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.Anemia, Aplastic: A form of anemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements.Hemolytic Agents: Substances that are toxic to blood in general, including the clotting mechanism; hematotoxins may refer to the hematopoietic system.Fanconi Anemia: 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)Anemia, Hemolytic, Congenital Nonspherocytic: 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.Hemolytic-Uremic Syndrome: 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, Hypochromic: 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, Macrocytic: Anemia characterized by larger than normal erythrocytes, increased mean corpuscular volume (MCV) and increased mean corpuscular hemoglobin (MCH).Anemia, Pernicious: 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)Anemia, Sickle Cell: 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.Hemolysin Proteins: 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.Security Measures: Regulations to assure protection of property and equipment.Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.Coombs Test: 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.Anemia, Megaloblastic: A disorder characterized by the presence of ANEMIA, abnormally large red blood cells (megalocytes or macrocytes), and MEGALOBLASTS.Infectious Anemia Virus, Equine: 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.Anemia, Refractory: A severe sometimes chronic anemia, usually macrocytic in type, that does not respond to ordinary antianemic therapy.Complement Hemolytic Activity Assay: 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.Erythropoietin: 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.Hemolytic Plaque Technique: 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)Equine Infectious Anemia: 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.Erythroblastosis, Fetal: 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.Phenylhydrazines: Diazo derivatives of aniline, used as a reagent for sugars, ketones, and aldehydes. (Dorland, 28th ed)Chicken anemia virus: 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.Spherocytosis, Hereditary: 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.Anemia, Dyserythropoietic, Congenital: 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.Iron: 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.Heinz Bodies: 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.Erythrocyte Count: The number of RED BLOOD CELLS per unit volume in a sample of venous BLOOD.Anemia, Diamond-Blackfan: 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)Fanconi Anemia Complementation Group Proteins: 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.Pregnancy Complications, Hematologic: 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.Reticulocyte Count: 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.Hematocrit: 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.Erythrocyte Aging: 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.Osmotic Fragility: 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.Erythropoiesis: 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.Erythrocytes, Abnormal: Oxygen-carrying RED BLOOD CELLS in mammalian blood that are abnormal in structure or function.Anemia, Neonatal: The mildest form of erythroblastosis fetalis in which anemia is the chief manifestation.Blood Transfusion: The introduction of whole blood or blood component directly into the blood stream. (Dorland, 27th ed)Glucosephosphate Dehydrogenase Deficiency: 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.Hematinics: 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.Anemia, Refractory, with Excess of Blasts: Chronic refractory anemia with granulocytopenia, and/or thrombocytopenia. Myeloblasts and progranulocytes constitute 5 to 40 percent of the nucleated marrow cells.Erythrocyte Indices: 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).Erythrocyte Membrane: The semi-permeable outer structure of a red blood cell. It is known as a red cell 'ghost' after HEMOLYSIS.Fanconi Anemia Complementation Group C Protein: 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.Rh-Hr Blood-Group System: 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.Fanconi Anemia Complementation Group D2 Protein: 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.Fanconi Anemia Complementation Group A Protein: 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.Hemoglobinometry: Measurement of hemoglobin concentration in blood.Complement System Proteins: 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).Streptolysins: Exotoxins produced by certain strains of streptococci, particularly those of group A (STREPTOCOCCUS PYOGENES), that cause HEMOLYSIS.Ferritins: 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.Pallor: A clinical manifestation consisting of an unnatural paleness of the skin.Erythrocyte Transfusion: The transfer of erythrocytes from a donor to a recipient or reinfusion to the donor.Complement Factor H: 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).Shiga Toxin: 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.Blood Group Incompatibility: 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, Abnormal: 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.Splenectomy: Surgical procedure involving either partial or entire removal of the spleen.Antimicrobial Cationic Peptides: 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.Splenomegaly: Enlargement of the spleen.Thrombotic Microangiopathies: 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.Molecular Sequence Data: 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.Hemoglobinuria, Paroxysmal: 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.Reticulocytes: 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.Complement Activation: 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.Rh Isoimmunization: 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.Bacterial Toxins: 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.Fanconi Anemia Complementation Group G Protein: 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.Thrombocytopenia: A subnormal level of BLOOD PLATELETS.Horses: 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.Plasma Exchange: 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.Thalassemia: 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.Sheep: 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.Sea Cucumbers: A class of Echinodermata characterized by long, slender bodies.Chromium Isotopes: 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.beta-Thalassemia: 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.Bone Marrow: 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.MethemoglobinPyruvate Kinase: 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.Spherocytes: Small, abnormal spherical red blood cells with more than the normal amount of hemoglobin.Iron, Dietary: 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.Escherichia coli Infections: Infections with bacteria of the species ESCHERICHIA COLI.Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule.Blood Transfusion, Intrauterine: In utero transfusion of BLOOD into the FETUS for the treatment of FETAL DISEASES, such as fetal erythroblastosis (ERYTHROBLASTOSIS, FETAL).Water Movements: The flow of water in enviromental bodies of water such as rivers, oceans, water supplies, aquariums, etc. It includes currents, tides, and waves.Amino Acid Sequence: 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.Escherichia coli O157: 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.Blood Cell Count: 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.Suppression, Genetic: Mutation process that restores the wild-type PHENOTYPE in an organism possessing a mutationally altered GENOTYPE. The second "suppressor" mutation may be on a different gene, on the same gene but located at a distance from the site of the primary mutation, or in extrachromosomal genes (EXTRACHROMOSOMAL INHERITANCE).Hepcidins: 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.Favism: 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.Autoantibodies: Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.Treatment Outcome: 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.Primaquine: 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)Fetal Hemoglobin: 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.Hemoglobinuria: 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.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Complement C3: 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.Spectrin: 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.alpha-Thalassemia: 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.Glucosephosphate DehydrogenasePrevalence: 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.Erythroblasts: 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.Infant, Newborn: An infant during the first month after birth.Pregnancy: The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.Hemoglobin, Sickle: 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.Shiga Toxin 2: 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.Hematologic Diseases: Disorders of the blood and blood forming tissues.Complement Factor I: 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.Vitamin B 12 Deficiency: 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)Complement C5: 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.Malaria: 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.Spleen: An encapsulated lymphatic organ through which venous blood filters.Reticulocytosis: 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.Shiga Toxin 1: 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.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Escherichia coli: 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.Risk Factors: 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 Pathway, Alternative: 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.Isavirus: A genus in the family ORTHOMYXOVIRIDAE containing one species: Infectious salmon anemia virus.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Pancytopenia: Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets.Rabbits: 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.Iron Overload: 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)Blood Grouping and Crossmatching: 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.Dapsone: 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)Retrospective Studies: 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.Mitomycin: 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.Shiga-Toxigenic Escherichia coli: 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.Fanconi Anemia Complementation Group F Protein: 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.Red-Cell Aplasia, Pure: Suppression of erythropoiesis with little or no abnormality of leukocyte or platelet production.Bacterial Proteins: Proteins found in any species of bacterium.Fanconi Anemia Complementation Group E Protein: 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.Complement C4: 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.Purpura, Thrombocytopenic, Idiopathic: 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.Virulence: 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.Hemolysin Factors: Plasmids controlling the synthesis of hemolysin by bacteria.Isoantibodies: Antibodies from an individual that react with ISOANTIGENS of another individual of the same species.Parvovirus B19, Human: The type species of ERYTHROVIRUS and the etiological agent of ERYTHEMA INFECTIOSUM, a disease most commonly seen in school-age children.Folic Acid Deficiency: 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)Kidney Failure, Chronic: 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.Parvoviridae Infections: Virus infections caused by the PARVOVIRIDAE.Erythrocyte Deformability: Ability of ERYTHROCYTES to change shape as they pass through narrow spaces, such as the microvasculature.Psoroptidae: Family of parasitic MITES, in the superfamily Sarcoptoidea, order Astigmata. Genera include Psoroptes and Chorioptes.Homozygote: An individual in which both alleles at a given locus are identical.Immunoglobulin G: The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.Elliptocytosis, Hereditary: An intrinsic defect of erythrocytes inherited as an autosomal dominant trait. The erythrocytes assume an oval or elliptical shape.Vitamin B 12: 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.Chronic Disease: 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)Bilirubin: A bile pigment that is a degradation product of HEME.Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.Complement C3b Inactivator Proteins: 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.Fish Venoms: 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.Trihexosylceramides: 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).Haptoglobins: 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.Hydrops Fetalis: 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.Pedigree: 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.Blood Group Antigens: Sets of cell surface antigens located on BLOOD CELLS. They are usually membrane GLYCOPROTEINS or GLYCOLIPIDS that are antigenically distinguished by their carbohydrate moieties.Blood Proteins: Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.Immunosuppressive Agents: 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.Hemagglutination: The aggregation of ERYTHROCYTES by AGGLUTININS, including antibodies, lectins, and viral proteins (HEMAGGLUTINATION, VIRAL).Melitten: 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.Anion Exchange Protein 1, Erythrocyte: 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.Antilymphocyte Serum: Serum containing GAMMA-GLOBULINS which are antibodies for lymphocyte ANTIGENS. It is used both as a test for HISTOCOMPATIBILITY and therapeutically in TRANSPLANTATION.Cucumaria: A genus of large SEA CUCUMBERS possessing the primitive radial configuration of podia in all five ambulacral areas.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Parasitemia: The presence of parasites (especially malarial parasites) in the blood. (Dorland, 27th ed)Ferrous Compounds: Inorganic or organic compounds that contain divalent iron.Hematology: A subspecialty of internal medicine concerned with morphology, physiology, and pathology of the blood and blood-forming tissues.Diarrhea: 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.Sickle Cell Trait: The condition of being heterozygous for hemoglobin S.Hookworm Infections: 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.Receptors, Transferrin: 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.Toxins, Biological: Specific, characterizable, poisonous chemicals, often PROTEINS, with specific biological properties, including immunogenicity, produced by microbes, higher plants (PLANTS, TOXIC), or ANIMALS.Anti-Bacterial Agents: Substances that reduce the growth or reproduction of BACTERIA.Renal Dialysis: Therapy for the insufficient cleansing of the BLOOD by the kidneys based on dialysis and including hemodialysis, PERITONEAL DIALYSIS, and HEMODIAFILTRATION.Streptococcus: 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.Aeromonas: 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.Fatal Outcome: 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.Hemoglobin C Disease: 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.Phenacetin: 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)Complement C8: 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, Falciparum: 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.Methemoglobinemia: 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)Severity of Illness Index: Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.Erythrocyte Volume: Volume of circulating ERYTHROCYTES . It is usually measured by RADIOISOTOPE DILUTION TECHNIQUE.Bone Marrow Transplantation: 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.Cnidarian Venoms: 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.Prospective Studies: 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.Intrinsic Factor: 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.Antigens, CD46: 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.Complement C3b: 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.Complement Inactivator Proteins: 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.Follow-Up Studies: 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.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.

Extraction of erythrocyte membrane proteins by sulfhydryl inhibitors. (1/616)

Human red cell membrane proteins were extracted by incubation of the ghost with hypotonic phosphate buffer (pH 7.4), N-ethylmaleimide and p-hydroxy-mercuribenzoate. In paroxysmal nocturnal hemoglobinuria (PNH), hereditary spherocytosis (HS) and hereditary elliptocytosis, the amount of proteins extracted by these procedures was significantly less than the amount extractable from the ghost of normal and aplastic anemia red cells. Polypeptide patterns of red cell membranes in these hematological disorders were essentially similar to those of normal ghosts. Analysis of the supernatant by SDS polyacrylamide gel electrophoresis revealed that this reduction was mainly due to the reduced amount of peripheral proteins extracted. The extraction of peripheral proteins by sulfhydryl reagents was accompanied by shape changes resulting in the formation of membrane vesicles, suggesting an important role of peripheral proteins in the maintenance of ghost shape. It is also suggested that qualitative abnormalities of peripheral proteins such as altered reactivity to sulfhydryl reagents and/or strong binding to the membrane are present in PNH, HS and hereditary elliptocytosis red cells.  (+info)

Reduced glutathione accelerates the oxidative damage produced by sodium n-propylthiosulfate, one of the causative agents of onion-induced hemolytic anemia in dogs. (2/616)

The oxidative effects of sodium n-propylthiosulfate, one of the causative agents of onion-induced hemolytic anemia in dogs, were investigated in vitro using three types of canine erythrocytes, which are differentiated by the concentration of reduced glutathione and the composition of intracellular cations. After incubation with sodium n-propylthiosulfate, the methemoglobin concentration and Heinz body count in all three types of erythrocytes increased and a decrease in the erythrocyte reduced glutathione concentration was then observed. The erythrocytes containing high concentrations of potassium and reduced glutathione (approximately five times the normal values) were more susceptible to oxidative damage by sodium n-propylthiosulfate than were the normal canine erythrocytes. The susceptibility of the erythrocytes containing high potassium and normal reduced glutathione concentrations was intermediate between those of erythrocytes containing high concentrations of potassium and reduced glutathione and normal canine erythrocytes. In addition, the depletion of erythrocyte reduced glutathione by 1-chloro-2, 4-dinitrobenzene resulted in a marked decrease in the oxidative injury induced by sodium n-propylthiosulfate in erythrocytes containing high concentrations of potassium and reduced glutathione. The generation of superoxide in erythrocytes containing high concentrations of potassium and reduced glutathione was 4.1 times higher than that in normal canine erythrocytes when the cells were incubated with sodium n-propylthiosulfate. These observations indicate that erythrocyte reduced glutathione, which is known as an antioxidant, accelerates the oxidative damage produced by sodium n-propylthiosulfate.  (+info)

Rumen bacteria are involved in the onset of onion-induced hemolytic anemia in sheep. (3/616)

The mechanism of onion-induced hemolytic anemia in ruminants was investigated. The ether-extract obtained from the mixture of rumen fluid and onion juice incubated at 38.5 degrees C for 9 hr induced oxidative damage in sheep erythrocytes in vitro, indicating the production of certain oxidants in the mixture. The increase of the oxidative effect in the mixture was inhibited completely by the removal of rumen microorganisms and partly by treatment with antibiotics and by oxygen gas. The sheep fed onions (50 g/kg body weight/day) for 15 days developed more severe Heinz body hemolytic anemia than did the sheep fed the equivalent amount of onions with 5 g/day ampicillin sodium salt. The results indicated that certain rumen bacteria appear to be involved in the onset of onion-induced hemolytic anemia in sheep.  (+info)

Erythroid accelerating activity of rat serum in early stage of drug induced hemolysis. (4/616)

An increase in the number of erythroblasts can be seen to some extent in the bone marrow of rats in the early stage of experimentally induced hemolytic anemia prior to any elevation in the plasma erythropoietin (Epo) level. This observation suggests that there is another erythroid stimulating factor present other than Epo. We studied the enhancing effect of serum, taken sequentially during experimentally induced hemolysis in rats, on erythroid proliferation, differentiation and maturation in vitro. Single intraperitoneal injection of 60 mg/kg of acetylphenylhydrazine (APH) induced self-limited hemolytic anemia in rats, in which the hematocrit dropped rapidly with a nadir at day 4 after APH injection, followed by a gradual increase with return to normal level by day 8. Serum obtained consecutively every day after APH injection from day 1 to day 7 was applied to an in vitro culturing system of erythroid progenitors. Addition of day 1 serum, in which an elevation of Epo level had not occurred, to a conventional methyl-cellulose culture of rat bone marrow mononuclear cells (BM-MNCs) resulted in a significant increase in the number of colonies derived from colony forming unit erythroid, but not in burst forming unit erythroid. This erythropoietic activity of the serum was particularly evident in the presence of Epo. In the liquid culture of BM-MNCs, day 1 serum also showed some enhancing effect on erythroblast formation. We were able to see significant differences in these erythroid enhancing activities induced by serum drawn on day 1 in comparison to the serum drawn on subsequent days. These results suggest that an unknown erythroid enhancing factor besides Epo stimulates erythropoiesis in the early stage of hemolytic anemia or sudden hypoxia before there is a measurable rise in the serum Epo level. We propose that this factor be termed erythroid accelerating factor (EAF).  (+info)

Spur cell anaemia and hepatic iron stores in patients with alcoholic liver disease undergoing orthotopic liver transplantation. (5/616)

BACKGROUND: Following orthotopic liver transplantation (OLT) histological examination of explant livers from patients with alcoholic liver disease (ALD) sometimes shows extensive iron deposits in a distribution suggestive of homozygous haemochromatosis. AIMS: To use haemochromatosis gene (HFE) assays to distinguish between ALD with notable siderosis and hereditary haemochromatosis. To evaluate the possible influence of spur cell haemolytic anaemia on hepatic iron loading. PATIENTS: Thirty seven patients with ALD were abstinent for at least six months prior to OLT. Twenty three patients had transferrin saturations greater than 55%, 16 also had increased serum ferritin (>350 micrograms/l). Eight of 37 (22%) explant livers had grade 3 or 4 hepatic iron deposition, predominantly in hepatocytes. Of these, four had a hepatic iron index greater than 1. 9 and most seemed to have spur cell haemolytic anaemia. METHODS: Mutation analysis for C282Y and H63D mutations was performed on DNA extracts from peripheral blood or explant liver. Spur cell haemolytic anaemia was diagnosed when the haemoglobin was 105 g/l in the presence of notable acanthocytosis. RESULTS: None of the eight patients with grade 3 or 4 hepatic iron had evidence of the C282Y mutation. Two of the eight were heterozygous for H63D. None of the remaining 28 patients tested showed homozygous HFE mutations. Spur cell anaemia was present in six of the eight patients with heavy iron deposition and only one of the remaining patients. CONCLUSIONS: The HFE mutation was not present in these patients with advanced ALD and heavy iron loading. Spur cell haemolytic anaemia provides an alternative potential mechanism for the heavy iron loading.  (+info)

The molecular basis of a case of gamma-glutamylcysteine synthetase deficiency. (6/616)

Gamma-glutamylcysteine synthetase catalyzes the first step in glutathione synthesis. The enzyme consists of 2 subunits, heavy and light, with the heavy subunit serving as the catalytic subunit. A patient with hemolytic anemia and low red blood cell glutathione levels was found to have a deficiency of gamma-glutamylcysteine synthetase activity. Examination of cDNA from the patient and her mother showed that she was homozygous and that her mother was heterozygous for a A-->T transversion at nt1109 producing a deduced amino acid change of His370Leu. The partial genomic structure of the catalytic subunit of gamma-glutamylcysteine synthetase (GLCLC) was determined, providing some intron/exon boundaries to make it possible to sequence an affected part of the coding region from genomic DNA. The 1109A-->T mutation was not present in the DNA of 38 normal subjects. In the course of these studies we found a diallelic polymorphism in nt +206 of an intron and another polymorphism that consisted of a duplication of a CAGC at cDNA nt1972-1975 in the 3' untranslated region. The 2 polymorphisms were found to be only in partial linkage disequilibrium.  (+info)

Molecular basis and enzymatic properties of glucose 6-phosphate dehydrogenase volendam, leading to chronic nonspherocytic anemia, granulocyte dysfunction, and increased susceptibility to infections. (7/616)

We have investigated the blood cells from a woman with a low degree of chronic nonspherocytic hemolytic anemia and frequent bacterial infections accompanied by icterus and anemia. The activity of glucose 6-phosphate dehydrogenase (G6PD) in her red blood cells (RBCs) was below detection level, and in her leukocytes less than 3% of normal. In cultured skin fibroblasts, G6PD activity was approximately 15% of normal, with 4- to 5-fold increased Michaelis constant (Km) for NADP and for glucose 6-phosphate. Activated neutrophils showed a decreased respiratory burst. Family studies showed normal G6PD activity in the RBCs from all family members, including both parents and the 2 daughters of the patient. Sequencing of polymerase chain reaction (PCR)-amplified genomic DNA showed a novel, heterozygous 514C-->T mutation, predicting a Pro172-->Ser replacement. Analysis of G6PD RNA from the patient's leukocytes and fibroblasts showed only transcripts with the 514C-->T mutation. This was explained by the pattern of X-chromosome inactivation, studied by means of the human androgen receptor (HUMARA) assay, which proved to be skewed in the patient, her mother, and one of the patient's daughters. Thus, the patient has inherited a de novo mutation in G6PD from her father and an X-chromosome inactivation determinant from her mother, causing exclusive expression of the mutated G6PD allele. Purified mutant protein from an Escherichia coli expression system showed strongly decreased specific activity, increased Km for NADP and for glucose 6-phosphate, and increased heat lability, which indicates that the defective phenotype is due to 2 synergistic molecular dysfunctions: decreased catalytic efficiency and protein instability.  (+info)

Reversal of metabolic block in glycolysis by enzyme replacement in triosephosphate isomerase-deficient cells. (8/616)

Inherited deficiency of the housekeeping enzyme triosephosphate isomerase (TPI) is the most severe clinical disorder of glycolysis. Homozygotes manifest congenital hemolytic anemia and progressive neuromuscular impairment, which in most cases pursues an inexorable course with fatal outcome in early childhood. No effective therapy is available. Hitherto specific enzyme replacement has not been attempted in disorders of glycolysis. Primary skeletal muscle myoblasts and Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines generated from homozygous TPI-deficient patients were cultured in the presence of exogenous enzyme or cocultured with human K562 erythroleukemia cells as an exogenous source of TPI. Uptake of active enzyme by TPI-deficient cells resulted in reversal of intracellular substrate accumulation, with a reduction in dihydroxyacetone phosphate (DHAP) concentration to levels seen in TPI-competent cells. Evidence of successful metabolic correction of TPI deficiency in vitro establishes the feasibility of enzyme replacement therapy, and has important implications for the potential role of allogeneic bone marrow transplantation and gene therapy as a means of sustained delivery of functional enzyme in vivo.  (+info)

Post-partum renal failure with microangiopathic haemolytic anaemia. Long-term survival after anticoagulant therapy.<...Post-partum renal failure with microangiopathic haemolytic anaemia. Long-term survival after anticoagulant therapy.<...
TY - JOUR. T1 - Post-partum renal failure with microangiopathic haemolytic anaemia. Long-term survival after anticoagulant therapy.. AU - Ponticelli, C.. AU - Imbasciati, E.. AU - Tarantino, A.. AU - Graziani, G.. AU - Redaelli, B.. PY - 1972. Y1 - 1972. UR - http://www.scopus.com/inward/record.url?scp=0015277359&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0015277359&partnerID=8YFLogxK. M3 - Article. C2 - 5043088. AN - SCOPUS:0015277359. VL - 9. SP - 27. EP - 41. JO - Experimental Nephrology. JF - Experimental Nephrology. SN - 0028-2766. IS - 1. ER - ...
Severe Hemolytic Anemia Post-Renal Transplantation Produced by Donor Anti-D Passenger Lymphocytes: Case Report and Literature...Severe Hemolytic Anemia Post-Renal Transplantation Produced by Donor Anti-D Passenger Lymphocytes: Case Report and Literature...
Severe Hemolytic Anemia Post-Renal Transplantation Produced by Donor Anti-D Passenger Lymphocytes: Case Report and Literature Review Academic Article ...
Drug induced Hemolytic Anemia - Clinicals, Diagnosis, and Management | Explain Medicine - Medical JoyworksDrug induced Hemolytic Anemia - Clinicals, Diagnosis, and Management | Explain Medicine - Medical Joyworks
Hemolytic Anemia is a condition where there is a destruction of red blood cells prematurely leading to anaemia with release of bilirubin in to the circulation. There are main 2 types of haemolytic anaemia: acquired and hereditary. There are also different types of acquired haemolytic anaemia such as immune mediated, infection induced, microangiopathic haemolytic anaemia and hereditary haemolytic anaemia such as glucose 6 phosphate deficiency, pyruvate kinase deficiency, hereditary spherocytosis and haemoglobinopathies. Drug induced haemolytic anaemia can be immune mediated where there is formation of autoantibodies against the red blood cell membrane after penicillin or immune complex formation after quinine therapy. It may be drug-dependent or drug-independent. Anaemia can be triggered by drugs such as primaquine, sulfonamide and aspirin in people with glucose 6 phosphate deficiency. Drugs also can trigger the anaemia in auto immune haemolytic anaemia. Eg:-Penicillin produces large amounts of ...
Thrombocytopenia Microangiopathic Hemolytic AnemiaThrombocytopenia Microangiopathic Hemolytic Anemia
Tips to help with your thrombocytopenia: Thrombocytopenia Microangiopathic Hemolytic Anemia. My thrombocytopenia, Online resources for thrombocytopenia.
Microangiopathic hemolytic anemia, noncardiac pulmonary edema, and renal failure after treatment of metastatic adenocarcinoma...Microangiopathic hemolytic anemia, noncardiac pulmonary edema, and renal failure after treatment of metastatic adenocarcinoma...
Claycomb C, Berkovic M. Microangiopathic hemolytic anemia, noncardiac pulmonary edema, and renal failure after treatment of metastatic adenocarcinoma of the colon with 5-fluorouracil and mitomycin-C: report of a case. J Am Osteopath Assoc 1986;86(8):499. doi: https://doi.org/10.7556/jaoa.1986.86.8.499.. Download citation file:. ...
Immune-Mediated Hemolytic Anemia (IMHA) - Veterinary Specialty CenterImmune-Mediated Hemolytic Anemia (IMHA) - Veterinary Specialty Center
Immune-Mediated Hemolytic Anemia (IMHA) is a serious and sometimes life-threatening auto-immune condition in which the immune system attacks and destroys a patients red blood cells, causing anemia.. Cause IMHA is caused by an abnormal immune response in which the patients body targets red blood cells for destruction. Primary IMHA has no known cause, meaning the immune system was not triggered to attack the red blood cells for any identifiable reason. Secondary IMHA is suspected when an anemic patient is diagnosed with a new infection, cancer, or has recently been started on medication or received a vaccination that stimulated the immune system. Primary IMHA is more common than secondary IMHA, but because of differences in therapy and prognosis, a search for an immune trigger is generally recommended.. The immune system has both pro-inflammatory and anti-inflammatory chemical triggers as well as recognition of its own cells; an auto-immune or immune-mediated condition is one in which these ...
Mechanical hemolytic anemia - WikipediaMechanical hemolytic anemia - Wikipedia
Mechanical hemolytic anemia is a form of hemolytic anemia due to mechanically induced damage to red blood cells. Red blood cells, while flexible, may in some circumstances succumb to physical shear and compression. This may result in hemoglobinuria. The damage is induced through repetitive mechanical motions such as prolonged marching (march hemoglobinuria) and marathon running. Mechanical damage can also be induced through the chronic condition microangiopathic hemolytic anemia or due to prosthetic heart valves. Repetitive impacts to the body may cause mechanical trauma and bursting (hemolysis) of red blood cells. This has been documented to have occurred in the feet during running and hands from Conga or Candombe drumming. Defects in red blood cell membrane proteins have been identified in some of these patients. Free haemoglobin is released from lysed red blood cells and filtered into the urine. March hematuria, occurs when blood is seen in the urine after repetitive impacts on the body, ...
Ankyrin and the hemolytic anemia mutation, nb, map to mouse chromosom by R A. White, C S. Birkenmeier et al.Ankyrin and the hemolytic anemia mutation, nb, map to mouse chromosom" by R A. White, C S. Birkenmeier et al.
Mice with normoblastosis, nb/nb, have a severe hemolytic anemia. The extreme fragility and shortened lifespan of the mutant erythrocytes result from a defective membrane skeleton. Previous studies in our laboratory indicated a 50% deficiency of spectrin and an absence of normal ankyrin in erythrocyte membranes of nb/nb mice. We now report genetic mapping data that localize both the nb and erythroid ankyrin (Ank-1) loci to the centromeric end of mouse chromosome 8. Using immunological and biochemical methods, we have further characterized the nature of the ankyrin defect in mutant erythrocytes. We do not detect normal sized (210 kDa) erythroid ankyrin by immunoblot analysis in nb/nb reticulocytes. However, nb/nb reticulocytes do contain a 150-kDa ankyrin immunoreactive protein. The 150-kDa protein is present with normal-sized ankyrin in nb/+ reticulocytes but is not found in +/+ reticulocytes. Our genetic and biochemical data indicate that the nb mutation results from a defect in the
Cold Agglutinin Hemolytic Anemia: Management with an Environmental Suit | Annals of Internal Medicine | American College of...Cold Agglutinin Hemolytic Anemia: Management with an Environmental Suit | Annals of Internal Medicine | American College of...
Cold Agglutinin hemolytic anemia due to cold autoantibodies associated with Mycoplasma pneumoniae is rare. Optimal treatment includes antibiotics and maintenance of a constant warm environment for the patient. This treatment, however, may result in a prolonged, costly, and confining hospitalization.. We report the use of an environmental suit for a patient with severe hemolysis due to M. pneumoniae pneumonia. This suit provides a constant temperature and has enabled the patient to journey outside his room, despite winter temperatures, yet avoid further hemolytic episodes. Early discharge was possible and has facilitated the patients return to home and work as well as ...
Reversible posterior leucoencephalopathy in scleroderma | Annals of the Rheumatic DiseasesReversible posterior leucoencephalopathy in scleroderma | Annals of the Rheumatic Diseases
A 34 year old Chinese woman with limited scleroderma presented with rapid onset of mental confusion and generalised tonic-clonic seizures. Her blood pressure control had been unsatisfactory in the preceding 4 weeks despite the use of three anti-hypertensive agents, which included an angiotensin converting enzyme inhibitor. Malignant hypertension (blood pressure 240/140 mm Hg on admission) was evident, with typical fundoscopic abnormalities, microangiopathic haemolytic anaemia, and rapidly deteriorating renal function with acute oligouric renal failure (increase in serum creatinine from baseline of 86 to 495 μmol/l in 3 days). There was, however, no evidence of left ventricular failure.. Treatment was given in the intensive care unit with infusions of labetalol (up to 150 mg/h) and iloprost (up to 10 μg/h), large doses of captopril (150 mg/day), and haemodialysis. An urgent magnetic resonance imaging (MRI) scan of the brain showed marked vasogenic oedema distributed symmetrically at the cortex, ...
Auto-immune Hemolytic Anemia - DogtimeAuto-immune Hemolytic Anemia - Dogtime
Auto-immune Hemolytic Anemia is a life threatening disease where the body attacks its own red blood cells. Symptoms of Auto-immune Hemolytic Anemia are jaundice, fainting, pale gums, lips and eye margins, dark tea colored urine, lethargy and rapid
Hemolytic AnemiaHemolytic Anemia
What is Hemolytic Anemia ? Hemolytic anemia is a rare blood disorder in which red blood cells are rapidly destroyed. The severity of this type of anemia is dete
Krames Online - When Your Child Has Hemolytic AnemiaKrames Online - When Your Child Has Hemolytic Anemia
Hemolytic anemia occurs when the body does not have enough healthy red blood cells (RBCs). This is because the cells are destroyed too early. The body also does not make new RBCs fast enough to replace the ones that are destroyed. There are many types of hemolytic anemia.
Top Hemolytic Anemia Hospitals in Gurgaon | CredihealthTop Hemolytic Anemia Hospitals in Gurgaon | Credihealth
View details of top hemolytic anemia hospitals in Gurgaon. Get guidance from medical experts to select best hemolytic anemia hospital in Gurgaon
I Have Warm-reacting-antibody Hemolytic AnemiaI Have Warm-reacting-antibody Hemolytic Anemia
Do You Have Warm-reacting-antibody Hemolytic Anemia? Join friendly people sharing true stories in the I Have Warm-reacting-antibody Hemolytic Anemia group. Find support forums, advice and chat with groups who share this life experience. A Warm-reacti...
State of the Art: Haemoplasmas - Lessons Learnt From Cats - WSAVA2013 - VINState of the Art: Haemoplasmas - Lessons Learnt From Cats - WSAVA2013 - VIN
Candidatus Mycoplasma turicensis: 0.4-26% cats. Pathogenicity. M. haemofelis is the most pathogenic feline haemoplasma species. Acute infection often results in severe haemolytic anaemia (especially in young cats), although at other times only mild anaemia is seen. Chronic infection is not usually associated with anaemia. Cats do not need to be immunocompromised or splenectomised to succumb to M. haemofelis clinical disease. Epidemiological studies have only variably demonstrated associations between anaemia and M. haemofelis infection, likely because these studies usually include chronically M. haemofelis-infected asymptomatic cats. Persistent autoagglutination or positive Coombs testing, indicating the presence of RBC-bound antibodies, are found in anaemic cats with acute M. haemofelis infection,1 although these antibodies usually appear only after the start of the development of anaemia, suggesting that they are as a result of haemoplasma-induced haemolysis rather than initiating ...
Anemia thin blood : Dvt treatment guidelines 2017Anemia thin blood : Dvt treatment guidelines 2017
Plasma cells are mature B lymphocytes that engage in the production of one specific antibody.Microangiopathic hemolytic anemia occurs when the red cell membrane is damaged in circulation,.Characteristic red blood cell abnormalities are anemia, sickle cell anemia and spherocytosis.The preferred and most reliable diagnosis of malaria is microscopic examination of blood films, because each of the four major parasite species has distinguishing characteristics.Others tests to determine anemia include the red blood cell count and the hemoglobin count.. Doctors give unbiased, trusted information on the benefits and side effects of Mephyton to treat Anemia: Dr.Since your body has fewer red blood cells when you have thalassemia, you may have symptoms of a low blood count, or anemia ...
Hemolytic Anemia of Pregnancy with Reports of Cases | Annals of Internal Medicine | American College of PhysiciansHemolytic Anemia of Pregnancy with Reports of Cases | Annals of Internal Medicine | American College of Physicians
Hemolytic anemia of pregnancy is a specific form of anemia, occurring usually during the latter months of pregnancy, or during the puerperium.. Despite the fact that these women frequently show a definite blood picture, and the clinical manifestations of primary anemia, it would seem that this disease is a specific type of anemia of pregnancy, because if the patient survives the acute attack, the blood picture usually returns to normal, and apparently remains so. This latter fact definitely removes the disease from the heading of primary anemia.. The literature on the subject is not voluminous, and much work remains to ...
CONTACT - LUMOXITI™ (moxetumomab pasudotox-tdfk) for HCL - HCPsCONTACT - LUMOXITI™ (moxetumomab pasudotox-tdfk) for HCL - HCPs
Hemolytic Uremic Syndrome (HUS), including life threatening cases, has been reported in patients treated with LUMOXITI and is characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and progressive renal failure. In the combined safety database of HCL patients treated with LUMOXITI, HUS occurred in 7% (9/129) of patients, including Grade 3 in 3% (4/129) and Grade 4 in 0.8% (1/129). Most cases of HUS occurred in the first 9 days (range: 1 to 16) of a treatment cycle, however, cases have also been reported on other days throughout the cycle. The median time to resolution of HUS was 11.5 days (range: 2 to 44). All cases resolved, including those who discontinued LUMOXITI.. Avoid LUMOXITI in patients with prior history of severe thrombotic microangiopathy (TMA) or HUS. Administer prophylactic intravenous fluids before and after LUMOXITI infusions. In Study 1053, patients with a platelet count ≥ 100,000/mm3 received low-dose aspirin on Days 1 through 8 of each 28-day ...
Burr Cell & Thrombocytopenia<...Burr Cell & Thrombocytopenia<...
Burr Cell & Thrombocytopenia Symptom Checker: Possible causes include Microangiopathic Hemolytic Anemia & Folate-Deficiency Anemia & Hemolytic Uremic Syndrome. Check the full list of possible causes and conditions now! Talk to our Chatbot to narrow down your search.
Comparison of the Immunity Status in-Between Children with β-Thalassaemia Major Receiving Different Treatment Modalities: A...Comparison of the Immunity Status in-Between Children with β-Thalassaemia Major Receiving Different Treatment Modalities: A...
Abstract Background: β-thalassaemia major is one of the chronic hemolytic anemias resulting from defect in β-globin chain. It requires frequent blood transfusio..
RightAnswer Knowledge SolutionsRightAnswer Knowledge Solutions
INTRAVENOUS: COMMON: Nausea, vomiting, anorexia, mucositis, fever, and myelosuppression (eg, leukopenia, thrombocytopenia). Leukopenia and thrombocytopenia may occur anytime within 8 weeks after onset of therapy with an average time of 4 weeks. Recovery after cessation of therapy was within 10 weeks. Approximately 25% of leukopenia or thrombocytopenic episodes did not recover. OTHER EFFECTS: Alopecia, diarrhea, ileus, confusion, drowsiness, fatigue, lethargy, headache, syncope, weakness, skin findings (eg, extravasation, desquamation, induration, pruritus, pain on injection, paresthesias, contact dermatitis, necrosis, cellulitis, ulceration, and tissue sloughing at the injection site), renal dysfunction, thrombophlebitis, hepatotoxicity, pulmonary toxicity (eg, hemoptysis, dyspnea, cough, pneumonitis, alveolitis, and pulmonary fibrosis). Hemolytic uremic syndrome, consisting mainly of microangiopathic hemolytic anemia (hematocrit equal to or less than 25%), thrombocytopenia (equal to or less ...
Hemolytic Anemia in ChildrenHemolytic Anemia in Children
The hemolytic anemias are a group of disorders in which the red blood cells are destroyed faster than the bone marrow can make them. The term for destruction of red blood cells is hemolysis.
Heritable Hemolytic Anemia/PKD archivesHeritable Hemolytic Anemia/PKD archives
Heritable Hemolytic Anemia/PKD is where the red cells have a genetically controlled defective pyruvate kinase activity. This is not a curable anemia.
Traumatic Hemolytic Anemia - Net Health BookTraumatic Hemolytic Anemia - Net Health Book
Traumatic hemolytic anemia can come from trauma. This causes schistocytes seen on a blood smear. Several medical conditions can cause this form of anemia.
Child has hemolytic anemia since birth. Done spenectomy. What could be the reason for low hemoglobin?Child has hemolytic anemia since birth. Done spenectomy. What could be the reason for low hemoglobin?
Question - Child has hemolytic anemia since birth. Done spenectomy. What could be the reason for low hemoglobin?. Ask a Doctor about Blood transfusion, Ask a Pediatrician
When Your Child Has Hemolytic AnemiaWhen Your Child Has Hemolytic Anemia
Hemolytic anemia occurs when the body doesnt have enough healthy red blood cells (RBCs). Read on to learn about the causes, symptoms, diagnosis, and treatment of this condition.
hemolytic anemiahemolytic anemia
... definition, an anemic condition characterized by the destruction of red blood cells: seen in some drug reactions and in certain infectious and hereditary disorders. See more.
What is Hemolytic Anemia? (with pictures)What is Hemolytic Anemia? (with pictures)
Hemolytic anemia is a type of condition in which there is an abnormally fast break down of red blood cells. Generally speaking...
Haemolytic anaemia steroid treatment | Hemolytic anemia - WikipediaHaemolytic anaemia steroid treatment | Hemolytic anemia - Wikipedia
A mild normochromic, normocytic anaemia is a common finding and usually a consequence of other diseases, including (1) anaemia of chronic disorders-associated with chronic infection, all forms of inflammatory diseases, and malignant disease; mechanism
Malaria Drug Association With Hemolytic Anemia Unclear - MPRMalaria Drug Association With Hemolytic Anemia Unclear - MPR
Artesunate, a drug used in the treatment of severe malaria, may or may not be associated with hemolytic anemia, so the U.S. Centers for Disease Control and Prevention recommends close monitoring of patients treated with the drug for four weeks after administration of the agent.
Reader Responses: Would rituximab re-treatment help this patient with hemolytic anemia? - ASH Clinical NewsReader Responses: Would rituximab re-treatment help this patient with hemolytic anemia? - ASH Clinical News
Reader Responses: Would rituximab re-treatment help this patient with hemolytic anemia? - Viewpoints, You Make the Call: Readers Response - ASH Clinical News
Heme cases Mar 24 teaching aid - SOM 214 Hemolytic anemias Classifications Intrinsic vs Extrinsic = mechanism Hereditary vs...Heme cases Mar 24 teaching aid - SOM 214 Hemolytic anemias Classifications Intrinsic vs Extrinsic = mechanism Hereditary vs...
View Notes - Heme cases Mar 24_teaching aid from PHARM HEM at UCSD. Feb 24, 2011 SOM 214 Hemolytic anemias Classifications: Intrinsic vs. Extrinsic = mechanism Hereditary vs. Acquired = chronicity,
Hemolytic Anemia - Symptoms, Diagnosis and TreatmentHemolytic Anemia - Symptoms, Diagnosis and Treatment
Complete information about Hemolytic Anemia, including signs and symptoms; conditions that suggest it; contributing risk factors; conditions suggested by it.
Cardiomyopathy and Hemolytic anemia, related diseases and genetic alterations | MENDELIAN.COCardiomyopathy and Hemolytic anemia, related diseases and genetic alterations | MENDELIAN.CO
CARDIOMYOPATHY and HEMOLYTIC ANEMIA related symptoms, diseases, and genetic alterations. Get the complete information with our medical search engine f
Buy Chinese herb remedies for Hemolytic AnemiaBuy Chinese herb remedies for Hemolytic Anemia
Chinese herbs shop remedies for Hemolytic Anemia. Our Chinese herbal products are inexpensive, safe, effective and shipped within 24 hours of order approval.
3T T2* MRI DISTINGUISHES MS FROM MICROANGIOPATHIC LESIONS | Journal of Neurology, Neurosurgery & Psychiatry3T T2* MRI DISTINGUISHES MS FROM MICROANGIOPATHIC LESIONS | Journal of Neurology, Neurosurgery & Psychiatry
Methods Forty patients were studied. Initially a test cohort of 10 patients with multiple sclerosis and 10 patients with microangiopathic white matter lesions underwent brain 3T MRI. Anonymised scans were analysed blind to clinical data, and simple diagnostic rules were devised, which were applied to a validation cohort of 20 patients (13 with multiple sclerosis and 7 with microangiopathic lesions).. ...
Health Article - G6PD Test - AARPHealth Article - G6PD Test - AARP
A G6PD deficiency is an inherited disorder (by X-linked recessive transmission). It can lead to a certain type of anemia known as hemolytic anemia. Anemia is a blood disorder in which the body doesnt have enough red blood cells.. G6PD protects oxygen-rich red blood cells (RBCs) from chemicals called reactive oxygen species (ROS). ROS build up in your body during a fever, infection, or when you take certain medications. If your G6PD levels are too low, your RBCs wont be protected from these chemicals. The blood cells will die, leading to anemia.. Certain foods, medications, infections, and severe stress can trigger a hemolytic episode, which is the rapid destruction of RBCs. In people with hemolytic anemia, the body cant produce enough RBCs to replace those that have been destroyed. Your doctor may order a G6PD test if they suspect you have hemolytic anemia based on symptoms such as:. ...
Health Article | Health & Wellness Library | University Hospitals | Cleveland, OHHealth Article | Health & Wellness Library | University Hospitals | Cleveland, OH
You may need this test to tell your healthcare provider whether you have antibodies that have attached to your red blood cells. You may need this test if you have symptoms of hemolytic anemia after a blood transfusion. A baby may need this blood test if the babys mother makes antibodies against the babys red blood cells and passes those antibodies to the baby inside the womb. This condition is called hemolytic disease of the newborn.. The most common cause of hemolytic anemia is when your immune system makes antibodies to your own red blood cells by mistake. When your immune system makes antibodies against your own healthy cells, it is called autoimmune disease. Symptoms or signs of hemolytic anemia may include:. ...
neutropenia Archives - CriticalCareDVMneutropenia Archives - CriticalCareDVM
It should come as no surprise to anybody who follows this blog that I love hematology and immunology! In previous posts Ive written about various immune-mediated problems, including immune-mediated hemolytic anemia, immune-mediated thrombocytopenia, and immune-mediated polyarthropathy. This week Im sharing information about another immune-mediated condition: immune-mediated neutropenia or IMN. I hope you find the material … [Read more…]. ...
idiopathic Archives - CriticalCareDVMidiopathic Archives - CriticalCareDVM
My favorite aspect of practicing medicine is treating diseases caused by dysfunction of the immune system. In previous blogs, I reviewed two common immune-mediated diseases - immune-mediated hemolytic anemia and immune-mediated thrombocytopenia. A less commonly appreciated condition of immune system dysfunction is immune-mediated polyarthropathy or IMPA, a disease where the immune system attacks a pets joints. … [Read more…] ...
German Wirehaired Pointer Club of America :: View topic - Is this serious?German Wirehaired Pointer Club of America :: View topic - Is this serious?
4- Finally and most importantly, over vaccination is now believed to be at the source of many auto-immune diseases. Although Veterinary colleges all teach their students that following the first sets of vaccines a puppy receives, re-vaccinations should be done every 3 to 4 years and should end when the dog reaches 7 to 9 years of age, Vets continue to send reminder cards to their clients yearly. People dont get vaccinated every year, and neither should animals. Even the department of agriculture of most countries recognises this fact when they require you to vaccinate your dogs against rabies every 3 years. By constantly activating the immune system of our dogs, their cells learn to react against much of their own normal systems, inflicting various autoimmune diseases such as lupus, immune-mediated arthritis, immune-mediated hemolytic anemia and much more... If your dog suffer from any autoimmune disease, it is recommanded that he does not receive anymore vaccines with the exception of Rabies ...
Overview of Hemolytic Anemia - Hematology and Oncology - Merck Manuals Professional EditionOverview of Hemolytic Anemia - Hematology and Oncology - Merck Manuals Professional Edition
Learn about the causes, symptoms, diagnosis & treatment of Anemias Caused by Hemolysis from the Professional Version of the Merck Manuals.
10 Symptoms of Hemolytic Anemia - Facty Health10 Symptoms of Hemolytic Anemia - Facty Health
Red blood cells or erythrocytes have the most difficult task in the entire body. They carry oxygen from your lungs to the heart and the rest of the body. Bone marrow makes the red blood cells. Usually, there is an abundance of erythrocytes available.
Childrens Hospital of The Kings Daughters Health SystemChildren's Hospital of The King's Daughters Health System
Treatment will depend on your childs symptoms, age, and general health. It will also depend on how severe the condition is.. A child with hemolytic anemia is often treated by a hematologist, an expert in blood disorders. The treatment for hemolytic anemia will vary depending on the cause of the illness and how severe the anemia is. Some children do not need treatment. For those that do, treatment may include:. ...
Papers with the keyword Penicillin anemia eosinophilia | Read by QxMDPapers with the keyword Penicillin anemia eosinophilia | Read by QxMD
Sera from 125 patients receiving mean total doses of beta-lactam therapy of 215 g over a mean of 14 days were assayed by radioimmunoassay. Titres of anti-penicilloyl antibodies, expressed in arbitrary units of specific IgG per microliter of serum (u/microliter), ranged from undetectable (less than 3 u/microliter) to 1,650 u/microliter. There was a higher prevalence of elevated IgG levels in patients who developed haemolytic anaemia or neutropenia compared with patients with no adverse reactions but only in those patients who developed haemolytic anaemia were the antibody titres significantly higher ...
ABO Discrepancy and Hemolytic Anemia Post Liver Transplant due to Passenger Lymphocyte Syndrome : Laboratory Medicine - oiABO Discrepancy and Hemolytic Anemia Post Liver Transplant due to Passenger Lymphocyte Syndrome : Laboratory Medicine - oi
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Diabetes, Thyroiditis & Hemolytic Anemia | Kerry Blue Terrier FoundationDiabetes, Thyroiditis & Hemolytic Anemia | Kerry Blue Terrier Foundation
The Kerry Blue Terrier Foundation (KBTF) is pleased to announce that it has contributed funds to an important research study on autoimmune diseases in dogs.
Microangiopathic hemolytic anemia - WikipediaMicroangiopathic hemolytic anemia - Wikipedia
In medicine (hematology) microangiopathic hemolytic anemia (MAHA) is a microangiopathic subgroup of hemolytic anemia (loss of red blood cells through destruction) caused by factors in the small blood vessels. It is identified by the finding of anemia and schistocytes on microscopy of the blood film. In diseases such as hemolytic uremic syndrome, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, and malignant hypertension, the endothelial layer of small vessels is damaged with resulting fibrin deposition and platelet aggregation. As red blood cells travel through these damaged vessels, they are fragmented resulting in intravascular hemolysis. The resulting schistocytes (red cell fragments) are also increasingly targeted for destruction by the reticuloendothelial system in the spleen, due to their narrow passage through obstructed vessel lumina. It is seen in systemic lupus erythematosus, where immune complexes aggregate with platelets, forming intravascular thrombi. ...
CHAPTER 57 DRUG-RELATED IMMUNE HEMOLYTIC ANEMIA | Free Medical TextbookCHAPTER 57 DRUG-RELATED IMMUNE HEMOLYTIC ANEMIA | Free Medical Textbook
CHAPTER 57 DRUG-RELATED IMMUNE HEMOLYTIC ANEMIA Williams Hematology CHAPTER 57 DRUG-RELATED IMMUNE HEMOLYTIC ANEMIA CHARLES H. PACKMAN Definitions and History Etiology and Pathogenesis Hapten or Drug Adsorption Mechanism Ternary Complex Mechanism: Drug-Antibody-Target Cell Complex Autoantibody Mechanism Nonimmunologic Protein Adsorption Clinical Features Laboratory Features Differential Diagnosis Therapy, Course, and Prognosis Therapy Course and Prognosis Chapter References…
Home remedy and cure of Haemolytic AnaemiaHome remedy and cure of Haemolytic Anaemia
The first deficiency to be demonstrated was a haemolytic Anemia described in premature infants. Infant formulations now contain vitamin E. Haemolytic anaemia is a breakdown of red cells with haemolysis which results in anaemia. There is sequestration of the red cells in the spleen which may enlarge.. A haemolytic anaemia is where the red blood cells are being broken down resulting in the patient becoming anaemic. There are a number of things which can attack the red blood cells. In autoimmune haemolytic anaemia it seems that the body is producing its own attack - that is, it is producing antibodies which it would normally produce to fight infections to fight its own cells. There are a lot of autoimmune diseases of different kinds and this haemolytic anaemia might be part of one of those diseases or it might be a problem in its own right - then it tends to get called idiopathic autoimmune haemolytic anaemia.. Acquired haemolytic anaemia may also be caused by the presence of antibodies ...
Hemolytic Anemia Resulting from Infections with Microorganisms | Williams Hematology, 9e | AccessHemOnc | McGraw-Hill MedicalHemolytic Anemia Resulting from Infections with Microorganisms | Williams Hematology, 9e | AccessHemOnc | McGraw-Hill Medical
SUMMARY Hemolytic anemia is a prominent part of the clinical presentation of patients infected with organisms such as the Plasmodium sp., Babesia, and Bartonella, which directly invade the erythrocyte. Malaria is the most common cause of hemolytic anemia on a worldwide basis, and much has been learned about how the parasite enters the erythrocyte and the mechanism of anemia. Falciparum malaria, in particular, can cause severe and sometimes fatal hemolysis (blackwater fever). Other organisms cause hemolytic anemia by producing a hemolysin (e.g., Clostridium perfringens), by stimulating an immune response (e.g., Mycoplasma pneumoniae), by enhancing macrophage recognition and hemophagocytosis, or by as yet unknown mechanisms. The many different infections that have been associated with hemolytic anemia are tabulated and references to the original studies provided.. ...
Hereditary hemolytic anemia with increased red cell adenosine deaminase (45- to 70-fold) and decreased adenosine triphosphate |...Hereditary hemolytic anemia with increased red cell adenosine deaminase (45- to 70-fold) and decreased adenosine triphosphate |...
Hereditary hemolytic anemia, a dominantly transmitted disorder, has affected 12 family members spanning three generations. The concentration of adenosine triphosphate in the red cells was about half that of comparably reticulocyte-rich blood. Since adenosine deaminase and adenosine kinase compete for a common substrate, the greatly increased activity of the former may interfere with nucleotide salvage via the latter. ...
Acquired immune hemolytic anemia associated with IgA erythrocyte coating: investigation of hemolytic mechanisms | Blood |...Acquired immune hemolytic anemia associated with IgA erythrocyte coating: investigation of hemolytic mechanisms | Blood |...
We have investigated the hemolytic mechanisms in a patient with acquired immune hemolytic anemia whose red cells appeared to be coated with IgA alone. The clinical course was similar to that of patients with hemolytic anemia mediated by warm-reacting IgG antibody. Splenic sequestration of red cells was demonstrated, and marked reduction of hemolysis occurred after corticosteroid therapy. Antibody was eluted from the patients red cells and used to sensitize normal red cells in vitro. These sensitized red cells were not lysed by fresh autologous serum, nor did they fix detectable amounts of C3. However, red cells sensitized by eluted antibody were lysed by normal human peripheral blood monocytes in a system designed to demonstrate antibody-dependent cell-mediated cytotoxicity. Monocyte-mediated hemolysis of sensitized red cells was inhibited by the addition of low concentrations of normal serum IgA to the system, but not by IgG. The ability of the eluate to induce monocyte-mediated hemolysis was ...
Recurrent Oxaliplatin-Induced Immune Hemolytic Anemia by Chemotherapy for Metastatic Colon Cancer: A Case ReportRecurrent Oxaliplatin-Induced Immune Hemolytic Anemia by Chemotherapy for Metastatic Colon Cancer: A Case Report
ABSTRACT. We report herein the case of a 55-year-old man who presented an acute hemolysis following a 6th cycle of FOLFOX regimen for a metastatic colorectal cancer; this patient had previously received 12 cycles in an adjuvant setting. He had presented attenuated signs during the previous cycle. This corresponded to an oxaliplatin-induced immune hemolytic anemia. This unfrequent side effect of oxaliplatin needs to be known in order to avoid severe complications.. 1. Introduction. Oxaliplatin is used in the treatment of colorectal cancer in adjuvant or metastatic setting. The side effects are generally moderate: hypersensitivity, digestive disorders, hematological toxicity, acroparesthesia exacerbated by the cold. More rarely, oxaliplatin can be responsible for immune-induced cytopenia that can sometimes threaten the vital prognosis. We report a rare case of a patient presenting with autoimmune hemolytic anemia induced by oxaliplatin after several months of treatment, with rapid and favorable ...
EDITORS QUIZ: GI SNAPSHOT | GutEDITOR'S QUIZ: GI SNAPSHOT | Gut
Spur cell anaemia (acanthocytosis), a rare acquired haemolytic anaemia observed mainly in the end stages of alcoholic cirrhosis, is characterised by an increased ratio of free cholesterol to phospholipid in the erythrocyte membranes that results in multispiculated erythrocytes (acanthocytes). These acanthocytes undergo rapid splenic destruction and consequently have a shortened survival. Recent studies have indicated that alcoholic iron overload may be associated with spur cell anaemia rather than hereditary haemochromatosis. Patients usually need frequent blood transfusions and the prognosis is extremely poor. Liver transplantation, which improves hepatic function and resolves spur cell anaemia, has been the most effective treatment. Our patient did not choose liver transplantation. She had a poor response to conservative treatment with multiple blood transfusions and died of liver failure seven months later. ...
Acute Autoimmune Hemolytic Anemia Following DTP Vaccination: Report of a Fatal Case and Review of the...'Acute Autoimmune Hemolytic Anemia Following DTP Vaccination: Report of a Fatal Case and Review of the...
the child was given her second doses of the oral polio virus, hepatitis B, and diphtheria, tetanus, and pertussis (DTP) vaccines, and within four days she exhibited lethargy, a low level fever, and lack of appetite. She was unresponsive when admitted to the hospital three days later, suffering from severe anemia and low hemoglobin levels. Tests for Haemophilus influenza, Streptococcus pneumoniae, and Neiseria meningitidis were negative or did not appear conclusively as cause or contributor to the current condition. The infant continued to experience severe hemolysis and died 41 hours after admission. Although the study could not prove it conclusively, by eliminating other causes of autoimmune hemolytic anemia (AIHA), the researchers suggest that, in this case, there is a causal relationship to the second DTP vaccination. A 1992 report from the Institute of Medicine concluded, however, that there is insufficient evidence of either the presence or absence of such a connection.. ...
How We Investigate Drug-Induced Immune Hemolytic Anemia - PubMedHow We Investigate Drug-Induced Immune Hemolytic Anemia - PubMed
Drugs are a rare cause of immune hemolytic anemia, but an investigation for a drug antibody may be warranted if a patient has definitive evidence of immune hemolysis, other more common causes of hemolysis have been excluded, and there is a good temporal relationship between the administration of a d …
Haemolytic anaemia | Article about haemolytic anaemia by The Free DictionaryHaemolytic anaemia | Article about haemolytic anaemia by The Free Dictionary
Looking for haemolytic anaemia? Find out information about haemolytic anaemia. A decrease in the blood concentration of hemoglobin and the number of erythrocytes, due to the inability of the mature erythrocytes to survive in the... Explanation of haemolytic anaemia
Hemolytic anemias due to abnormalities in red cell spectrin: a brief by S E. Lux, L C. Wolfe et al.Hemolytic anemias due to abnormalities in red cell spectrin: a brief " by S E. Lux, L C. Wolfe et al.
Lux, S E.; Wolfe, L C.; Pease, B; Tomaselli, M B.; John, K M.; and Bernstein, S E., " Hemolytic anemias due to abnormalities in red cell spectrin: a brief review." (1981). Faculty Research 1980 - 1989. 159 ...
Chapter 433. Hemolytic Anemia | Rudolphs Pediatrics, 22e | AccessPediatrics | McGraw-Hill MedicalChapter 433. Hemolytic Anemia | Rudolph's Pediatrics, 22e | AccessPediatrics | McGraw-Hill Medical
The classic laboratory finding of hemolysis is anemia with an elevated reticulocyte count. The reticulocytosis reflects normal bone marrow function and occurs in response to the premature RBC destruction; reticulocytes are larger than older erythrocytes and have a blue-purple color known as polychromasia (Fig. 433-1). Reticulocytosis generally occurs 3 to 5 days after a sudden drop in hemoglobin concentration but is relatively constant in children with congenital hemolytic anemia. Making the diagnosis of hemolytic anemia begins with recognizing the constellation of signs and symptoms, then obtaining a complete blood count with reticulocyte count, and finally examining the peripheral blood smear. Additional laboratory findings supporting the diagnosis of hemolysis include elevated total serum bilirubin and lactate dehydrogenase (LDH; LDH being released from RBCs during hemolysis). Intravascular hemolysis also causes decreased or undetectable levels of haptoglobin, but this test is not specific so ...
Occurrence of G6PD Enzyme Deficiency among Children Suffering from Hemolytic Anemia in Gaza - PalestineOccurrence of "G6PD" Enzyme Deficiency among Children Suffering from Hemolytic Anemia in Gaza - Palestine
Background: The Glucose-6-phosphate dehydrogenase (G6PD) deficiency has been considered as the commonest enzymopathic inherited disorder of red blood cells, which affecting more than 500 million people worldwide. The G6PD gene in human is X-linked so males are more affected than females. The mutation in the G6PD gene may lead to the production of a G6PD enzyme that has diminished functionality and/or stability, leading to wide range of biochemical and clinical presentations principally neonatal jaundice and acute hemolytic anemia triggered by an exogenous agent in most cases. More than 176 mutations, and 500 different variants have been described to date for the G6PD gene, however, the Mediterranean mutation c.563 C,T, whether associated with c.1311 C,T polymorphism or not, is among most common variants that lead to enzyme deficiency and often associated with Favism. Objectives: The main objective of this study is to determine the frequency of the Mediterranean mutation (c.563 C,T) and its ...
Successful treatment of scleroderma renal crisis with enalapril. | Postgraduate Medical JournalSuccessful treatment of scleroderma renal crisis with enalapril. | Postgraduate Medical Journal
A patient with scleroderma renal crisis is described. At presentation he had severe hypertension, deteriorating renal function, microangiopathic haemolytic anaemia, and elevated levels of renin, aldosterone and noradrenaline. Enalapril controlled blood pressure, stabilized renal function, lowered aldosterone and noradrenaline levels, and improved peripheral circulation. It appears that converting-enzyme inhibitors can favourably alter the outlook of this otherwise fatal disorder.. ...
Hereditary hemolytic anemia - Causes,Symptoms,Diagnosis,Treatment,Analysis,diseaseHereditary hemolytic anemia - Causes,Symptoms,Diagnosis,Treatment,Analysis,disease
Inherited in a dominant and recessive manner. And each of these options is characterized by the presence of fetal hemoglobin. The most severe disease is considered to be a big thalassemia, which is expressed already in the neonatal period and ending fatally. Asymptomatic forms are due to the presence of HbA, HbF, and others formed early appearance of the child: "tower skull", wide-set eyes, broad flat nose. There is an increase in the abdomen as a result of increased parenchymal organs, primarily the spleen ...
Non RhD isoimmunization causing severe hemolytic disease of fetus and newborn in Rh positive pregnancies: report of 2 cases...Non RhD isoimmunization causing severe hemolytic disease of fetus and newborn in Rh positive pregnancies: report of 2 cases...
Non RhD isoimmunization causing severe hemolytic disease of fetus and newborn in Rh positive pregnancies: report of 2 cases with review of literature
Horses and Zebras: September 2016Horses and Zebras: September 2016
If there are fragments, it is consistent with a microangiopathic hemolytic anemia. Fragments are broken apart red blood cells; the red blood cells are broken apart in the intravascular system when there is damage and clot formation in blood vessels that the red blood cells get trapped in and ripped apart. There could also be other indicators of hemolysis including: elevated LDH, elevated indirect bilirubin, and decreased haptoglobin. It is not an immune related cause of hemolysis so the DAT (direct antiglobulin test) should be negative ...
Autoimmune Hemolytic Anemia - how long after taking predisone should the pain stop?Autoimmune Hemolytic Anemia - how long after taking predisone should the pain stop?
1 Answer - Posted in: anemia, hemolytic anemia - Answer: I found no answer to your question. This is the best, simplest explanation ...
Cefuroxime-induced immune hemolysis<...Cefuroxime-induced immune hemolysis<...
TY - JOUR. T1 - Cefuroxime-induced immune hemolysis. AU - Malloy, Colleen Ann. AU - Kiss, Joseph E.. AU - Challapalli, Malliswari. PY - 2003/7/1. Y1 - 2003/7/1. N2 - Drug-induced immune hemolytic anemia (IHA) is rare but is being reported with increasing frequency. The most commonly cited cause of drug-induced IHA has been receipt of second and third generation cephalosporin antibiotics. We report the first case of IHA associated with cefuroxime administration.. AB - Drug-induced immune hemolytic anemia (IHA) is rare but is being reported with increasing frequency. The most commonly cited cause of drug-induced IHA has been receipt of second and third generation cephalosporin antibiotics. We report the first case of IHA associated with cefuroxime administration.. UR - http://www.scopus.com/inward/record.url?scp=0041743122&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0041743122&partnerID=8YFLogxK. U2 - 10.1016/S0022-3476(03)00210-5. DO - ...
Stem cells: The therapeutic role in the treatment of diabetes mellitus - University of Huddersfield RepositoryStem cells: The therapeutic role in the treatment of diabetes mellitus - University of Huddersfield Repository
References: Ahuja, Y.R., Vijayalakshmi, V., Stem cell test: A practical tool in toxicogenomics (2007) Toxicology, 231 (1), pp. 1-10; Ainsworth, C.D., Crowther, M.A., Treleaven, D., Evanovttch, D., Webert, K.E., Blajchman, M.A., Severe hemolytic anemia post-renal transplantation produced by donor anti-D passenger lymphocytes, case report and literature review (2009) Transfusion Medical Review, 23 (2), pp. 155-159; Amit, M., Carpenter, M.K., Clonally derived human embryonic stem cell lines maintain pluripotency and proliferative potential for prolonged periods of culture (2000) Developmental Biology, 227 (2), pp. 271-278; Amit, M., Itskovitz-Eldor, J., Maintenance of human embryonic stem cells in animal serum- and feeder layer-free culture conditions (2006) Methods Molecular Biology, 331, pp. 105-113; Amit, M., Margulets, V., Human feeder layers for human embryonic stem cells (2003) Biological Reproduction, 68 (6), pp. 2150-2156; Andrews, P.W., From teratocarcinomas to embryonic stem cells (2002) ...
Zinc - wikidocZinc - wikidoc
Even though zinc is an essential requirement for a healthy body, too much zinc can be harmful. Excessive absorption of zinc can also suppress copper and iron absorption. The free zinc ion in solution is highly toxic to plants, invertebrates, and even vertebrate fish. The Free Ion Activity Model (FIAM) is well-established in the literature, and shows that just micromolar amounts of the free ion kills some organisms. A recent example showed 6 micromolar killing 93% of all daphnia in water.[4] Swallowing a post 1982 American one cent piece (97.5% zinc) can also cause damage to the stomach lining due to the high solubility of the zinc ion in the acidic stomach.[5] Zinc toxicity, mostly in the form of the ingestion of US pennies minted after 1982, is commonly fatal in dogs where it causes a severe hemolytic anemia.[6] In pet parrots zinc is highly toxic and poisoning can often be fatal[7]. There is evidence of induced copper deficiency at low intakes of 100-300 mg Zn/d. The USDA RDA is 15 mg Zn/d. ...
Hows Dave Doing?: Auto Immune Hemolytic AnemiaHow's Dave Doing?: Auto Immune Hemolytic Anemia
AIHA is the current problem - in addition to the CLL, of course. Dave has had some ups and downs the last few weeks, and hes due to start Chemo again tomorrow. But Im not convinced that his blood counts are adequate (that he can withstand a round of chemo.) The doctor has been increasing his Prednisone, but based on his appearance, I have a feeling his counts are down again. He had more blood drawn this morning, so tomorrow morning, when we meet with the doctor, well know for sure ...
Piperacillin-Induced Immune Hemolytic Anemia in an Adult with Cystic FibrosisPiperacillin-Induced Immune Hemolytic Anemia in an Adult with Cystic Fibrosis
Case Reports in Medicine is a peer-reviewed, Open Access journal that publishes case reports and case series in all areas of clinical medicine.
Anemias, Sickle Cell - Medical Dictionary online-medical-dictionary.orgAnemias, Sickle Cell - Medical Dictionary online-medical-dictionary.org
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 ...
Clinical Approaches to Managing and Treating Adverse Vaccine Reactions by W. Jean Dodds, DVM - Truth4Pets | Truth4PetsClinical Approaches to Managing and Treating Adverse Vaccine Reactions by W. Jean Dodds, DVM - Truth4Pets | Truth4Pets
Potent adjuvanted killed vaccines like those for rabies virus also can trigger immediate and delayed (vaccinosis) adverse vaccine reactions. Genetic predisposition to these disorders in humans has been linked to the leucocyte antigen D-related gene locus of the major histocompatibility complex, and is likely to have parallel associations in domestic animals.. It must be recognized, however, that we have the luxury of asking such questions today only because the risk of disease has been effectively reduced by the widespread use of vaccination programs.. Adverse Events Associated with Vaccination The clinical signs associated with vaccine reactions typically include fever, stiffness, sore joints and abdominal tenderness, susceptibility to infections, neurological disorders and encephalitis, collapse with autoagglutinated red blood cells and icterus (autoimmune hemolytic anemia, AIHA, also called immune-mediated hemolytic anemia, IMHA), or generalized petechiae and ecchymotic hemorrhages ...
JCI - Mutations in factor H reduce binding affinity to C3b and heparin and surface attachment to endothelial cells in hemolytic...JCI - Mutations in factor H reduce binding affinity to C3b and heparin and surface attachment to endothelial cells in hemolytic...
Hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. Recent studies have identified a factor H-associated form of HUS, caused by gene mutations that cluster in the C-terminal region of the complement regulator factor H. Here we report how three mutations (E1172Stop, R1210C, and R1215G; each of the latter two identified in three independent cases from different, unrelated families) affect protein function. All three mutations cause reduced binding to the central complement component C3b/C3d to heparin, as well as to endothelial cells. These defective features of the mutant factor H proteins explain progression of endothelial cell and microvascular damage in factor H-associated genetic HUS and indicate a protective role of factor H for tissue integrity during thrombus formation.. ...
JCI - Mutations in factor H reduce binding affinity to C3b and heparin and surface attachment to endothelial cells in hemolytic...JCI - Mutations in factor H reduce binding affinity to C3b and heparin and surface attachment to endothelial cells in hemolytic...
Hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. Recent studies have identified a factor H-associated form of HUS, caused by gene mutations that cluster in the C-terminal region of the complement regulator factor H. Here we report how three mutations (E1172Stop, R1210C, and R1215G; each of the latter two identified in three independent cases from different, unrelated families) affect protein function. All three mutations cause reduced binding to the central complement component C3b/C3d to heparin, as well as to endothelial cells. These defective features of the mutant factor H proteins explain progression of endothelial cell and microvascular damage in factor H-associated genetic HUS and indicate a protective role of factor H for tissue integrity during thrombus formation.. ...
Article abstract | American Journal of Case ReportsArticle abstract | American Journal of Case Reports
BACKGROUND:Thrombotic thrombocytopenic purpura (TTP) in children is a rare life-threatening syndrome, characterized by microangiopathic hemolytic anemia, thrombocytopenia with renal dysfunction, neurologic symptoms, and fever. TTP is usually caused b...
Hemolytic Anemia | NaturalBloodHealth.comHemolytic Anemia | NaturalBloodHealth.com
The following testimonial letter was translated from Spanish.). As believers in God, we are are sure that Carao was an answer sent by the Lord in response to our prayers. For more than 2 years, David had been taking Prednizolona, in relatively large doses (up to 20 mg. daily) for a child of his age (4 years) and when the dosage was reduced (following the doctors instructions) the autoimmune hemolytic anemia reappeared. On 4 occasions, David required blood transfusions.. When he started taking Carao, he immediately began to improve. read more ». ...
Browsing Peter Agre by Author Bennet, VBrowsing Peter Agre by Author "Bennet, V"
Patients from two families with chronic hemolytic anemia have been studied. The erythrocytes are very fragile and appear microcytic with a great variety of shapes. Clinical evaluation failed to identify traditionally ...
FDA Alert: Avastin (bevacizumab) - Jul 14, 2008FDA Alert: Avastin (bevacizumab) - Jul 14, 2008
Audience: Oncologists, other healthcare professionals. [Posted 07/14/2008] Genentech, Inc. informed healthcare professionals of reports of several cases of microangiopathic hemolytic anemia (MAHA) in patients with solid tumors receiving Avastin in combination with sunitinib malate. Avastin is not approved for use in combination with sunitinib malate and this combination is not recommended. Twenty-five patients were enrolled in a Phase I dose-escalation study combining Avastin and sunitinib malate. The study consisted of 3 cohorts using a fixed dose of Avastin at 10mg/kg/IV every 2 weeks and escalating doses of sunitinib that included 25, 37.5, and 50 mg orally daily given in a 4 weeks on/ 2 weeks off schedule. Five of 12 patients at the highest sunitinib dose level exhibited laboratory findings consistent with MAHA. Two of these cases were considered severe with evidence of thrombocytopenia, anemia, reticulocytosis, reductions in serum haptoglobin, schistocytes on peripheral smear, modest ...
Hemolytic anemia - WikipediaHemolytic anemia - Wikipedia
In a healthy person, a red blood cell survives 90 to 120 days in the circulation, so about 1% of human red blood cells break down each day[citation needed]. The spleen (part of the reticulo-endothelial system) is the main organ that removes old and damaged RBCs from the circulation. In healthy individuals, the breakdown and removal of RBCs from the circulation is matched by the production of new RBCs in the bone marrow. In conditions where the rate of RBC breakdown is increased, the body initially compensates by producing more RBCs; however, breakdown of RBCs can exceed the rate that the body can make RBCs, and so anemia can develop. Bilirubin, a breakdown product of hemoglobin, can accumulate in the blood, causing jaundice. In general, hemolytic anemia occurs as a modification of the RBC life cycle. That is, instead of being collected at the end of its useful life and disposed of normally, the RBC disintegrates in a manner allowing free iron-containing molecules to reach the blood. With their ...
Internet Scientific PublicationsInternet Scientific Publications
We discuss the case of a patient with PAH of multiple etiologies, and report to the best of our knowledge the first case of APS and factor V deficiency associated with MMM.. The etiology of PAH in this case was not that of emphysema or interstitial lung disease as evidenced by minimal parenchymal involvement on imaging studies. However, negative perfusion lung scan and doppler ultrasound of lower extremities could not exclude the possibility of pulmonary microthrombosis (6,8). Thrombotic microangiopathy has been associated with APS (10,26), and MPD (8,18). In fact, recurrent pulmonary embolism is assumed to be the major cause of PAH in APS (5,10); and, thromboembolism secondary to thrombophilia (in MMM) is well described (7,8,18).. Although titers of aPL were not available in our patient, the diagnosis of APS was satisfied by other major criteria. These major criteria were past episodes of vascular thrombosis (microangiopathic hemolytic anemia, myocardial infarction, and stroke), laboratory ...
Notes from Dr. RW: TTP presenting as complete heart blockNotes from Dr. RW: TTP presenting as complete heart block
Although we typically think of a pentad of manifestations of TTP and, in fact, have a treatment threshold consisting of microangiopathic hemolytic anemia and thrombocytopenia otherwise unexplained, the disease can cause manifestations in multiple organs. Here is a discussion of cardiac manifestations. ...
Features associated with, and the impact of, hemolytic anemia in patients with systemic lupus erythematosus: LX, results from a...Features associated with, and the impact of, hemolytic anemia in patients with systemic lupus erythematosus: LX, results from a...
Durán, S., Apte, M., Alarcón, G. S., Marion, M. C., Edberg, J. C., Kimberly, R. P., Zhang, J., Langefeld, C. D., ViLá, L. M. and Reveille, J. D. (2008), Features associated with, and the impact of, hemolytic anemia in patients with systemic lupus erythematosus: LX, results from a multiethnic cohort. Arthritis & Rheumatism, 59: 1332-1340. doi: 10.1002/art.24020 ...
Hemolytic Anemia | Boston Childrens HospitalHemolytic Anemia | Boston Children's Hospital
Learn more about Hemolytic Anemia symptoms, diagnosis, and treatments from experts at Boston Childrens, ranked best Childrens Hospital by US News.
Hemolytic Anemia | National Heart, Lung, and Blood Institute (NHLBI)Hemolytic Anemia | National Heart, Lung, and Blood Institute (NHLBI)
Learn more about the causes, symptoms, complications, and treatments for hemolytic anemia, and how to participate in an NHLBI clinical trial.
Chloroquine g6pdChloroquine g6pd
A chloroquine dose of 600 mg base (= 1,000 mg salt) should be given initially, followed by 300 mg base (= 500 mg salt) at 6, 24, and 48 hours after the initial dose for a total chloroquine dose of 1,500 mg base (=2,500 mg salt) Glucose-6-phosphate dehydrogenase (G6PD) deficiency-May cause hemolytic anemia in patients with this condition. Excretion of chloroquine is quite slow,but is increased by acidification of the urine G6PD deficiency is an inherited disease (passed on from previous generations), and cannot be caught by being in contact with someone else. chloroquine g6pd Relapsing and increasingly frequent recrudescent infections cause repeated symptomatic illnesses, worsening the risk of anaemia and severe and fatal disease [ 5, 6 ] Chloroquine is used to prevent and treat malaria. DRUGS TO AVOID IN G6PD DEFICIENCY DEFINITE RISK OF HAEMOLYSIS POSSIBLE RISK OF HAEMOLYSIS Pharmacological Class • Chloroquine & derivatives • Proguanil • Pyrimethamine • Quinidine • Quinine Refer to ...
UniProtKB/SwissProt variant VAR 002488UniProtKB/SwissProt variant VAR 002488
Anemia, non-spherocytic hemolytic, due to G6PD deficiency (NSHA) [MIM:300908]: A disease characterized by G6PD deficiency, acute hemolytic anemia, fatigue, back pain, and jaundice. In most patients, the disease is triggered by an exogenous agent, such as some drugs, food, or infection. Increased unconjugated bilirubin, lactate dehydrogenase, and reticulocytosis are markers of the disorder. Although G6PD deficiency can be life-threatening, most patients are asymptomatic throughout their life. {ECO:0000269,PubMed:12524354, ECO:0000269,PubMed:1303180, ECO:0000269,PubMed:1303182, ECO:0000269,PubMed:1536798, ECO:0000269,PubMed:1611091, ECO:0000269,PubMed:1889820, ECO:0000269,PubMed:1945893, ECO:0000269,PubMed:20007901, ECO:0000269,PubMed:26479991, ECO:0000269,PubMed:2836867, ECO:0000269,PubMed:2912069, ECO:0000269,PubMed:30988594, ECO:0000269,PubMed:7858267, ECO:0000269,PubMed:7959695, ECO:0000269,PubMed:8193373, ECO:0000269,PubMed:8490627, ECO:0000269,PubMed:8533762, ECO:0000269,PubMed:8733135, ...
Protein Function Globins and Antibodies 3/12/ ppt downloadProtein Function Globins and Antibodies 3/12/ ppt download
13 Changes in surface rarely change the function of hemoglobin with the exception of the sickle cell mutation. Internal residues cause the hemoglobin to contort to different shapes and alter its binding properties. Heinz bodies are precipitated aggregates of hemoglobin. Usually cause hemolytic anemia characteristic by cell lysis. Hb Hammersmith Phe CD1(42)   Ser. The Phe wedges the heme in place, without it the heme falls out of the protein. Hb Bristol Val E11(67)   Asp occludes O 2 from the pocket. Hb Bibba substitutes a Pro in the middle of H helix kinks the chain. Hb Savannah replaces Gly B6(24)  Val where the B helix crosses the E helix. ...
Annals of General Hospital Psychiatry | Full text | Psychotic mania in glucose-6-phosphate-dehydrogenase-deficient subjectsAnnals of General Hospital Psychiatry | Full text | Psychotic mania in glucose-6-phosphate-dehydrogenase-deficient subjects
This description of psychotic mania in a substantial proportion of G6PD-deficient subjects attending our department is to be discussed in the context of existing literature. The role of G6PD deficiency in psychiatric disorders has not been definitely established, studies varying from reports of acute psychotic cases [6,7] to surveys of enzyme activity in hospitalized populations [8-10,14]. G6PD deficiency was also used as a traditional X-chromosome marker in linkage studies [4,15-17]. The first study dates back to 1962, when Dern et al [6] reported a not-otherwise-described temporary psychosis during primaquine administration in two G6PD-deficient subjects several weeks after the subsidence of acute hemolytic anemia.. In 1976, Nasr reported two consecutive acute psychotic episodes in a young Afro-American woman [7]. An abstract of the description of the latter case is worthy of mention: "She was in good mental health until one week prior to admission, when she started to become irritable and ...
Crowdfunding to help pay for mylos medical treatment for immune-mediates haemolytic anemia and non-regenerative anemia on...Crowdfunding to help pay for mylo's medical treatment for immune-mediates haemolytic anemia and non-regenerative anemia on...
Weʼre raising money to help pay for mylos medical treatment for immune-mediates haemolytic anemia and non-regenerative anemia. Support this JustGiving Crowdfunding Page.
Tafenoquine (Oral Route) Description and Brand Names - Mayo ClinicTafenoquine (Oral Route) Description and Brand Names - Mayo Clinic
Before taking this medicine, you and your child should be tested for G6PD deficiency or favism (blood disorder). Tafenoquine may cause hemolytic anemia in patients with these conditions. Talk to your doctor if you have concerns about this. This medicine may cause some people to be agitated, irritable, or display other abnormal behaviors. Make sure the doctor knows if you have trouble sleeping, get upset easily, have a big increase in energy, or start to act reckless. Also tell the doctor if you have sudden or strong feelings, such as feeling nervous, angry, restless, violent, or scared. If you or your caregiver notice any of these side effects, tell your doctor right away. This medicine may cause a serious allergic reaction, including angioedema, which can be life-threatening and requires immediate medical attention. Tell your doctor right away if you have a rash, itching, hoarseness, trouble breathing, trouble swallowing, or large, hive-like swelling on face, eyelids, lips, tongue, throat, ...
Nomifensine | CTDNomifensine | CTD
An isoquinoline derivative that prevents dopamine reuptake into synaptosomes. The maleate was formerly used in the treatment of depression. It was withdrawn worldwide in 1986 due to the risk of acute hemolytic anemia with intravascular hemolysis resulting from its use. In some cases, renal failure also developed. (From Martindale, The Extra Pharmacopoeia, 30th ed, p266 ...
Canine Haemolytic Anaemia - Complementary TherapiesCanine Haemolytic Anaemia - Complementary Therapies
Canine Haemolytic Anaemia - As a vet, I used a range of Complementary Therapies in addition to a short course of pharmaceuticals and successfully treated my dog in only 4 weeks.
North Madison Veterinary Clinic, Care GuidesNorth Madison Veterinary Clinic, Care Guides
Immune-mediated hemolytic anemia (IMHA) is a type of illness known as an autoimmune disease. Autoimmune diseases result when the bodys immune system does not recognize itself; cells that normally attack invading viruses and bacteria begin attacking the bodys own cells, causing damage. In dogs and cats with IMHA, the bodys red blood cells come under attack. When red blood cells are severely damaged, they can burst; this is known as hemolysis. Therefore, IMHA is a condition in which red blood cells are attacked by the bodys immune system and destroyed by hemolysis, resulting in anemia (an inadequate quantity of red blood cells). Red blood cells can be destroyed within the blood vessels or in the spleen, liver, or bone marrow (where they are produced).. Read More ...
Care GuidesCare Guides
Immune-mediated hemolytic anemia (IMHA) is a type of illness known as an autoimmune disease. Autoimmune diseases result when the bodys immune system does not recognize itself; cells that normally attack invading viruses and bacteria begin attacking the bodys own cells, causing damage. In dogs and cats with IMHA, the bodys red blood cells come under attack. When red blood cells are severely damaged, they can burst; this is known as hemolysis. Therefore, IMHA is a condition in which red blood cells are attacked by the bodys immune system and destroyed by hemolysis, resulting in anemia (an inadequate quantity of red blood cells). Red blood cells can be destroyed within the blood vessels or in the spleen, liver, or bone marrow (where they are produced).. Read More ...
Care GuidesCare Guides
Immune-mediated hemolytic anemia (IMHA) is a type of illness known as an autoimmune disease. Autoimmune diseases result when the bodys immune system does not recognize itself; cells that normally attack invading viruses and bacteria begin attacking the bodys own cells, causing damage. In dogs and cats with IMHA, the bodys red blood cells come under attack. When red blood cells are severely damaged, they can burst; this is known as hemolysis. Therefore, IMHA is a condition in which red blood cells are attacked by the bodys immune system and destroyed by hemolysis, resulting in anemia (an inadequate quantity of red blood cells). Red blood cells can be destroyed within the blood vessels or in the spleen, liver, or bone marrow (where they are produced).. Read More ...
HemoglobinemiaHemoglobinemia
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Shih TzuShih Tzu
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Human genetic resistance to malariaHuman genetic resistance to malaria
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Adenosine deaminaseAdenosine deaminase
MicroangiopathyMicroangiopathy
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CampesterolCampesterol
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CisplatinCisplatin
Entlebucher Mountain DogEntlebucher Mountain Dog
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ଜଣ୍ଡିସ୍ - ଉଇକିପିଡ଼ିଆଜଣ୍ଡିସ୍ - ଉଇକିପିଡ଼ିଆ
黃疸 - 維基百科，自由的百科全書黃疸 - 維基百科，自由的百科全書
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Jaundice - Simple English Wikipedia, the free encyclopediaJaundice - Simple English Wikipedia, the free encyclopedia
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குருதிச்சோகை - தமிழ் விக்கிப்பீடியாகுருதிச்சோகை - தமிழ் விக்கிப்பீடியா
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阿司匹林 - 維基百科，自由的百科全書阿司匹林 - 維基百科，自由的百科全書
Hemolytic disease of the newbornHemolytic disease of the newborn
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AnemiaAnemia, HemolyticAnemia, Hemolytic, AutoimmuneAnemia, Hemolytic, CongenitalHemolysisAnemia, AplasticHemolytic AgentsFanconi AnemiaAnemia, Hemolytic, Congenital NonspherocyticHemolytic-Uremic SyndromeAnemia, HypochromicAnemia, MacrocyticAnemia, PerniciousAnemia, Sickle CellHemolysin ProteinsSecurity MeasuresErythrocytesCoombs TestAnemia, MegaloblasticInfectious Anemia Virus, EquineAnemia, RefractoryComplement Hemolytic Activity AssayErythropoietinHemolytic Plaque TechniqueEquine Infectious AnemiaErythroblastosis, FetalPhenylhydrazinesChicken anemia virusSpherocytosis, HereditaryAnemia, Dyserythropoietic, CongenitalIronHeinz BodiesErythrocyte CountAnemia, Diamond-BlackfanFanconi Anemia Complementation Group ProteinsPregnancy Complications, HematologicReticulocyte CountHematocritErythrocyte AgingOsmotic FragilityErythropoiesisErythrocytes, AbnormalAnemia, NeonatalBlood TransfusionGlucosephosphate Dehydrogenase DeficiencyHematinicsAnemia, Refractory, with Excess of BlastsErythrocyte IndicesErythrocyte MembraneFanconi Anemia Complementation Group C ProteinRh-Hr Blood-Group SystemFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group A ProteinHemoglobinometryComplement System ProteinsStreptolysinsFerritinsPallorErythrocyte TransfusionComplement Factor HShiga ToxinBlood Group IncompatibilityHemoglobins, AbnormalSplenectomyAntimicrobial Cationic PeptidesSplenomegalyThrombotic MicroangiopathiesMolecular Sequence DataHemoglobinuria, ParoxysmalReticulocytesComplement ActivationRh IsoimmunizationBacterial ToxinsFanconi Anemia Complementation Group G ProteinThrombocytopeniaHorsesPlasma ExchangeThalassemiaSheepSea CucumbersChromium Isotopesbeta-ThalassemiaBone MarrowMethemoglobinPyruvate KinaseSpherocytesIron, DietaryEscherichia coli InfectionsHemoglobinopathiesBlood Transfusion, IntrauterineWater MovementsAmino Acid SequenceEscherichia coli O157Blood Cell CountSuppression, GeneticHepcidinsFavismAutoantibodiesTreatment OutcomePrimaquineFetal HemoglobinHemoglobinuriaRecombinant ProteinsComplement C3Spectrinalpha-ThalassemiaGlucosephosphate DehydrogenasePrevalenceErythroblastsInfant, NewbornPregnancyHemoglobin, SickleShiga Toxin 2Hematologic DiseasesComplement Factor IVitamin B 12 DeficiencyComplement C5MalariaSpleenReticulocytosisShiga Toxin 1Base SequenceEscherichia coliRisk FactorsComplement Pathway, AlternativeIsavirusTime FactorsPancytopeniaRabbitsIron OverloadBlood Grouping and CrossmatchingDapsoneRetrospective StudiesMitomycinShiga-Toxigenic Escherichia coliFanconi Anemia Complementation Group F ProteinRed-Cell Aplasia, PureBacterial ProteinsFanconi Anemia Complementation Group E ProteinComplement C4Purpura, Thrombocytopenic, IdiopathicVirulenceHemolysin FactorsIsoantibodiesParvovirus B19, HumanFolic Acid DeficiencyKidney Failure, ChronicParvoviridae InfectionsErythrocyte DeformabilityPsoroptidaeHomozygoteImmunoglobulin GElliptocytosis, HereditaryVitamin B 12Chronic DiseaseBilirubinMethyldopaComplement C3b Inactivator ProteinsFish VenomsTrihexosylceramidesHaptoglobinsHydrops FetalisPedigreeBlood Group AntigensBlood ProteinsImmunosuppressive AgentsHemagglutinationMelittenAnion Exchange Protein 1, ErythrocyteAntilymphocyte SerumCucumariaPhenotypeParasitemiaFerrous CompoundsHematologyDiarrheaSickle Cell TraitHookworm InfectionsReceptors, TransferrinToxins, BiologicalAnti-Bacterial AgentsRenal DialysisStreptococcusAeromonasFatal OutcomeHemoglobin C DiseasePhenacetinComplement C8Malaria, FalciparumMethemoglobinemiaSeverity of Illness IndexErythrocyte VolumeBone Marrow TransplantationCnidarian VenomsProspective StudiesIntrinsic FactorAntigens, CD46Complement C3bComplement Inactivator ProteinsFollow-Up StudiesDisease Models, Animal
Hemolytic anemia | Define Hemolytic anemia at Dictionary.comHemolytic anemia | Define Hemolytic anemia at Dictionary.com
Hemolytic Anemia - Symptoms, Diagnosis and TreatmentHemolytic Anemia - Symptoms, Diagnosis and Treatment
Infectious hemolytic anemias - ONAInfectious hemolytic anemias - ONA
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Traumatic Hemolytic Anemia - Net Health BookTraumatic Hemolytic Anemia - Net Health Book
I Have Warm-reacting-antibody Hemolytic AnemiaI Have Warm-reacting-antibody Hemolytic Anemia
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Heme cases Mar 24 teaching aid - SOM 214 Hemolytic anemias Classifications Intrinsic vs Extrinsic = mechanism Hereditary vs...Heme cases Mar 24 teaching aid - SOM 214 Hemolytic anemias Classifications Intrinsic vs Extrinsic = mechanism Hereditary vs...
Hemolytic anemia - WikipediaHemolytic anemia - Wikipedia
Autoimmune hemolytic anemia - WikipediaAutoimmune hemolytic anemia - Wikipedia
Hemolytic anemia: MedlinePlus Medical EncyclopediaHemolytic anemia: MedlinePlus Medical Encyclopedia
Hemolytic Anemia (for Parents) - Norton ChildrensHemolytic Anemia (for Parents) - Norton Children's
Immune hemolytic anemia: MedlinePlus Medical EncyclopediaImmune hemolytic anemia: MedlinePlus Medical Encyclopedia
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Autoimmune hemolytic anemia: Causes, types, and symptomsAutoimmune hemolytic anemia: Causes, types, and symptoms
How is acquired autoimmune hemolytic anemia (AIHA) treated?How is acquired autoimmune hemolytic anemia (AIHA) treated?
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congenital hemolytic anemiacongenital hemolytic anemia
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Autoimmune Hemolytic AnemiaAutoimmune Hemolytic Anemia
Microangiopathic hemolytic anemia | Define Microangiopathic hemolytic anemia at Dictionary.comMicroangiopathic hemolytic anemia | Define Microangiopathic hemolytic anemia at Dictionary.com
When are major challenges in the diagnosis of hemolytic anemias?When are major challenges in the diagnosis of hemolytic anemias?
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Donath-Landsteiner Hemolytic Anemia: Practice Essentials, Pathophysiology, EtiologyDonath-Landsteiner Hemolytic Anemia: Practice Essentials, Pathophysiology, Etiology
Contribution of 3,4-Dichlorophenylhydroxylamine in Propanil-Induced Hemolytic Anemia | SpringerLinkContribution of 3,4-Dichlorophenylhydroxylamine in Propanil-Induced Hemolytic Anemia | SpringerLink
Experimental onion-induced hemolytic anemia in dogs. - PubMed - NCBIExperimental onion-induced hemolytic anemia in dogs. - PubMed - NCBI
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Hemolytic anemiaHemolytic anemia
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsInformation ScienceNamed GroupsHealth Care
AnemiaAnemia, HemolyticAnemia, Hemolytic, AutoimmuneAnemia, Hemolytic, CongenitalHemolysisAnemia, AplasticHemolytic AgentsFanconi AnemiaAnemia, Hemolytic, Congenital NonspherocyticHemolytic-Uremic SyndromeAnemia, HypochromicAnemia, MacrocyticAnemia, PerniciousAnemia, Sickle CellHemolysin ProteinsSecurity MeasuresErythrocytesCoombs TestAnemia, MegaloblasticInfectious Anemia Virus, EquineAnemia, RefractoryComplement Hemolytic Activity AssayErythropoietinHemolytic Plaque TechniqueEquine Infectious AnemiaErythroblastosis, FetalPhenylhydrazinesChicken anemia virusSpherocytosis, HereditaryAnemia, Dyserythropoietic, CongenitalIronHeinz BodiesErythrocyte CountAnemia, Diamond-BlackfanFanconi Anemia Complementation Group ProteinsPregnancy Complications, HematologicReticulocyte CountHematocritErythrocyte AgingOsmotic FragilityErythropoiesisErythrocytes, AbnormalAnemia, NeonatalBlood TransfusionGlucosephosphate Dehydrogenase DeficiencyHematinicsAnemia, Refractory, with Excess of BlastsErythrocyte IndicesErythrocyte MembraneFanconi Anemia Complementation Group C ProteinRh-Hr Blood-Group SystemFanconi Anemia Complementation Group D2 ProteinFanconi Anemia Complementation Group A ProteinHemoglobinometryComplement System ProteinsStreptolysinsFerritinsPallorErythrocyte TransfusionComplement Factor HShiga ToxinBlood Group IncompatibilityHemoglobins, AbnormalSplenectomyAntimicrobial Cationic PeptidesSplenomegalyThrombotic MicroangiopathiesMolecular Sequence DataHemoglobinuria, ParoxysmalReticulocytesComplement ActivationRh IsoimmunizationBacterial ToxinsFanconi Anemia Complementation Group G ProteinThrombocytopeniaHorsesPlasma ExchangeThalassemiaSheepSea CucumbersChromium Isotopesbeta-ThalassemiaBone MarrowMethemoglobinPyruvate KinaseSpherocytesIron, DietaryEscherichia coli InfectionsHemoglobinopathiesBlood Transfusion, IntrauterineWater MovementsAmino Acid SequenceEscherichia coli O157Blood Cell CountSuppression, GeneticHepcidinsFavismAutoantibodiesTreatment OutcomePrimaquineFetal HemoglobinHemoglobinuriaRecombinant ProteinsComplement C3Spectrinalpha-ThalassemiaGlucosephosphate DehydrogenasePrevalenceErythroblastsInfant, NewbornPregnancyHemoglobin, SickleShiga Toxin 2Hematologic DiseasesComplement Factor IVitamin B 12 DeficiencyComplement C5MalariaSpleenReticulocytosisShiga Toxin 1Base SequenceEscherichia coliRisk FactorsComplement Pathway, AlternativeIsavirusTime FactorsPancytopeniaRabbitsIron OverloadBlood Grouping and CrossmatchingDapsoneRetrospective StudiesMitomycinShiga-Toxigenic Escherichia coliFanconi Anemia Complementation Group F ProteinRed-Cell Aplasia, PureBacterial ProteinsFanconi Anemia Complementation Group E ProteinComplement C4Purpura, Thrombocytopenic, IdiopathicVirulenceHemolysin FactorsIsoantibodiesParvovirus B19, HumanFolic Acid DeficiencyKidney Failure, ChronicParvoviridae InfectionsErythrocyte DeformabilityPsoroptidaeHomozygoteImmunoglobulin GElliptocytosis, HereditaryVitamin B 12Chronic DiseaseBilirubinMethyldopaComplement C3b Inactivator ProteinsFish VenomsTrihexosylceramidesHaptoglobinsHydrops FetalisPedigreeBlood Group AntigensBlood ProteinsImmunosuppressive AgentsHemagglutinationMelittenAnion Exchange Protein 1, ErythrocyteAntilymphocyte SerumCucumariaPhenotypeParasitemiaFerrous CompoundsHematologyDiarrheaSickle Cell TraitHookworm InfectionsReceptors, TransferrinToxins, BiologicalAnti-Bacterial AgentsRenal DialysisStreptococcusAeromonasFatal OutcomeHemoglobin C DiseasePhenacetinComplement C8Malaria, FalciparumMethemoglobinemiaSeverity of Illness IndexErythrocyte VolumeBone Marrow TransplantationCnidarian VenomsProspective StudiesIntrinsic FactorAntigens, CD46Complement C3bComplement Inactivator ProteinsFollow-Up StudiesDisease Models, Animal
AIHAJaundiceOccursSymptoms of hemolyticIntrinsicPyruvate kinase defCongenital Nonspherocytic Hemolytic AnemiaMicroangiopathic haemolyDisseminated intravasculForm of hemolytic anemiaAcuteIMHASevere hemolytic anemiaDiagnosisSpleenOccurCoombsDiseasesG6PDNewbornBilirubinDeficiencyPenicillinBoneHemolysisDrug-Induced Immune Hemolytic AnemiaUremic syndromeAuto Immune Hemolytic AnemiaSynonymsAntibodiesNonspherocytic hemolytic anemiaAntibody Hemolytic AnemiaImmune Hemolytic AnemiasIdiopathic autoimmune hemolyType of hemolytic anemiaDiseaseCauses hemolytic anemiaThromboticDisordersCause hemolytic anemiasNonimmune hemolytic anemiasHereditary hemolytic anemiasSignsSymptoms of Autoimmune HemolyCommon symptoms of hemolytic anemiaPossible causes of hemolytic anemiaChronicAutoimmune hemolytic anaemiaSickleCold antibodyImmunohemolytic anemiaDiagnosis of hemolytic anemiaChildren with hemolytic anemiaHematopoietic stem cell transBlood cellsAcute hemolytic anemiaIntravascular hemolytic anemia
AIHA1
Jaundice1
  • While most red blood cells live for three to four months, hemolytic anemia can translate to much quicker breakdown, resulting in fewer than normal blood cells, excess bleeding, low iron counts, and jaundice . (wise-geek.com)
Occurs1
Symptoms of hemolytic1
Intrinsic2
Pyruvate kinase def1
Congenital Nonspherocytic Hemolytic Anemia1
Microangiopathic haemoly1
Disseminated intravascul1
  • Other such conditions are extremely high blood pressure (malignant hypertension), thrombotic thrombocytopenic purpura, disseminated intravascular coagulation (DIC), disseminated cancer, hemolytic-uremic syndrome, lupus erythematosus and polyarteritis nodosa that can also lead to traumatic hemolytic anemia because of damaged small blood vessels. (nethealthbook.com)
Form of hemolytic anemia2
  • A rare form of hemolytic anemia, called erythroblastosis fetalis, can occur in newborns and is normally caused by the mother having a negative blood type that conflicts with the baby's positive blood type (called Rh incompatibility). (wise-geek.com)
  • When this is not prevented, this form of hemolytic anemia can be very severe for the newborn, resulting in brain damage. (wise-geek.com)
Acute1
IMHA2
Severe hemolytic anemia1
Diagnosis1
Spleen2
Occur1
Coombs2
  • Here's how readers responded to a You Make the Call question about treatment of Coombs-positive hemolytic anemia in a patient who declines to undergo splenectomy . (ashclinicalnews.org)
  • Even though there is no information about the type of Coombs-positive hemolytic anemia this specific patient has, my therapeutic intervention would consist of first re-challenging with 4 weekly courses of low-dose rituximab (100 mg/m 2 fixed dose), plus cyclophosphamide and dexamethasone. (ashclinicalnews.org)
Diseases1
G6PD1
Newborn1
Bilirubin1
Deficiency1
Penicillin2
Bone1
  • This is an uncommon anemia that develops when red blood cells are destroyed faster than bone marrow can replace them. (diagnose-me.com)
Hemolysis20
Drug-Induced Immune Hemolytic Anemia3
Uremic syndrome5
Auto Immune Hemolytic Anemia4
Synonyms1
Antibodies17
Nonspherocytic hemolytic anemia11
Antibody Hemolytic Anemia13
Immune Hemolytic Anemias1
Idiopathic autoimmune hemoly3
Type of hemolytic anemia2
Disease13
Causes hemolytic anemia3
Thrombotic1
  • The thrombotic thrombocytopenic purpura and hemolytic uremic syndromes: overview of pathogenesis (Experience of The Oklahoma TTP-HUS Registry, 1989-2007). (medscape.com)
Disorders10
Cause hemolytic anemias2
Nonimmune hemolytic anemias1
Hereditary hemolytic anemias4
  • In hereditary hemolytic anemias, the underlying molecular defect affects and determines red blood cell vesiculation, resulting in shedding microvesicles of different compositions and concentrations. (frontiersin.org)
  • Despite extensive research into red blood cell biochemistry and physiology, little is known about red cell deformability and vesiculation in hereditary hemolytic anemias, and the associated pathophysiological role is incompletely assessed. (frontiersin.org)
  • Also, we review recent scientific findings on the molecular defects of hereditary hemolytic anemias, and their correlation with red blood cell deformability and vesiculation. (frontiersin.org)
  • Integrating bio-analytical findings on abnormalities of red blood cells and their microvesicles will be critical for a better understanding of the pathophysiology of hereditary hemolytic anemias. (frontiersin.org)
Signs14
Symptoms of Autoimmune Hemoly1
Common symptoms of hemolytic anemia1
Possible causes of hemolytic anemia2
Chronic7
Autoimmune hemolytic anaemia2
Sickle1
Cold antibody1
Immunohemolytic anemia1
Diagnosis of hemolytic anemia3
Children with hemolytic anemia2
Hematopoietic stem cell trans2
Blood cells31
Acute hemolytic anemia1
Intravascular hemolytic anemia1
Malaria Drug Association With Hemolytic Anemia Unclear - MPR
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Overview of Hemolytic Anemia - Hematology and Oncology - Merck Manuals Professional Edition
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Quiz: Overview of Hemolytic Anemia - Merck Manuals Professional Edition
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Microangiopathic hemolytic anemia | Define Microangiopathic hemolytic anemia at Dictionary.com
Microangiopathic hemolytic anemia | Define Microangiopathic hemolytic anemia at Dictionary.com (dictionary.com)
Autoimmune hemolytic anemia | Define Autoimmune hemolytic anemia at Dictionary.com
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Hemolytic Anemia
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