The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.
A condition of inadequate circulating red blood cells (ANEMIA) or insufficient HEMOGLOBIN due to premature destruction of red blood cells (ERYTHROCYTES).
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.
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.
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.
A syndrome of HEMOLYSIS, elevated liver ENZYMES, and low blood platelets count (THROMBOCYTOPENIA). HELLP syndrome is observed in pregnant women with PRE-ECLAMPSIA or ECLAMPSIA who also exhibit LIVER damage and abnormalities in BLOOD COAGULATION.
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.
The semi-permeable outer structure of a red blood cell. It is known as a red cell 'ghost' after HEMOLYSIS.
Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.
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.
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.
The oxygen-carrying proteins of ERYTHROCYTES. They are found in all vertebrates and some invertebrates. The number of globin subunits in the hemoglobin quaternary structure differs between species. Structures range from monomeric to a variety of multimeric arrangements.
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.
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.
Diazo derivatives of aniline, used as a reagent for sugars, ketones, and aldehydes. (Dorland, 28th ed)
A disease characterized by chronic hemolytic anemia, episodic painful crises, and pathologic involvement of many organs. It is the clinical expression of homozygosity for hemoglobin S.
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)
Agglutination of ERYTHROCYTES by a virus.
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).
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.
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.
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).
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.
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.
A bile pigment that is a degradation product of HEME.
The aggregation of ERYTHROCYTES by AGGLUTININS, including antibodies, lectins, and viral proteins (HEMAGGLUTINATION, VIRAL).
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.
Immunizing agent containing IMMUNOGLOBULIN G anti-Rho(D) used for preventing Rh immunization in Rh-negative individuals exposed to Rh-positive red blood cells.
The taking of a blood sample to determine its character as a whole, to identify levels of its component cells, chemicals, gases, or other constituents, to perform pathological examination, etc.
Yellow discoloration of the SKIN; MUCOUS MEMBRANE; and SCLERA in the NEWBORN. It is a sign of NEONATAL HYPERBILIRUBINEMIA. Most cases are transient self-limiting (PHYSIOLOGICAL NEONATAL JAUNDICE) occurring in the first week of life, but some can be a sign of pathological disorders, particularly LIVER DISEASES.
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.
A nutritional condition produced by a deficiency of VITAMIN E in the diet, characterized by posterior column and spinocerebellar tract abnormalities, areflexia, ophthalmoplegia, and disturbances of gait, proprioception, and vibration. In premature infants vitamin E deficiency is associated with hemolytic anemia, thrombocytosis, edema, intraventricular hemorrhage, and increasing risk of retrolental fibroplasia and bronchopulmonary dysplasia. An apparent inborn error of vitamin E metabolism, named familial isolated vitamin E deficiency, has recently been identified. (Cecil Textbook of Medicine, 19th ed, p1181)
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.
Exotoxins produced by certain strains of streptococci, particularly those of group A (STREPTOCOCCUS PYOGENES), that cause HEMOLYSIS.
A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.
The number of RED BLOOD CELLS per unit volume in a sample of venous BLOOD.
Oxygen-carrying RED BLOOD CELLS in mammalian blood that are abnormal in structure or function.
The effects, both local and systemic, caused by the bites of SPIDERS.
The major human blood type system which depends on the presence or absence of two antigens A and B. Type O occurs when neither A nor B is present and AB when both are present. A and B are genetic factors that determine the presence of enzymes for the synthesis of certain glycoproteins mainly in the red cell membrane.
A condition characterized by an abnormal increase of BILIRUBIN in the blood, which may result in JAUNDICE. Bilirubin, a breakdown product of HEME, is normally excreted in the BILE or further catabolized before excretion in the urine.
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.
Small glycoproteins found on both hematopoietic and non-hematopoietic cells. CD59 restricts the cytolytic activity of homologous complement by binding to C8 and C9 and blocking the assembly of the membrane attack complex. (From Barclay et al., The Leukocyte Antigen FactsBook, 1993, p234)
Ability of ERYTHROCYTES to change shape as they pass through narrow spaces, such as the microvasculature.
Serologic tests in which a known quantity of antigen is added to the serum prior to the addition of a red cell suspension. Reaction result is expressed as the smallest amount of antigen which causes complete inhibition of hemagglutination.
A species of gram-negative, aerobic bacteria that is the etiologic agent of epidemic typhus fever acquired through contact with lice (TYPHUS, EPIDEMIC LOUSE-BORNE) as well as Brill's disease.
Stable chromium atoms that have the same atomic number as the element chromium, but differ in atomic weight. Cr-50, 53, and 54 are stable chromium isotopes.
A 105-kDa serum glycoprotein with significant homology to the other late complement components, C7-C9. It is a polypeptide chain cross-linked by 32 disulfide bonds. C6 is the next complement component to bind to the membrane-bound COMPLEMENT C5B in the assembly of MEMBRANE ATTACK COMPLEX. It is encoded by gene C6.
The process by which blood or its components are kept viable outside of the organism from which they are derived (i.e., kept from decay by means of a chemical agent, cooling, or a fluid substitute that mimics the natural state within the organism).
A spider of the genus Loxosceles, found in the midwestern and other parts of the United States, which carries a hemolytic venom that produces local necrosis or ulceration.
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.
Plasmids controlling the synthesis of hemolysin by bacteria.
An examination of chemicals in the blood.
An autosomal recessive glycogen storage disease in which there is deficient expression of 6-phosphofructose 1-kinase in muscle (PHOSPHOFRUCTOKINASE-1, MUSCLE TYPE) resulting in abnormal deposition of glycogen in muscle tissue. These patients have severe congenital muscular dystrophy and are exercise intolerant.
A 93-kDa serum glycoprotein encoded by C7 gene. It is a polypeptide chain with 28 disulfide bridges. In the formation of MEMBRANE ATTACK COMPLEX; C7 is the next component to bind the C5b-6 complex forming a trimolecular complex C5b-7 which is lipophilic, resembles an integral membrane protein, and serves as an anchor for the late complement components, C8 and C9.
The type (and only) species of RUBIVIRUS causing acute infection in humans, primarily children and young adults. Humans are the only natural host. A live, attenuated vaccine is available for prophylaxis.
Solutions that have a lesser osmotic pressure than a reference solution such as blood, plasma, or interstitial fluid.
The most common etiologic agent of GAS GANGRENE. It is differentiable into several distinct types based on the distribution of twelve different toxins.

Changes in haematological parameters and iron metabolism associated with a 1600 kilometre ultramarathon. (1/3524)

OBJECTIVE: To investigate haematological variations and iron related changes in the serum of participants in a 1600 kilometre ultramarathon run. PARTICIPANTS: Seven male and two female participants in a 1600 km foot race. METHODS: Blood samples were obtained from the participants before, after four and 11 days of running, and at the end of the event. Samples were analysed by standard methods for haemoglobin, packed cell volume, total red cell count, mean red cell volume, mean red cell haemoglobin, total white cell count and differential, platelets, reticulocytes, iron, ferritin, total iron binding capacity, percentage transferrin saturation, haptoglobin, and bilirubin and corrected for changes in plasma volume. RESULTS: The following variables decreased during the event (p < 0.05): haemoglobin, packed cell volume, mean red cell volume, percentage lymphocytes, percentage monocytes, serum iron, total iron binding capacity, and percentage transferrin saturation. Increases (p < 0.05) were found in plasma volume, total red cell count (day 4 only), total white cell count, percentage and absolute numbers of neutrophils and reticulocytes, absolute numbers of lymphocytes and monocytes (day 4 only), absolute numbers of eosinophils (day 11 and race end), absolute numbers of basophils (race end only), platelets, ferritin, haptoglobin, and bilirubin (day 4 only). CONCLUSION: Ultramarathon running is associated with a wide range of changes in haematological parameters, many of which are related to the normal acute phase response to injury. These should not be confused with indicators of disease.  (+info)

Improved methods using the reverse transcriptase polymerase chain reaction to detect tumour cells. (2/3524)

Reverse transcriptase polymerase chain reaction (RT-PCR) is increasingly used to detect small numbers of circulating tumour cells, though the clinical benefit remains controversial. The largest single contributing factor to the controversy of its value is the different approaches to sample processing. The aim of this study was to compare the sensitivity and reproducibility of RT-PCR for the detection of tumour cells after four commonly used different methods of sample processing. Using RT-PCR, one tumour cell spiked in 2 ml of whole blood was detected after analysis of separated mononuclear cell RNA, whole blood total or poly-A+ RNA. No false positives were identified with any method. However, the reproducibility of tumour cell detection was reduced after isolation of the mononuclear cell fraction. Only analysis of poly-A+ RNA had a sensitivity of 100% in all the cell spiking experiments. In patient blood samples, analysis of poly-A+ RNA increased the number of blood samples positive for tyrosine hydroxylase (TH) mRNA compared with those positive after analysis of total RNA. This may reflect high levels of cDNA reducing the efficiency of the PCR. Isolation of poly-A+ RNA increases the sensitivity and reproducibility of tumour cell detection in peripheral blood.  (+info)

Antioxidative activity of 4-oxy- and 4-hydroxy-nitroxides in tissues and erythrocytes from rats. (3/3524)

AIM: To compare the activities of antioxidation of 4-oxy- and 4-hydroxy-nitroxides in tissues and RBC from rats. METHODS: The homogenates of liver, heart, and kidneys of rats were used to determine malondialdehyde (MDA) formation using TBA colorimetric method. H2O2-caused hemolysis was measured spectrometrically. Superoxide anion from zymosan-stimulated neutrophils of rats was assayed by NBT reduction method. RESULTS: Nitroxide free radicals OTMPO and HTMPO inhibited MDA generation caused by .OH generation system (MIC 10.5 and 21 mumol.L-1, respectively), antagonized hemolysis induced by H2O2 (MIC: 338 and 168 mumol.L-1, respectively), but did not affect O2- formation from activated neutrophils. 1-Hydroxyl compounds OTMPOH and HTMPOH possessed similarly potent antilipoperoxidative activities. But nonfree radical OTMP and HTMP had no effect on peroxidation of tissues. CONCLUSION: Nitroxides exert their antilipoperoxidative effect by specifically scavenging .OH free radicals in biological system. Trapping of .OH free radicals by nitroxides is not by reduction of NO. group in nitroxides. Both NO. group and NOH group are essential active groups.  (+info)

Isolation and characterization of Vibrio parahaemolyticus causing infection in Iberian toothcarp Aphanius iberus. (4/3524)

High mortality among laboratory cultured Iberian toothcarp Aphanius iberus occurred in February 1997 in Valencia (Spain). The main signs of the disease were external haemorrhage and tail rot. Bacteria isolated from internal organs of infected fish were biochemically homogeneous and identified as Vibrio parahaemolyticus. The bacteria were haemolytic against erythrocytes from eel Anguilla anguilla, amberjack Seriola dumerili, toothcarp A. iberus and humans, and were Kanagawa-phenomenon-negative. Infectivity tests showed that the virulence for A. iberus was dependent on salinity. Finally, all strains were virulent for amberjack and eel.  (+info)

Hemolysis associated with 25% human albumin diluted with sterile water--United States, 1994-1998. (5/3524)

Since 1994, a shortage of 5% human albumin, a product used off-label during therapeutic plasma exchange (TPE), has existed in the United States. Because of this shortage, hospital pharmacists may prepare 5% solution of human albumin by diluting 25% human albumin with 0.9% NaCl or, when sodium load is a concern, 5% dextrose. However, if sterile water alone is used as the diluent, the osmolarity (tonicity) of the albumin solution is reduced and may cause hemolysis in recipients. This report describes two of 10 episodes of hemolysis (one fatal) among persons who received 25% human albumin diluted with sterile water and emphasizes that sterile water alone should not be used to dilute albumin.  (+info)

Novel techniques for in vivo hemolysis studies in guinea pigs. (6/3524)

The in vivo toxic-hemolytic studies using small experimental animals are complicated by difficulties in preventing hemolysis during repeated collection of blood specimens and in measuring hemoglobin concentration in small amounts of plasma sample. To solve these problems we tried to develope the new techniques for the in vivo hemolysis studies using guinea pigs. The hemolysis accident was minimized to 2.75 mg/dl by collecting the blood directly into heparinized microhematocrit tubes by small longitudinal incision in the auricular artery. The hemoglobin in a small amount of sample (10 microliters) was determined by the new analytical system using a microflow spectrophotometer with a modified cyanmethemoglobin method. The standard curve of the hemoglobin concentration in the system revealed a line of Y = 1.8X + 0.79 (r = 0.999), CV < 1% with a minimum detectable concentration of 1.25 mg/dl. By using the new techniques, it was found that the plasma hemoglobin concentration in normal animals were 7.27 +/- 0.44 mg/dl (mean +/- S.E.). The in vivo hemolytic activity of saponin was observed dose-dependently at doses of 30-50 mg/kg, i.v. in the guinea pigs. It is concluded that the present techniques are useful for in vivo hemolytic studies in small experimental animals such as guinea pigs.  (+info)

The hemolytic activity of bracken extracts in guinea pigs. (7/3524)

This study was conducted to elucidate the hemolytic activity of a new toxic substance in bracken fern. A crude extract (CE) was prepared from the methanol extracts of bracken by the column chromatography. When the CE was injected subcutaneously in guinea pigs, the hemoglobinuria and hemolysis were observed within 6 hr, and 3 days later edema and hemorrhages in the urinary bladder were observed. The CE was then fractionated by high performance liquid chromatography (HPLC), and three (HF, BF and CF) of the fractions showed the toxic activities in guinea pigs. The HF caused the hemolysis, whereas both the BF and the CF caused the hemorrhagic cystitis without any hemolytic activities. The HF was further fractionated by the HPLC, resulting of the 3 fractions (HF-I, II and III). The hemolysis was caused only with the HF-II, and HF-II as well as HF did not cause the hemorrhagic cystitis. HPLC analysis revealed that both BF and CF contains braxin B and braxin C, respectively, and both HF and HF-II do not contain braxin A, B or C. These facts suggest that bracken fern contains a new toxic substance (hemolysin) which induces the acute hemolysis in guinea pigs.  (+info)

The rgg gene of Streptococcus pyogenes NZ131 positively influences extracellular SPE B production. (8/3524)

Streptococcus pyogenes produces several extracellular proteins, including streptococcal erythrogenic toxin B (SPE B), also known as streptococcal pyrogenic exotoxin B and streptococcal proteinase. Several reports suggest that SPE B contributes to the virulence associated with S. pyogenes; however, little is known about its regulation. Nucleotide sequence data revealed the presence, upstream of the speB gene, of a gene, designated rgg, that was predicted to encode a polypeptide similar to previously described positive regulatory factors. The putative Rgg polypeptide of S. pyogenes NZ131 consisted of 280 amino acids and had a predicted molecular weight of 33,246. To assess the potential role of Rgg in the production of SPE B, the rgg gene was insertionally inactivated in S. pyogenes NZ131, which resulted in markedly decreased SPE B production, as determined both by immunoblotting and caseinolytic activity on agar plates. However, the production of other extracellular products, including streptolysin O, streptokinase, and DNase, was not affected. Complementation of the rgg mutant with an intact rgg gene copy in S. pyogenes NZ131 could restore SPE B production and confirmed that the rgg gene product is involved in the production of SPE B.  (+info)

There are two main types of hemolysis:

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

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

Some common causes of hemolysis include:

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

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

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

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

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

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

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

The symptoms of hemoglobinuria may include:

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

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

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

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

In severe cases of hemoglobinuria, complications can include:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Blood group incompatibility can occur in various ways, including:

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

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

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

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

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

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

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

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

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

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

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

Symptoms of neonatal jaundice may include:

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

Treatment for neonatal jaundice may include:

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

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

Causes and risk factors:

1. Poor diet: A diet that is lacking in vitamin E can lead to a deficiency. Foods that are low in vitamin E include processed foods, sugary drinks, and refined carbohydrates.
2. Malabsorption: Certain medical conditions, such as celiac disease, can lead to malabsorption of nutrients, including vitamin E.
3. Pregnancy and lactation: Pregnant and breastfeeding women have a higher requirement for vitamin E, and a deficiency can occur if they do not consume enough.
4. Chronic diseases: Certain chronic diseases, such as Crohn's disease, can increase the risk of vitamin E deficiency.
5. Genetic disorders: Some genetic disorders, such as abetalipoproteinemia, can lead to a deficiency in vitamin E.


1. Fatigue and weakness
2. Muscle weakness
3. Loss of appetite
4. Nerve damage
5. Poor wound healing
6. Increased risk of infections
7. Decreased immune function
8. Anemia
9. Skin problems, such as acne and dermatitis
10. Eye problems, such as cataracts and retinal degeneration.


Vitamin E deficiency is diagnosed based on a combination of clinical symptoms, medical history, and laboratory tests, including:

1. Blood tests: Measurement of serum vitamin E levels can help determine if there is a deficiency.
2. Dietary assessment: A dietitian or nutritionist may evaluate the patient's diet to identify any potential sources of vitamin E deficiency.
3. Physical examination: A healthcare provider may perform a physical examination to look for signs of vitamin E deficiency, such as skin problems or muscle weakness.

Treatment and Prevention:

1. Dietary changes: Increasing the intake of foods rich in vitamin E, such as nuts, seeds, and vegetable oils, can help prevent and treat vitamin E deficiency.
2. Supplementation: Vitamin E supplements can be used to treat and prevent vitamin E deficiency. The recommended daily intake of vitamin E varies by age and sex, but generally ranges from 5-15 mg/day.
3. Addressing underlying causes: If the deficiency is caused by an underlying medical condition, such as Crohn's disease or abetalipoproteinemia, treating the condition can help resolve the deficiency.
4. Supportive care: Patients with severe vitamin E deficiency may require supportive care, such as intravenous nutrition or respiratory support, to manage their symptoms.

Prognosis and Complications:
The prognosis for vitamin E deficiency is generally good if the underlying cause is identified and treated promptly. However, untreated severe vitamin E deficiency can lead to complications such as:

1. Skin problems: Vitamin E deficiency can cause skin problems, such as acne, dermatitis, and wound healing difficulties.
2. Muscle weakness: Vitamin E is important for muscle function, and deficiency can lead to muscle weakness and wasting.
3. Neurological problems: Vitamin E deficiency can cause neurological problems, such as peripheral neuropathy and seizures.
4. Increased risk of infections: Vitamin E is important for immune function, and deficiency can increase the risk of infections.
5. Reproductive problems: Vitamin E deficiency can cause reproductive problems, such as infertility and miscarriage.

Also known as: Hereditary spherocytosis (HSS)

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Some common types of spiders that are known to bite humans include black widows, brown recluses, and hobos. Black widow spider bites are characterized by a red, burning sensation at the site of the bite, while brown recluse spider bites can cause necrotic lesions and severe systemic reactions. Hobo spider bites are similar to brown recluse spider bites and can also cause necrotic lesions and systemic reactions.

Treatment for spider bites typically involves supportive care, such as wound cleaning and dressing, antibiotics, and pain management. In severe cases, hospitalization may be necessary to monitor and treat complications.

Prevention is key when it comes to spider bites, and this includes avoiding areas where spiders are known to live, wearing protective clothing and insect repellent, and seeking medical attention promptly if a bite occurs. Early diagnosis and treatment can help to minimize the risk of complications and improve outcomes for patients with spider bites.

There are several possible causes of hyperbilirubinemia, including:

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

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

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

The main symptoms of GSD-VII are muscle weakness, fatigue, and an inability to produce insulin or grow properly. Affected individuals may also experience seizures, developmental delays, and liver disease. GSD-VII is typically diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis.

Treatment for GSD-VII typically involves managing the symptoms and preventing complications. This may include a high-carbohydrate diet, vitamin supplements, and medications to control seizures and other symptoms. In severe cases, liver transplantation may be necessary.

GSD-VII is a rare disease, and its prevalence is not well established. However, it is estimated to affect approximately 1 in 100,000 individuals worldwide. GSD-VII can occur in individuals of any ethnicity or geographic location.

The prognosis for GSD-VII varies depending on the severity of the disease and the presence of complications. With proper management, affected individuals can lead active and fulfilling lives. However, liver disease and other complications can significantly impact quality of life and life expectancy.

There is currently no cure for GSD-VII, but research is ongoing to develop new treatments and improve existing ones. In addition, genetic counseling and testing can help identify individuals who carry the mutated gene and are at risk of passing it on to their children.

Paxillus involutus ingestion can cause hemolysis. Spaceflight can cause hemolysis. Hemolysis may result from intrinsic defects ... Extravascular hemolysis refers to hemolysis taking place in the liver, spleen, bone marrow, and lymph nodes. In this case ... Hemolysis or haemolysis (/hiːˈmɒlɪsɪs/), also known by several other names, is the rupturing (lysis) of red blood cells ( ... From hemo- + -lysis, from Ancient Greek: [n] αἷμα (haîma, "blood") + λύσις (lúsis, "loosening"). Hemolysis inside the body can ...
Beta-hemolysis (β-hemolysis), sometimes called complete hemolysis, is a complete lysis of red cells in the media around and ... A substance that causes hemolysis is a hemolysin. When alpha-hemolysis (α-hemolysis) is present, the agar under the colony is ... Other synonymous terms are incomplete hemolysis and partial hemolysis. Alpha hemolysis is caused by hydrogen peroxide produced ... display alpha hemolysis. This is sometimes called green hemolysis because of the color change in the agar. ...
... describes hemolysis that happens mainly inside the vasculature. As a result, the contents of the red ... Intravascular hemolysis is the state when the red blood cell ruptures as a result of the complex of complement autoantibodies ... Extravascular hemolysis Haptoglobin and hemopexin are not recyclable. Stanley L Schrier. William C Mentzer; Jennifer S Tirnauer ... Schaer, D. J.; Buehler, P. W.; Alayash, A. I.; Belcher, J. D.; Vercellotti, G. M. (2012-12-20). "Hemolysis and free hemoglobin ...
"Intravascular hemolysis". eClinpath. Retrieved 2019-05-08. "Bilirubin and hemolytic anemia". eClinpath. Retrieved 2019-05-08. ... concentrations are low or depleted as a result of severe or prolonged hemolysis. Both Hp and Hx are acute-phase proteins, the ...
... haptoglobin levels will be decreased in case of intravascular hemolysis or severe extravascular hemolysis. In the process of ... In intravascular hemolysis, free hemoglobin will be released into circulation and hence haptoglobin will bind the hemoglobin. ... "Intravascular hemolysis". eClinpath. Retrieved 8 May 2019. "Entrez Gene: HP". Trayhurn P, Wood IS (September 2004). "Adipokines ... A decrease in haptoglobin can support a diagnosis of hemolysis, especially when correlated with a decreased hemoglobin, and ...
... there are two principal mechanisms of hemolysis; intravascular and extravascular. Intravascular hemolysis describes hemolysis ... Extravascular hemolysis refers to hemolysis taking place in the liver, spleen, bone marrow, and lymph nodes. In this case ... Chronic hemolysis leads to an increased excretion of bilirubin into the biliary tract, which in turn may lead to gallstones. ... Intravascular hemolysis may occur when red blood cells are targeted by autoantibodies, leading to complement fixation, or by ...
Haemolysis is reported. It has also been reported to cause post kidney failure in children. Like other antibiotics, ceftriaxone ... Guleria VS, Sharma N, Amitabh S, Nair V (September-October 2013). "Ceftriaxone-induced hemolysis". Indian Journal of ...
"What is Hemolysis?" (PDF). Becton-Dickinson. Archived (PDF) from the original on 2008-06-25. Retrieved 2008-06-01. Akerblom O, ...
"Microbiology Primer: Hemolysis". Archived from the original on 2008-12-11. Retrieved 2008-12-12. "Streptococcaceae Answers". ... that enlarges the area of hemolysis formed by the β-hemolysin elaborated from Staphylococcus aureus. Although the test is ...
Neter, E (1956). "Bacterial Hemagglutination and Hemolysis". Statler Research Laboratories and Department of Pediatrics, ...
... hemolysis can also occur. MD is not persistent, meaning that it will dissipate after a short time. It is, however, still quite ...
Stalnikowicz R, Amitai Y, Bentur Y (2004). "Aphrodisiac drug-induced hemolysis". Journal of Toxicology. Clinical Toxicology. 42 ...
Rao, D. Sheshagiri; Barik, Ramachandra; Siva Prasad, Akula (1 September 2016). "Hemolysis induced by PMIVSD occluder". Indian ...
Hemolysis or Kidney stone disease). "Chenopodium giganteum D.Don". Plants of the World Online. Board of Trustees of the Royal ...
Crenellation Cytorrhysis Hemolysis Plasmolysis "Crenate". Oxford Dictionaries. Archived from the original on July 31, 2012. ...
Can occur hemolysis and erythrocytes. It occurs mostly in moist soil in shade, at the height of 1000-3000 m as climbs over ...
No hemolysis has been observed. Growth has been documented on trypticase soy agar, but the size of the colonies are roughly ...
Histophilus does not exhibit consistent hemolysis. Their ability to reduce nitrogen allows them to be facultative anaerobes and ...
... display alpha-hemolysis. Alpha-hemolysis is also termed incomplete hemolysis or partial hemolysis because the cell membranes of ... Beta-hemolysis (β-hemolysis), sometimes called complete hemolysis, is a complete lysis of red cells in the media around and ... Streptococcus pyogenes, or GAS, displays beta hemolysis. Some weakly beta-hemolytic species cause intense hemolysis when grown ... When alpha-hemolysis (α-hemolysis) is present, the agar under the colony will appear dark and greenish due to the conversion of ...
Hemolysis leads to elevated bilirubin levels. After delivery, bilirubin is no longer cleared (via the placenta) from the ... Acute hemolytic transfusion reactions due to immune hemolysis may occur in patients who have no antibodies detectable by ... In the presence of significant hemolysis the smear will show schistocytes (fragmented red blood cells), reticulocytosis, and in ... hemolysis). This is a major cause of HDN, because 75% of pregnancies result in some contact between fetal and maternal blood, ...
"Immune Hemolysis: Diagnosis and Treatment Recommendations". Seminars in Hematology. Anemia in Clinical Practice. 52 (4): 304- ... "Drug-induced hemolysis: Cefotetan-dependent hemolytic anemia mimicking an acute intravascular immune transfusion reaction". ... Quinidine Penicillin in high doses can induce immune mediated hemolysis via the hapten mechanism in which antibodies are ...
Shirron, N; Korem, M; Shuster, A; Leikin-Frankel, A; Rosenberg, M (2008). "Effect of Alcohol on Bacterial Hemolysis". Curr. ... "Microbial alcohol-conferred hemolysis is a late response to alcohol stress". FEMS Yeast Res. 11 (4): 315-23. doi:10.1111/j.1567 ...
α-Hemolysis will only cause partial lysis of the red blood cells (the cell membrane is left intact) and will appear green or ... γ-Hemolysis (or nonhemolytic) is the term referring to a lack of hemolytic activity. BAPs also contain meat extract, tryptone, ... "Blood Agar Plates and Hemolysis Protocols". Archived from the original on 2012-02-02. Retrieved 2014-10-28. Fisher, Bruce; ...
Growth on rabbit blood shows slight hemolysis. In glucose broth, the cultures appear turbid with a smooth sediment and a final ...
Sharp MK, Mohammad SF (Sep 1998). "Scaling of hemolysis in needles and catheters". Annals of Biomedical Engineering. 26 (5): ... and 25G butterflies connected directly to vacuum tubes caused the same amount of hemolysis and gave the same coagulation panel ... that shear stress and hence hemolysis decrease with decreasing needle bore (but the decrease can be clinically insignificant). ...
Hemolysis, magnesium concentration in red blood cells is approximately three times greater than in serum, therefore hemolysis ... Hypermagnesemia is expected only in massive hemolysis. Chronic kidney disease, excretion of magnesium becomes impaired when ...
... mechanisms of hemolysis, red blood cell destruction; and iron overload, a serious chronic condition in which the body absorbs ...
Melrose, W. D.; Bell, P. A.; Jupe, D. M.; Baikie, M. J. (1990-01-01). "Alcohol-associated haemolysis in Zieve's syndrome: a ... ISBN 0-19-262515-2. Shukla, Sandhya; Sitrin, Michael (2015-07-09). "Hemolysis in Acute Alcoholic Hepatitis: Zieve's Syndrome". ...
... s also cause hemolysis of mammalian blood cells. The main purpose of the secretion of grammastin is defensive and ... Grammistins affect organisms by cytolysis and hemolysis. As well as being toxic they are also antibiotic and antimicrobial. " ...
... a clue to footstrike hemolysis. Runner's anemia as a benefit versus runner's hemolysis as a detriment". The American Journal of ... The impact forces from running can lead to red blood cell hemolysis and accelerate red blood cell production. This can shift ... Repetitive impacts to the body may cause mechanical trauma and bursting (hemolysis) of red blood cells. This has been ... "Rust Urine after Intense Hand Drumming Is Caused by Extracorpuscular Hemolysis". Clinical Journal of the American Society of ...
Multistate Outbreak of Hemolysis in Hemodialysis Patients -- Nebraska and Maryland, 1998 From May 13 through May 23, 1998, a ... To ascertain the extent of this problem, all episodes of hemolysis in dialysis patients using a Cobe Centrysystem 3 Blood ... In this outbreak, all episodes of hemolysis have been associated with blood tubing produced by a single manufacturer. ... Hemolysis (i.e., premature breakdown of red blood cells {RBCs}) associated with hemodialysis is rare (2,3). The most frequent ...
Hemolysis is the breakdown of red blood cells. ... Conditions that can cause hemolysis include:. *Immune reactions ...
Metformin-induced hemolysis with jaundice K D Lin et al. N Engl J Med. 1998. . ... Metformin-induced hemolysis with jaundice K D Lin, J D Lin, J H Juang ...
Haptoglobin testing in hemolysis: measurement and interpretation Andrew W Y Shih et al. Am J Hematol. 2014 Apr. ... Haptoglobin testing in hemolysis: measurement and interpretation Andrew W Y Shih, Andrew McFarlane, Madeleine Verhovsek ... The direct antiglobulin test: a critical step in the evaluation of hemolysis. Zantek ND, Koepsell SA, Tharp DR Jr, Cohn CS. ... As there is no single gold standard for hemolysis, validation studies must rely on a combination of factors, which are reviewed ...
Therefore, it would be desirable to account for flow induced hemolysis by... ... In rotary blood pumps the degree of hemolysis is of crucial importance. ... Keywords: CFD-simulation, rotary blood pump, hemolysis, Lagrangian modelling, Eulerian modelling, unsteady hemolysis. 1 ... CFD-simulation, rotary blood pump, hemolysis, Lagrangian modelling, Eulerian modelling, unsteady hemolysis. ...
You can tell that this is the type of hemolysis that has occurred because of the presence of areas that are lightened and a bit ... At times, there is too much hemolysis that is going on that it will make the body start - ProProfs Discuss ... This is a Beta Hemolysis because this shows a complete breakdown of the red blood cells. ... At times, there is too much hemolysis that is going on that it will make the body start to feel bad. There are some who may go ...
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Learn about hemolysis topic of Biology in details explained by subject experts on Register free for online ... Hemolysis Meaning. What is Hemolysis? Hemolysis or Hemolysis is the destruction of RBC (red blood cells) and the discharge of ... Classification of Hemolysis. Hemolysis can be categorized according to whether the Hemolysis is Extrinsic, i.e., from a source ... Hemolysis or hemolysis might occur in vivo (inside) or in vitro (outside) of the body. One reason for Hemolysis is hemolysins ...
Life-threatening haemolysis induced by henna in a Sudanese child with glucose-6-phosphate dehydrogenase deficiency ... Our case was a 6-year-old boy who had 2 episodes of haemolysis, the first at the age of 2 years when henna was applied to his ... This is hard to explain but the amount of henna applied may have been small; lawsone is reported to cause haemolysis in a dose- ... Intravascular haemolysis of various causes can result in acute tubular necrosis due to haemoglobinuria leading to acute renal ...
Hemolysis Prediction in Medical Devices Using Cell Deformation and Pore Formation Models. Haßler, Stefan Thomas (Corresponding ... Hemolysis Prediction in Medical Devices Using Cell Deformation and Pore Formation Models ... Sie sind hier:Hemolysis Prediction in Medical Devices Using Cell Deformation and Pore Formation Models ... Sie sind hier: Hemolysis Prediction in Medical Devices Using Cell Deformation and Pore Formation Models ...
Hemolysis. This medical term refers to the destruction of red blood cells, which can happen during a plasma donation. The ... If the attendant notices signs of hemolysis, they will stop the procedure and may call for additional help. ...
Optimized workflow in HbA1c determination with onboard hemolysis. In order to process whole blood samples by onboard hemolysis ... Analyzers which are capable to do onboard hemolysis, immersion depth of sample probe is insufficient to reach sedimented ...
Hemolysis 7-Eleven Store, Texas, USA, 1953 Restrained-Fuck,... ...
Evidence against immune haemolysis in falciparum malaria in Thailand Merry AH., Looareesuwan S., Phillips RE., Chanthavanich P ... No evidence that chloroquine or hydroxychloroquine induce hemolysis in G6PD deficiency * Integration of HIV services with ...
Browse by "Hemolysis". Classification: Biospecimen Aliquots and Components. Pre-analytical Factor: Hemolysis. ...
George T, Kumar PS, Jayanthi Bai N, Krishnamurthy S. Lipid antioxidants & hemolysis. Indian Journal of Biochemistry & ...
... ... Clinical studies have shown a strong positive correlation between priapism and high levels of intravascular hemolysis in men ... Clinical studies have shown a strong positive correlation between priapism and high levels of intravascular hemolysis in men ... However, there are no experimental studies that show that intravascular hemolysis promotes alterations in erectile function. ...
... positive acid hemolysis (Ham) test, with normal result of sucrose hemolysis test in one form of this disease (hereditary ... In addition, hemolysis may be observed as a result of physical injury to the RBC or following exposure to drugs, chemicals, or ... Evaluation for Hemolysis. Normally, RBCs survive in the circulation for 120 days. If the erythrocytic life span is shortened ... Anemia solely due to hemolysis does not occur until RBCs are being destroyed at 6-8 times the normal rate, reducing the mean ...
Hemolysis In glucose-6-phosphate dehydrogenase deficient individuals, hemolysis may occur. This reaction is frequently dose- ...
Hemolysis Transfusion-Related Acute Lung Injury (TRALI) General Laboratory Tests ADVERSE REACTIONS Adverse Drug Reaction ... IGIV recipients should be monitored for clinical signs and symptoms of hemolysis. If signs and/or symptoms of hemolysis are ... Hemolysis. IGIV products can contain blood group antibodies which may act as hemolysins and induce in vivo coating of red blood ... signs and symptoms of hemolysis, such as fatigue, increased heart rate, yellowing of the skin or eyes, and dark-colored urine ...
Hemolysis In glucose-6-phosphate dehydrogenase deficient individuals, hemolysis may occur. This reaction is frequently dose- ...
Hemolysis after immunoglobulin therapy was described in patients receiving high immunoglobulin dosages. The issue of hemolysis ... Hemolysis after immunoglobulin therapy was described in patients receiving high immunoglobulin dosages. The issue of hemolysis ... Hemolysis after immunoglobulin therapy was described in patients receiving high immunoglobulin dosages. The issue of hemolysis ... Hemolysis after immunoglobulin therapy was described in patients receiving high immunoglobulin dosages. The issue of hemolysis ...
Conservative Management of Alloimmune Hemolysis and Cholestasis With Extreme Laboratory Ab Conservative Management of ... Alloimmune Hemolysis and Cholestasis With Extreme Laboratory Abnormalities. Kotch, Chelsea; Friedman, David F; Wilkins, ...
... foot-strike hemolysis, march hemoglobinuria) refers to an apparent anemia that occurs in avid runners and in hikers or soldiers ... The hemolysis occurs during the foot strike with each step. Older red cells have more rigid membranes and are more susceptible ... 2) hemolysis during running or hiking, followed by hemoglobinuria, decreased haptoglobin levels, and schistocytes in the ... Runners anemia (foot-strike hemolysis, march hemoglobinuria) refers to an apparent anemia that occurs in avid runners and in ...
The acute event of hemolysis resolved with medical therapy, and all were successfully discharged. However, recurrent hemolysis ... The acute event of hemolysis resolved with medical therapy, and all were successfully discharged. However, recurrent hemolysis ... The acute event of hemolysis resolved with medical therapy, and all were successfully discharged. However, recurrent hemolysis ... The acute event of hemolysis resolved with medical therapy, and all were successfully discharged. However, recurrent hemolysis ...
Hemolysis, Elevated Liver Enzymes, and Low Platelets Syndrome. Hemolysis, elevated liver enzymes, and low platelets (HELLP) ... GrandMaison S, Sauve N, Weber F, Dagenais M, Durand M, Mahone M. Hepatic rupture in hemolysis, elevated liver enzymes, low ... Fitzpatrick KE, Hinshaw K, Kurinczuk JJ, Knight M. Risk factors, management, and outcomes of hemolysis, elevated liver enzymes ... Clinical utility of strict diagnostic criteria for the HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome. ...
  • Clinical studies have shown a strong positive correlation between priapism and high levels of intravascular hemolysis in men with SCD. (
  • However, there are no experimental studies that show that intravascular hemolysis promotes alterations in erectile function. (
  • Therefore, we aimed to evaluate the corpus cavernosum smooth muscle relaxant function in a murine model that displays intravascular hemolysis induced by phenylhydrazine (PHZ), as well as the role of intravascular hemolysis in increasing the stress oxidative in the penis. (
  • Our results show that intravascular hemolysis promotes increased corpus cavernosum smooth muscle relaxation associated with increased HO-1 expression, as well as increased oxidative stress associated with upregulation of gp91phox expression. (
  • Moreover, our study supports clinical studies that point to a strong positive correlation between priapism and high levels of intravascular hemolysis in men with SCD. (
  • However, acute intravascular hemolysis due to thrombus in the pump remains a clinical challenge. (
  • We screened for LVAD-related intravascular hemolysis among 115 consecutive patients surviving HeartMateII implantation and investigated the role of medical therapy in resolving the hemolysis. (
  • BACKGROUND: Intravascular hemolysis in sickle cell anemia could contribute to complications associated with nitric oxide deficiency, advancing age, and increased mortality. (
  • METHODS: The distribution of serum lactic dehydrogenase (LDH) values was used as a surrogate measure of intravascular hemolysis in a contemporaneous patient group and an historical adult population from the Cooperative Study of Sickle Cell Disease (CSSCD), all with sickle cell anemia. (
  • Hematological Effects: Isolated cases of acute intravascular hemolysis, hemolytic anemia and hemoglobinuria have been reported. (
  • Hemolysis or hemolysis causes hemoglobinuria due to the release of hemoglobin into the blood plasma , which plays a significant role in sepsis pathogenesis. (
  • Runner's anemia (foot-strike hemolysis, march hemoglobinuria) refers to an apparent anemia that occurs in avid runners and in hikers or soldiers who travel with heavy loads. (
  • In disease, Haemolysis meaning is associated with hemolytic anaemia. (
  • Clinical Profile and Severity of Hemolysis in Adult Patients of Primary Autoimmune Hemolytic Anemia and Their Response to Steroid: A Prospective Cohort Study from Single Institution. (
  • The findings also suggest that an important class of disease modifiers in sickle cell anemia affect the rate of hemolysis. (
  • Monitor rate of hemolysis. (
  • Slight Hemolysis usually has little effect on test results, while more superior Hemolysis mainly demands a recollection, as results are grossly affected. (
  • The test compounds also resulted slight hemolysis at very high doses substantiating a safer profile compared to the positive control QS-21. (
  • A case was defined as hypertension (an increase of greater than or equal to 30 mm Hg from the baseline systolic blood pressure) and evidence of hemolysis (i.e., positive 'pink test' {pink-appearing serum}) in a patient within 12 hours of initiating hemodialysis during May 13-20. (
  • A presumptive diagnosis of acute haemolysis due to G6PD deficiency was made and the child received 1 blood transfusion and folic acid after which he recovered fully. (
  • The acute event of hemolysis resolved with medical therapy, and all were successfully discharged. (
  • The liver diseases unique to pregnancy include hyperemesis gravidarum, acute fatty liver of pregnancy (AFLP), intrahepatic cholestasis of pregnancy (ICP), and hemolysis and elevated liver enzymes and low platelets (HELLP) syndrome. (
  • For example, Plasmodium falciparum malaria is suggested by the presence of more than one ring form in an RBC, and the infection produces pan-hemolysis of RBCs of all ages. (
  • Ventricular assist devices (VADs) have already helped many patients with heart failure but have the potential to assist more patients if current problems with blood damage (hemolysis, platelet activation, thrombosis and emboli, and destruction of the von Willebrand factor (vWf)) can be eliminated. (
  • Chronic hyper-hemolysis in sickle cell anemia: association of vascular complications and mortality with less frequent vasoocclusive pain. (
  • Leftto- right shunt did not stop even 35 hours after the cessation of streptokinase and severe anemia developed due to mechanical hemolysis. (
  • Mixed type AIHA cases were presented mostly with severe haemolysis , with minimum therapeutic response to prednisolone and maximum relapse / drug dependency. (
  • Comparison of radial haemolysis with haemagglutination inhibition in estimating rubella antibody. (
  • Laboratory investigations were performed to establish haemolytic anaemia and to assess severity of haemolysis . (
  • Because haptoglobin levels become depleted in the presence of large amounts of free hemoglobin, decreased haptoglobin is a marker of hemolysis. (
  • Hyper-hemolysis was influenced by fetal hemoglobin and alpha thalassemia, and was a risk factor for early death in the CSSCD population (Hazard Ratio = 1.97, P = 0.02). (
  • The issue of hemolysis after immunoglobulin administration at replacement doses has been considered of little clinical significance. (
  • Hemolysis is the breakdown of red blood cells. (
  • Hemolysis, the red blood cell breakdown process, is a test-dependent phenomenon and affects laboratory tests to varying degrees. (
  • If toxins or chemicals build up in your body, it may cause breakdown of red blood cells and destroy them, which is known as hemolysis. (
  • Hemolysis or hemolysis might occur in vivo (inside) or in vitro (outside) of the body. (
  • The results were compared with in vitro measurements of the pressure head in each VAD and the hemolysis index in two VADs. (
  • One reason for Hemolysis is hemolysins' action, toxins produced by particular pathogenic bacteria or fungi. (
  • The hemolysis occurs during the foot strike with each step. (
  • However, this hemolysis may make you severely anemic , which sometimes occurs very quickly. (
  • Hemolysis or Hemolysis is the destruction of RBC (red blood cells) and the discharge of their contents (cytoplasm) into surrounding fluid (e.g. blood plasma). (
  • In this study, computational fluid dynamics (CFD) was used to calculate the hemodynamics in three clinical VADs and two investigational VADs and the shear stress, residence time, and hemolysis were investigated. (
  • A comparative analysis of the blood damage related fluid dynamic parameters and hemolysis index was performed among the VADs. (
  • Results: Six patients had signs and symptoms of immunoglobulin-induced hemolysis. (
  • The present prospective study was conducted to evaluate the profile of clinical picture, severity of haemolysis , treatment response of steroid . (
  • From May 13 through May 23, 1998, a total of 30 patients in three states * developed hemolysis with or without chest pains, shortness of breath, nausea, or abdominal pain while undergoing hemodialysis (HD). (
  • Hemolysis after immunoglobulin therapy was described in patients receiving high immunoglobulin dosages. (
  • Study Design and Methods: This was a single-center observational study over a 2-year period on immunoglobulin-induced hemolysis in a cohort of 162 patients with PADs treated with immunoglobulin administered at replacement dosages. (
  • Conclusion: Hemolysis occurred in patients receiving immunoglobulin at replacement dosages. (
  • At the end of follow-up, three patients were transplanted, one patient died refusing LVAD exchange for recurrent hemolysis, and 4 remained alive on LVAD support. (
  • As there is no single gold standard for hemolysis, validation studies must rely on a combination of factors, which are reviewed in this article. (
  • This destruction of RBC is called Hemolysis. (
  • Hemolysis is the process of unnatural destruction of red blood cells. (
  • The decrease of C5 binding to C3b clusters in the presence of C5 inhibitors correlated with the levels of residual hemolysis. (
  • Hemolysis definition is preceded by understanding the process of formation of red blood cells. (
  • Hemolysis is the word for the process in which the red blood cells break down and release bilirubin. (
  • The issue of hemolysis in long-term recipients of immunoglobulin treatment administered at replacement dosages should be more widely recognized. (
  • Increased or accelerated Hemolysis reduces the lifespan of red blood cells, causing them to die instantly than the bone marrow can replace them. (
  • Intrinsic Hemolysis is due to defects within the red blood cells, their membranes, the structure of haemoglobin , or the metabolism of the cell. (
  • The importance of AP-produced C3b clusters for C5 activation in the presence of eculizumab was corroborated by the finding that residual hemolysis after forceful activation of the classical pathway could be reduced by blocking the AP. (
  • We have previously reported that intense hemolysis is associated with increased risk of vascular complications in a small cohort of adults with sickle cell disease. (
  • A new scalar transport model for hemolysis was developed. (
  • It is an X-linked recessive inborn error of metabolism which can result in haemolysis on exposure to a number of triggers, such as some infections, and certain medicines and foods. (
  • all had evidence of hemolysis on admission to the hospital. (
  • Hemolysis can be categorized according to whether the Hemolysis is Extrinsic, i.e., from a source outside the red blood cell or Intrinsic, i.e., due to a defect within the red cell. (
  • We report on a 6-year-old boy, previously undiagnosed with G6PD deficiency, who developed life-threatening haemolysis after application of henna to his skin. (

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