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)

We describe 21 patients with severe and life-threatening autoimmune cytopenias resistant to standard immunosuppression who were treated with the monoclonal antibody Campath-1H. Four patients had autoimmune neutropenia, four had autoimmune haemolytic anaemia, four had pure red cell aplasia, one had immune thrombocytopenia purpura (ITP), three had autoimmune haemolytic anaemia and ITP (Evan's syndrome), three had autoimmune pancytopenia (ITP, autoimmune neutropenia and autoimmune haemolytic anaemia), one had ITP (associated with acquired Glanzmann's disease) and autoimmune neutropenia, and one had ITP and red cell aplasia. Campath-1H was administered at a dose of 10 mg/d as an intravenous infusion for 10 d. Responses were seen in 15 patients, which were sustained in six. Relapse occurred in eight patients after Campath-1H treatment. Patients entering the study later, received cyclosporine after Campath-1H in an attempt to reduce the incidence of relapse. Three patients received a second course of Campath-1H; all responded but later relapsed. Fourteen patients are alive at a median of 12 months (range 4-61) after Campath-1H. Campath-1H represents an alternative therapeutic option for severe, refractory autoimmune cytopenias.
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PMID:The effect of treatment with Campath-1H in patients with autoimmune cytopenias. 1156 82

We describe 11 patients with severe refractory autoimmune cytopenias treated with the anti-CD20 monoclonal antibody rituximab. Six patients had autoimmune neutropenia (AIN), two had pure red cell aplasia (PRCA), one had AIN and autoimmune haemolytic anaemia, one had AIN and immune thrombocytopaenia purpura (ITP) and one had PRCA and ITP. Rituximab was administered at a dose of 375 mg/m(2) as an intravenous infusion weekly for 4 weeks. Six of eight patients with AIN and all three patients with PRCA did not respond. Two patients died: one with resistant AIN and autoimmune haemolytic anaemia died of pneumocytis pneumonia infection, and one with PRCA and ITP died of an acute exacerbation of bronchiectasis. Rituximab in AIN and PRCA appears to be less effective than Campath-1H when compared to historical data from our group. This supports the hypothesis that T cells may be important in the pathophysiology of AIN and PRCA.
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PMID:Lack of clinical efficacy of rituximab in the treatment of autoimmune neutropenia and pure red cell aplasia: implications for their pathophysiology. 1712 83

Immune-mediated hemolytic anemia is a well-recognized complication of hematopoietic stem cell transplantation. We report on a 6-year-old boy with X-linked adrenoleukodystrophy who developed severe delayed alloimmune hemolytic anemia associated with immune-mediated neutropenia and thrombocytopenia following major ABO incompatible unrelated cord blood transplantation. The patient's cytopenias were refractory to treatment with corticosteroids, cyclosporine, intravenous immune globulin, rituximab, and pentostatin. After one course of Campath-1H his hematologic parameters normalized, suggesting that the compound may be an effective therapy for complex immunohematologic disorders complicating hematopoietic stem cell transplantation. The case also emphasizes the importance of T-cells in transplant associated immune cytopenias.
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PMID:Successful treatment of refractory immune hemolysis following unrelated cord blood transplant with Campath-1H. 1741 90

Alemtuzumab, a humanized monoclonal antibody that targets CD52 antigens on lymphocytes and monocytes, has shown efficacy in preventing relapse in relapsing-remitting multiple sclerosis. Despite known severe (yet rare) renal side effects such as anti-glomerular basement membrane disease and membranous glomerulopathy, to our knowledge, alemtuzumab has never been documented to cause drug-induced thrombotic microangiopathy. We describe a 39-year-old woman with relapsing-remitting multiple sclerosis who developed acute kidney injury requiring renal replacement therapy after 1 dose of alemtuzumab, as well as microangiopathic hemolytic anemia and thrombocytopenia. Pathologic examination of a kidney biopsy specimen demonstrated extensive cortical necrosis and arteriolar fibrin thrombi with nonspecific immunofluorescence staining of immunoglobulin M and C3 and absence of immune deposits on electron microscopy. These findings were consistent with the diagnosis of acute thrombotic microangiopathy. She received dexamethasone and underwent plasmapheresis, which was unsuccessful at removing alemtuzumab. The patient received renal replacement therapy for approximately 7 weeks, followed by slow recovery of kidney function that returned close to her baseline.
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PMID:Acute Thrombotic Microangiopathy and Cortical Necrosis Following Administration of Alemtuzumab: A Case Report. 3052 35