Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 5 1/2-yr-old child developed severe anemia with erythroid hypoplasia and 50% ringed sideroblasts in his bone marrow. A serum inhibitor of erythropoiesis was demonstrated, utilizing syngeneic and autologous bone marrow in a plasma-clot culture system. The IgG fraction of the patient's serum effected similar suppression of erythroid colony formation. Prednisone therapy was ineffective, but following treatment with cyclophosphamide, normal erythropoiesis was established, ringed sideroblasts disappeared, and his serum no longer inhibited erythropoiesis in vitro. Cyclophosphamide was discontinued, and the patient has remained hematologically normal. This patient is an example of antibody-mediated sideroblastic anemia successfully treated with a cytotoxic drug.
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PMID:Antibody-mediated acquired sideroblastic anemia: response to cytotoxic therapy. 46 37

The authors describe an unusual case of hypoplastic anaemia. The condition developed shortly after birth as a typical case of Josephs-Blackfan Diamond and was favourably influenced only by a combined treatment with Prednison and Dianabol. The improvement, however, did not last long and after shorter or longer periods of time anaemia recurred again. Applying the same therapy the authors succeeded, despite the sometimes grave condition of the child, not only to save his life but also to normalize the erythrocyte count. It must be noted that the child showed viability for a long period of time no matter how pronounced the anaemia was. Thus, therapy was not necessary to be repeated often. Of special interest for this case were bone marrow examinations. During the first year of the child's life only 1 to 4 erythroblasts were seen the examination was performed several times. After the sixth year the bone marrow contained many erythroblasts although the type of anaemia remained unchanged. According to the authors this peculiarity could be explained only as a transition from a hypoplastic into a pseudohypoplastic anaemia.
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PMID:[On an unusual case of hypoplastic anaemia (author's transl)]. 88 7

A 4-year-old boy with pure red cell aplasia was investigated. Immunophenotypic analysis of peripheral blood lymphocytes revealed a marked increase of CD20+ cells, which fell from 25.9% in the active stage to 9.7% in remission. The plasma contained a suppressive activity against CFU-e and BFU-e formation by the patient's bone marrow cells, which disappeared when the disease went into remission. Prednisone (2 mg/kg/day) therapy was tried for 5 weeks, but produced no improvement. Subsequently, high-dose gamma-globulin therapy induced complete remission of anemia. A lymphoblastoid B cell line obtained from the patient before therapy produced a factor that suppressed erythropoiesis but not granulopoiesis. The suppressive activity resided in the immunoglobulin fraction and was adsorbed by an anti-immunoglobulin column. These results indicate that expansion of B cells producing an immunoglobulin which suppressed erythropoiesis was involved in the pathogenesis of the disease in this patient.
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PMID:A B cell line from a patient with pure red cell aplasia produces an immunoglobulin that suppresses erythropoiesis. 172 Mar 59

Clinico-haematological parameters in sixteen patients of paroxysmal nocturnal haemoglobinuria (PNH) are presented. Their modes of presentation included recurrent episodes of cola-coloured urine (6/16), refractory anaemia (9/16) and predominant thrombotic manifestations (1/16). Laboratory investigations revealed the presence of anaemia (16/16), reticulocytosis (14/16), thrombocytopenia (11/16), leucopenia (5/16) and cellular bone marrow (14/16). Two patients had hypoplastic bone marrow initially but subsequently developed PNH. The patients were treated with haematinics, prednisolone (16/16) and oxymethalone (2). Prednisone was effective in suppressing haemolytic episodes. Oxymethalone given to the 2 patients with hypoplastic bone marrow resulted in amelioration of anaemia in one but no effect in the other patient.
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PMID:A clinico-haematologic profile of paroxysmal nocturnal haemoglobinuria. 181 94

A case of acquired haemophilia A presenting with extensive spontaneous bruising and anaemia is reported. The anaemia was due to myelodysplastic syndrome (FAB: refractory anaemia with ringed sideroblasts). A factor-VII:C-specific inhibitor was also found. Prednisone and pyridoxine were given, and the inhibitor became undetectable after 4 weeks of therapy, but the abnormal ringed sideroblasts still persisted on repeated bone marrow biopsy.
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PMID:Myelodysplastic syndrome and acquired factor VIII inhibitor with severe subcutaneous haemorrhage. 190 70

To determine whether patients with systemic lupus erythematosus undergoing long-term peritoneal dialysis have persistent clinical and serologic remissions, the clinical courses of eight patients with end-stage renal disease in whom peritoneal dialysis was begun at Rush-Presbyterian-St. Luke's Medical Center between 1981 and 1986 were analyzed. Patients were followed for a mean of 90.1 +/- 28.8 months before dialysis and 20.8 +/- 4.7 months after the initiation of dialysis. Disease activity was quantified for each individual in terms of "flares" per year before and after the initiation of peritoneal dialysis, the means of which were 0.66 +/- 0.46 and 0.94 +/- 0.28, respectively. Comparison of these rates showed no statistical difference. Seven of the eight patients had at least one flare while receiving peritoneal dialysis, all of which required prednisone therapy (mean 31.3 mg per day). The clinical manifestations included fever, rash, myalgias, anemia, leukopenia, serositis, and cerebritis. Eighty-eight percent of these flares had associated worsening of serologic results. Prednisone was discontinued in only one patient at any time during peritoneal dialysis. This experience reveals that patients with lupus continue to show clinical and serologic disease activity and require maintenance prednisone therapy while receiving long-term peritoneal dialysis.
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PMID:Persistence of clinical and serologic activity in patients with systemic lupus erythematosus undergoing peritoneal dialysis. 349 20

Disulon (Dapsone) was used in 20 patients with Horton's disease, with the object of reducing steroid therapy. In a retrospective series, Dapsone was prescribed in 12 patients with severe complications of steroid therapy; it was possible to reduce the dose of steroids by about 50 p. 100 in under 3 months without causing a flare-up of the disease. In a prospective series of 8 patients, Dapsone was given at the outset with Prednisone; the results were compared with a control series of 8 patients--the dose of steroids could be reduced earlier, the total duration of steroid therapy was shorter, and the total dose of steroids was lower. The main side effect of Dapsone is haemolysis which may give rise to anaemia, the severity of which is usually dose-dependent. A daily dosage of 75 to 100 mg would seem to provide a good compromise between the anti-inflammatory and haemolytic effects. Dapsone should always be given in association with steroids in the treatment of temporal arteritis; a closer biological surveillance of patients treated with association is necessary.
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PMID:[Disulon in the treatment of Horton's disease. Experience with 20 patients]. 377 39

A case of thrombocytopenia in a Collie dogIdiopathic thrombocytopenia, the most common cause of the hemorrhagic syndrome in the dog, was diagnosed in an adult male Collie. The bleeding tendency was manifested by anemia, ecchymotic hemorrhages, melena and bilateral epistaxis. Hook-worms increased the anemia. The clinical diagnosis was confirmed by a reduced platelet count. Prednisone was the specific treatment.
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PMID:[A case of thrombocytopenia in a Collie dog (author's transl)]. 724 73

The purpose of this study was to evaluate a new regimen for the treatment of multiple myeloma based on alternating 3-week cycles of chemotherapy and interferon (rIFN alpha 2). In this prospective phase II clinical trial the Eastern Cooperative Oncology Group evaluated a regimen consisting of 2 cycles of VBMCP (Vincristine 1.2 mg/M(2) IV d1, BCNU 20 mg/M(2) IV d1, Melphalan 8 mg/M(2) PO dl-4, Cyclophosphamide 400 mg/M2 IV d1, Prednisone 40 mg/M(2) PO d1-7) followed by alternating 3-week cycles of VBMCP and rIFN alpha2 5 Mu/M(2) SC 3x/week. Treatment was administered for 2 years. Fifty-eight patients with previously untreated multiple myeloma were entered. Objective response (OR) required 50% decrease in M-protein with correction of severe anemia and no progression of skeletal disease. Complete remission (CR) was defined by disappearance of M-protein and normalization of the bone marrow morphology. Life table analysis was utilized to express survival and response duration. Fifty-four patients were evaluable. Objective response was seen in 80% of patients including CR in 30% (16 patients). The median response duration is 35 months, 46 months for patients with CR. The median survival is 42 months for all patients. Five year survival is 42%. Although 78% of patients had neutrophil nadirs <1000 x 10(9)/L, the incidence of severe infection was only 9%. These data demonstrate that VBMCP + interferon is an effective new regimen combining chemotherapy with a biological response modifier for the treatment of multiple myeloma. The incidence of CR is high, and the response and survival durations appear to be 1 year longer than usually seen with standard chemotherapy. A current ECOG randomized trial compares VBMCP + interferon with VBMCP alone.
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PMID:Complete remission induction with combined VBMCP chemotherapy and interferon (rIFN alpha 2b) in patients with multiple myeloma. 883 1

Immune dysregulation, a hallmark of chronic lymphocytic leukemia (CLL), manifests itself in three autoimmune diseases: warm autoimmune hemolytic anemia (AIHA); idiopathic thrombocytopenia (ITP); and, pure red cell aplasia (PRCA). AIHA occurs in 11% of advanced stage CLL patients. Prednisone is the first treatment of choice, with 90% responses and 65% complete responses. More than 60% of patients relapse when treatment is stopped. Intravenous immunoglobulin, the next line of treatment, causes responses in 40% of patients. While the data are very limited, cyclosporine A is a reasonable choice for third-line therapy. Alkylating agents, danazol, plasma exchange, immunoabsorption, vincristine-loaded platelets, splenectomy, and splenic irradiation are also reported to cause responses. The data on mechanisms of AIHA are most consistent with immune dysregulation leading to loss of tolerance to a self antigen which in turn leads to the immune-based hemolytic anemia. PRCA is underrecognized in CLL with 6% of CLL patients having PRCA when tested for it. Unlike AIHA, PRCA often occurs in early stage disease. Anemia, reticulocytopenia, and a marrow virtually devoid of red blood cell precursors are hallmarks of PRCA. Corticosteroid therapy is the first line of treatment. If a response is not obtained in 4 weeks, cyclosporine A should be added. Although the data on pathophysiology are very limited, PRCA appears to be the result of an abnormal T cell that both fails in its normal function to support growth and inhibits the growth of erythroid progenitor cells. ITP occurs in 2-3% of CLL patients, occurs in early stage disease and may be a presenting manifestation. Initial therapy for ITP mirrors the guidelines for primary ITP. Initial therapy should consist of prednisone. Seventy percent of patients respond. Splenectomy is a reasonable second-line treatment. Autoimmune phenomena, largely related to blood cells, are based in the immune dysregulation of CLL. Longer survivals in CLL patients, more treatment regimens per patient, and more immunosuppression with modern treatments, allow us to predict an increasing incidence of autoimmune blood cell diseases in CLL.
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PMID:Autoimmune disease and chronic lymphocytic leukemia: autoimmune hemolytic anemia, pure red cell aplasia, and autoimmune thrombocytopenia. 948 30


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