Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002878 (hemolytic anemia)
 7,530 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The illegitimate glycosphingolipid antigens of the P blood group system and of the Forssman (Fs) tissue antigen in adenocarcinoma which are foreign to the host suggest the self-nonself concept which applies also to numerous other diseases such as rheumatoid arthritis, lupus, gluomerulonephritis, and idiopathic acute hemolytic anemia. In the presence of the glycosphingolipid antigens such as ABO, P, and Fs, the normal serum of the homozygote recessive precursor contains antibodies for the missing antigen(s). The expected antibody to the Fs antigen was present in about 75% of normal men and women. In cancer sera, the incidence of anti-Fs was decreased to about 35-40%. On testing the normal population anti-Fs was present in 90% of the sera in the youngest group, and this value gradually diminished in the older groups; the incidence of the antibody in the 70-year age group was to about 60%. The rate of loss of anti-Fs with increasing years appears to parallel the gradual loss of anti-A and anti-B isoagglutinin titers. This phenomenon may be associated with the gradual diminution of protein synthesis with aging or the continuous accumulation of soluble immune complexes in the serum, or both. It is suggested that the self-nonself concept is also the basis for the pathogenesis of rhematoid arthritis, lupus erythematosus, idiopathic acute hemolytic anemia, and numerous other conditions classified as "autoimmune" diseases. Some of these diseases are induced by viruses or drugs or both. When a virus or drug attaches itself to the membrane of a tissue cell, the self is converted to nonself which, in rheumatoid arthiritis, alters its self Ig to nonself Ig.
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PMID:Self-nonself concept for cancer and diseases previously known as "autoimmune" diseases (illegitimate transferases/plasma exchange). 28 17

Ingestion of drugs can cause patients or blood donors to have a positive direct and sometimes indirect antiglobulin test. The most common cause of these positive reactions and immune hemolytic anemia due to drugs is the formation of red cell autoantibodies. These autoantibodies will react with the patient's own red cells and usually most other normal red cells in vitro without the drug being present. The prototype drug causing this type of reaction is alpha methyldopa (Aldomet). Other drugs cause positive antiglobulin tests by three different mechanisms, the drug antibodies reacting with red cells in vitro only in the presence of the drug. The first of these mechanisms causes positive reactions because the drug binds firmly to the red cell membrane, and antibody against the drug will combine with the drug on the membrane leading to IgG-sensitized red cells. The prototype drug for this mechanism is penicillin. The second mechanism involves chemical modification of the red cell membrane by the drug so that it takes up many proteins nonspecifically; the cephalosporins are the only group of drugs known to react in this fashion. The final mechanism involves the formation of an immune complex by the drug and its specific antibody. This immune complex will attach to cell membranes, usually activating complement in the process. Examples of drugs thought to operate by this mechanism are phenacetin, quinine, and quinidine. Some individuals have antibodies present in their serum that will react with chemical added to commercial blood bank reagents. Examples of these are antibodies to dyes added to ABO typing sera, antibodies to sodium caprylate in bovine albumin, and antibodies to chemicals added to red cell diluents, e.g., chloramphenicol, neomycin, and hydrocortisone. If these antibodies are present they can create problems in pretransfusion testing; in particular, they can present anomalies in ABO, Rh grouping, and antibody detection.
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PMID:Problems in pre-transfusion tests related to drugs and chemicals. 77 71

Six cases of immune hemolytic anemia attributed to donor-derived red cell antibodies after allogeneic bone marrow transplantation (BMT) are reported. In 2/6 cases, severe intravascular hemolysis was seen, 6/6 required increased red cell transfusion, and 1/6 was treated by plasma exchange. All recipients were receiving cyclosporine to prevent graft-v-host disease. Investigations showed that in each case, the donor lacked ABO or Rho(D) red cell antigens present in the recipient. The direct antiglobulin test was positive in 6/6. Relevant serum antibody (anti-A, four cases; anti-B, one case; anti-D, one case) was first detected one to three weeks after BMT. Eluates made from recipient red cells showed the same specificity as serum antibody. Maximum hemolysis occurred nine to 16 days after BMT, suggesting that active production of antibody by "passenger" donor lymphocytes was the likely mechanism of hemolysis, rather than passive transfer of antibody in the marrow infusion. Retrospective analysis of 21 consecutive cyclosporine-treated BMT patients receiving marrow lacking ABO or D antigens present in the recipient showed that (1) 15/18 patients tested had red cell antibody production against recipient red cell antigens; (2) despite the frequent presence of antibody specific for recipient red cell antigens, only 3/21 patients developed clinically significant hemolysis; (3) clinical hemolysis could not be predicted by donor or recipient red cell antibody titers. We conclude that although red cell antibody against recipient antigens is frequently produced after minor ABO and D mismatched BMT in cyclosporine-treated recipients, only 10% to 15% of cases develop clinically significant immune hemolysis. The data presented show that the most likely source of antibody is "passenger" donor lymphoid cells.
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PMID:Donor-derived red blood cell antibodies and immune hemolysis after allogeneic bone marrow transplantation. 307 41

Immune hemolytic anemia in patients after organ transplantation has been reported generally to be graft-cell-derived due to elaboration by the donor's "passenger" lymphocytes of the antibodies directed against the recipient's red cell antigens. In contrast, this report presents a case that illustrates postoperative red cell alloantibody production by the recipient of an orthotopic liver transplant. Anti-Jka, -c, and -S, detected in the recipient's serum 9 days after transplantation, resulted in significant hemolysis. These alloantibodies had not been present in the recipient's serum before transplantation or in the sera of the liver or blood donors. In addition, anti-Jka and -c were eluted from posttransfusion red cells. The patient was transfused during surgery with crossmatch-compatible blood, that carried the alloantigens Jka, c, and S. The liver donor's red cells also carried the Jka, c, and S antigens. The recipient's pretransplantation red cell phenotyping was Jk(a-), c-, S-. The recipient had received only one transfusion 10 years prior to this operation, after which time he was noted to have anti-K. Immunosuppression initially consisted of cyclosporine, azathioprine, and prednisolone. This is believed to be the first report of delayed immune hemolysis due to non-ABO antibodies in a liver transplant patient treated with cyclosporine.
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PMID:Delayed immune hemolysis in a patient receiving cyclosporine after orthotopic liver transplantation. 313 Jun 96

Malaria is uncommonly acquired without mosquito transmission. Two patients presenting with malaria illustrate this rare phenomenon. The first was a 1-month-old child who had received an exchange blood transfusion for severe haemolytic anaemia due to ABO blood incompatibility. The second was a doctor who had taken blood from the first patient. The occurrence of both transfusion malaria and accidental malaria from the same blood transfusion must be very uncommon.
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PMID:Unusual forms of malaria transmission. A report of 2 cases. 354 51

5 patients with autoimmune haemolytic anaemia (AIHA) of warm type (4 idiopathic, 1 associated with systemic lupus erythematosus and thrombocytopenia) were treated with high doses of i.v. immunoglobulin (IgG; Sandoglobulin; 2.0 g/kg body weight). IgG therapy was ineffective in all 5 cases as indicated by a lack of clinical improvement, continuous signs of accelerated red blood cell (RBC) destruction, and an unchanged survival rate of 51Cr-labelled autologous RBC in 4 patients studied. IgG infused at equivalent doses into 5 healthy volunteers led to an increase of IgG coating of autologous RBC (irrespective of the ABO blood groups) without concomitant changes of haemoglobin, haematocrit or reticulocytes, increase of serum IgM in 3/5, a decrease of serum C4 in 5/5, and a decrease of serum haptoglobin in 2/5 individuals. We conclude that IgG at a dose of 2.0 g/kg body weight is ineffective in AIHA. This may be caused by an increased, though clinically inapparent, interaction of IgG-coated autologous RBC with the mononuclear phagocyte system.
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PMID:Lack of efficacy of high-dose intravenous immunoglobulin in autoimmune haemolytic anaemia: a clue to its mechanism. 401 19

The first case of haemolytic anaemia with thrombocytopenia and acute renal failure induced by ingestion of aspirin in a 22-year old woman is reported. An IgM anti-aspirin antibody which agglutinated erythrocytes of the patient and of ABO compatible donors in the presence of aspirin was isolated in the serum. In addition, the allergic nature of the patient's hypersensitivity to aspirin was confirmed by positive lymphocyte transformation and basophil degranulation tests in the presence of the drug.
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PMID:[Immunoallergic hemolytic anemia, thrombopenia and acute renal failure induced by aspirin]. 623 55

A new method for eluting red cell antibodies using chloroform has been shown to be effective. The method is similar to ether and xylene techniques but can be completed within 10 min after adequate cell washing. Comparison studies using ether, xylene and chloroform showed that antibodies eluted by chloroform yielded equivalent titration scores. Antibodies within the Ss blood group system were easily eluted using chloroform but not using ether. Also, the chloroform method yielded informative eluates when prepared from red cells of patients with warm antibody autoimmune hemolytic anemia, drug-induced immune hemolytic anemia, hemolytic disease of the newborn caused by ABO or Rh fetal maternal incompatibility, or from patients having a positive direct antiglobulin test as a result of alloantibodies stimulated by recent transfusion ("delayed transfusion reaction'). The advantages of chloroform elution are: (1) chloroform is nonflammable; (2) the eluate is readily obtained from the top layer after centrifugation; (3) no residual solvent remains in the eluate, and (4) the method is rapid.
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PMID:A new elution procedure using chloroform, a nonflammable organic solvent. 703 31

Seventy-one ABO incompatible (heterospecific) infants and 71 controls, who were free from other potential causes of jaundice, were studied to ascertain which cord blood tests reliably predict the severity of ABO haemolytic disease of the newborn (ABO HDN). The modified Direct Antiglobulin Test (spin DAGT) was positive in all infants who required treatment for haemolytic jaundice and only DAGT positive children showed evidence of impending haemolytic anaemia or compensated haemolysis in cord or capillary blood. Cord serum bilirubin concentration had some predictive value, particularly when the level exceeded 85 mumol/l, but it was a less reliable indicator and had greater value if used in association with the DAGT. The elution test, which is frequently used as a diagnostic tool in ABO HDN, had no predictive value and we felt that its putative value is due to overdiagnosis of ABO HDN in jaundiced heterospecific infants. We conclude that the spin DAGT, despite the weakness of the reaction, reliably identifies infants at risk from severe ABO HDN and is sufficiently sensitive to be used as a single screening test for the early detection of the disorder.
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PMID:Prediction of the severity of ABO haemolytic disease of the newborn by cord blood tests. 719 39

Hemolytic-uremic syndrome (HUS) accompanied by pneumococcal infections forms a characteristic subgroup of HUS. Pneumococcal neuraminidase splits off neuraminic acid from the glycoproteins present on the surface of red cells, thrombocytes and endothelial cells, and thus exposes the hidden Thomsen cryptantigen (T-Ag). The T-Ag can then react with a complement-fixing antibody of the IgM class which is present in all human plasmas after the age of 6 months. Early diagnosis of T-transformation should be attempted. Highly suggestive hints are: pneumonia, hemolytic anemia, reticulocytopenia, difficulties in ABO typing, a positive direct Coombs test and a positive minor cross-match. The definite diagnosis of T-transformation is established with the aid of anti-T agglutinins from Arachis hypogaea, the common peanut. Two children aged 19 and 22 months with pneumonia, Coombs-positive hemolytic anemia, HUS and exposure of the T-Ag on the red cell membrane are described. In one of them, circulating neuraminidase and circulating pneumococcal antigen of serotype 3 were found. In both children exchange transfusions resulted in elimination of circulating neuraminidase and of T-transformed red cells prone to hemolysis.
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PMID:[Neuraminidase-producing pneumococci in the pathogenesis of hemolytic-uremic syndrome]. 728 May 95


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