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Query: UMLS:C0002878 (hemolytic anemia)
 7,530 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study red cell autoantibodies with ABO specificity, the records of 4668 patients seen over 32 years were examined. Five group A patients had high thermal amplitude cold agglutinins showing anti-A, -A1 or -AI specificity; none had ever received blood or blood products. They presented as chronic cold haemagglutinin disease, autoimmune haemolytic anaemia or were discovered during investigation of pregnancy, carcinomatosis or anaemia. In vivo haemolysis was evident in all but the antenatal case; only the patient with autoimmune haemolytic anaemia required treatment, responding well to steroids. ABO-specific autoantibodies thus appear similar in reactions and clinical manifestations to autoantibodies in general.
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PMID:Autoimmune haemolysis and red cell autoantibodies with ABO blood group specificity. 779 42

A 52-yr-old man developed immune hemolytic anemia approximately 2 wk after receiving an ABO-minor-mismatch renal transplant. When a Group O organ is transplanted into a non-O recipient or a non-AB organ is transplanted into a Group AB recipient, hemolysis can occur and has been attributed to a form of graft-versus-host disease in which donor plasma cells carried along with the graft produce red blood cell antibodies. In this case, the diagnosis was confirmed when an antibody screen indicated that the organ recipient's serum agglutinated panel red blood cells of the recipient's ABO group. This type of hemolysis usually occurs 1 to 2 wk after transplantation, is limited in duration, and can be severe. If transfusion is required, blood of donor type should be used.
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PMID:Immune hemolytic anemia after renal transplantation secondary to ABO-minor-mismatch between the donor and recipient. 830 39

Hemolysis due to donor-derived red cell antibodies is a potential complication after minor ABO-mismatched solid organ transplantation. It has also been described in Rh-positive recipients receiving organs from previously isoimmunized Rh-negative donors. We report on a group O, Rh(D)-positive patient who received a heart-lung transplant from a group O, Rh(D)-negative donor presenting an anti-D antibody. Severe hemolytic anemia developed in the early postoperative period and lasted for 3 mo. Anti-D antibodies that were of donor origin were found in bronchoalveolar lavage fluid and serum. In addition, using the polymerase chain reaction for human leukocyte antigen class II genotyping, we were able to demonstrate the presence of a mixed population of donor and recipient cells in the lungs and the peripheral blood of the recipient. The chimeric state in the blood persisted until at least the fifty-seventh postoperative day. This first case report of hemolysis due to Rh(D) antibody after heart-lung transplantation emphasizes the need for routine red cell antibody screening of donors and for close monitoring of signs of red cell destruction in the recipient in cases of pretransplant donor isoimmunization.
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PMID:Severe hemolysis due to a donor anti-D antibody after heart-lung transplantation. Association with lung and blood chimerism. 834 16

We report on flow cytometric IgG subclass determinations of red cell antibodies using polyclonal FITC-labeled antibodies. The limit of detection of this method was 1 ng anti-D per 1 x 10(7) red cells. The inter- and intra-assay coefficients of variance were 8.2 and 2.3%, respectively. In 8 newborns with a positive direct antiglobulin test (DAT) in the gel centrifugation test (GCT), due to ABO antibodies, IgG1 was detected in all and IgG2 additionally in 4 of these cases. In 5 severe cases of hemolytic disease of the newborn (HDN) due to anti-D, large amounts of IgG1 were found, and in 3 of these 5, IgG3 in combination with IgG1. In 8 mild or moderate HDN cases (4 anti-D, 2 anti-E, 1 anti-Fya, 1 anti-Jka), phototherapy sufficed, and IgG1 was the only antibody. In 7 adult patients with malignant lymphoma and a positive DAT (GCT), only small amounts of IgG1 red cell autoantibodies could be demonstrated by flow cytometry. In 5 further patients with malignant lymphoma, a positive DAT, and severe hemolytic anemia, large amounts of IgG1 autoantibodies were found and IgG3 was also present in 3 of these cases. Flow-cytometric determination of IgG subclasses may be a useful tool in immunohematology, since subclass determinations were possible in all of these cases. This method is suited for clinical routine and offers the possibility of sufficient standardization.
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PMID:Flow cytometric analyses of the subclasses of red cell IgG antibodies. 858 93

We report three instances of antibody-mediated hemolytic anemia following ABO-mismatched, but compatible, renal (n = 2) and simultaneous pancreas-kidney (n = 1) transplantation. The two renal allograft recipients had received a 6-antigen matched transplant; one received polyclonal antilymphocyte globulin to treat an early rejection episode. The simultaneous pancreas-kidney transplant received polyclonal antilymphocyte globulin (ALG) as part of a quadruple therapy induction regimen. All three patients developed severe, but self-limited, antibody-mediated hemolytic anemia within two weeks of their transplants. Serologic testing demonstrated the hemolysis to be antibody mediated; furthermore, testing of the ALG lots demonstrated high titers of anti-red blood cell antibodies. The possible contribution of ALG and HLA matching to the hemolysis seen in these patients after ABO mismatched organ transplantation is discussed.
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PMID:Antibody-mediated hemolytic anemia following ABO-mismatched organ transplantation: contributory role of HLA matching and polyclonal antilymphocyte globulin. 866 12

The development of immune-mediated hemolytic anemia is a well-recognized complication after allogeneic bone marrow transplantation (BMT). The majority of reported cases, however, have been alloimmune in origin due to ABO or minor red blood cell antigen incompatibilities between the donor and recipient. In this study, we report seven adult patients who developed autoimmune hemolytic anemia (AIHA) between June 1985 and January 1993. These patients were identified from a total of 236 adult patients who received T cell-depleted (TCD) grafts as graft-versus-host disease (GVHD) prophylaxis. The onset of AIHA was at a median of 10 months (range 7-25 months) post-transplant and occurred in 5% of all patients transplanted with TCD grafts who survived at least 6 months. Six patients had a warm reacting autoantibody, while one patient had a cold-reacting antibody with a thermal amplitude up to 30 degrees C. All were receiving immunosuppressive treatment for GVHD at the time of diagnosis. Initial treatment in all patients consisted of steroids. Three of the seven had a partial response while the four remaining patients failed to respond to corticosteroids. Splenectomy was performed in three patients with two partial responses. Four patients were treated with additional therapeutic interventions, including plasmapheresis, immunoglobulin infusions, staphylococcus protein A column, or other immunosuppressive agents. In five cases, erythropoietin was administered as adjunctive treatment to maintain adequate hematocrit levels. Two patients are presently in complete remission after prolonged courses of steroids, while a third patient has compensated hemolysis requiring low-dose steroids. Four patients died due to either infectious complications or disseminated intravascular coagulation secondary to cold agglutinin disease. These data indicate that AIHA is a clinically significant and not infrequent complication in allogeneic marrow transplant recipients. The response to conventional treatment is generally unsatisfactory as even patients who ultimately remit require prolonged courses of immunosuppressive therapy.
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PMID:Autoimmune hemolytic anemia following T cell-depleted allogeneic bone marrow transplantation. 880 20

A 46-year-old woman with chronic myelogenous leukemia received allogeneic bone marrow transplantation from an unrelated human leukocyte antigen (HLA) matched (but mixed lymphocyte culture (MLC) positive to graft-versus host disease (GvHD) donor. The blood type of the recipient was A type Rh (+) while the donor blood type was B type Rh (+). The patient received busulfan 8 mg/kg, cyclophosphamide 120 mg/kg, and total-body irradiation 10 Gy before bone marrow transplantation. Short-term administration of methotrexate and cyclosporin was given for prophylaxis of GvHD. The mononuclear cells harvested from the donor were concentrated by COBE Spectra before bone marrow transplantation. Although engraftment of transplanted bone marrow in the recipient was confirmed on day 11, the patient suffered from severe anemia on day 10. Since the direct Coombs' test to A type red blood cells was positive, and anti-A antibody titer increased 16-fold, we diagnosed her anemia as hemolytic anemia caused by ABO mismatched transplantation. In addition to hemolytic anemia, she had skin symptoms of acute GvHD grade II, microangiopathic hemolytic anemia, and died of multiple organ failure on day 44. This experience indicated that some allogeneic transplant recipients are at risk of severe hemolytic anemia in the early stage after unrelated ABO mismatched donor and that it is necessary to establish proper treatment and prophylaxis.
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PMID:[Rapid onset of hemolytic anemia after allogeneic bone marrow transplantation from an unrelated ABO major mismatched donor]. 902 56

Passenger lymphocytes in grafted kidney have been reported to result in autoimmune hemolytic anemia (AIHA) in minor ABO incompatible transplants. We followed up 15 cases of minor ABO incompatible transplants for one year. Two patients developed severe but self-limited auto-immune hemolytic anemia within two weeks of renal transplantation. Both were blood group A and had received a kidney from a group O donor. Preoperative cross-match and antibody screen was negative; however subsequent to the hemolytic episode, group-specific blood was incompatible and patients were transfused with group O, cross-match compatible blood. Serological tests showed positive direct anti-globulin test (DAT) and anti-A was eluted from both cases.
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PMID:Acquired hemolytic anemia after minor ABO incompatible renal transplantation. 956 84

We report a bone marrow transplant which was HLA matched, with major and minor ABO and minor RhD incompatibility (anti-RhD antibody) between the donor and recipient. When engraftment occurred, the recipient developed an anti-RhD antibody of donor origin detected by direct and indirect antiglobulin tests (DAT, IAT) and showed signs of mild hemolytic anemia. With the disappearance of the recipient RBCs, the DAT became negative and the hemolysis disappeared, while the anti-RhD alloantibody persisted in the patient's serum. This case emphasizes the importance of close immuno-hematological monitoring in patients undergoing allogeneic BMT with ABO-RhD incompatibility between recipient and donor.
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PMID:Transmission of an anti-RhD alloantibody from donor to recipient after ABO-incompatible BMT. 963 84

Among 27 patients who received minor ABO-incompatible partial liver transplantations and 19 who received major ABO-incompatible partial liver transplantations from living donors, 2 developed hemolytic anemia within 2 weeks after transplantation. These 2 patients had received livers from their living fathers whose blood type was ABO-incompatible. B-to-A transplantation was performed in patient 1 and O-to-B transplantation was performed in patient 2. Anti-A IgM and IgG were detected in the serum of patient 1, and anti-B IgM and IgG were detected in the serum of patient 2. These antibodies were eluted from the red blood cells of the patients. The coexistence of donor-specific DNA in the peripheral blood of the patients proved that they had chimerism, and graft-versus-host antibody production due to passenger B lymphocytes in the donor's liver was subsequently confirmed.
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PMID:Hemolytic reaction due to graft-versus-host (GVH) antibody production after liver transplantation from living donors: report of two cases. 971 12


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