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 combination of oral zidovudine (250 mg twice daily) and subcutaneous interferon-alpha (10 x 10(6) units daily) was evaluated for clinical, antiretroviral, and immunological efficacy and for side effects in 17 patients with AIDS-related Kaposi's sarcoma. Fifteen patients were evaluable. During the study period of 12 weeks, tumor responses were complete in two patients and partial in two patients (27% major response rate). Minimal responses were seen in two patients (40% overall response rate). An anti-HIV effect (reduction of serum p24 antigen by 70% or more) was observed in seven of ten evaluable patients who were initially antigenemic. CD4 lymphocyte counts remained unchanged. In six patients who had either a tumor response or a marked decline of HIV antigenemia, the treatment was continued between 12 and 59 weeks beyond the study period. Two of four patients with tumor regression at 12 weeks had an additional tumor response in this period despite prior dose reduction of interferon due to toxicity. Late progression of KS was eventually observed in four of six patients on prolonged treatment. The responsiveness of Kaposi's sarcoma seen in this study in patients with low CD4 counts and prior constitutional symptoms (fever, weight loss) was unexpected and needs further confirmation by larger patient groups. Dose-limiting toxicities were bone marrow depression (severe anemia in four and neutropenia with anemia in two patients), subjective adverse experiences (fever, fatigue, myalgia; four patients) and both (two patients).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Combined treatment with zidovudine and lymphoblast interferon-alpha in patients with HIV-related Kaposi's sarcoma. 190 99

A number of studies have illustrated the effectiveness of hematopoietic growth factors in managing treatment-related cytopenias in patients with human immunodeficiency virus (HIV) infection. One of these factors, granulocyte-macrophage colony-stimulating factor, has been shown to restore absolute neutrophil counts in patients with acquired immunodeficiency syndrome (AIDS) and Kaposi's sarcoma receiving a combination of zidovudine (AZT) and interferon alfa. A combination of granulocyte colony-stimulating factor and erythropoietin has also been demonstrated to alleviate both neutropenia and anemia in patients with advanced AIDS or AIDS-related complex receiving zidovudine. Hematopoietic growth factors, in combination with each other and with antiretroviral agents, thus have an important supportive role to play in the treatment of patients with HIV disease.
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PMID:Antiretroviral therapy and immunomodulators in patients with AIDS. 201 46

Three hematopoietic stimulants have been used in patients with HIV infection and a variety of AIDS-related complications. Both G-CSF and GM-CSF have demonstrated the ability to correct leukopenia related to HIV infection and ameliorate the drug-related myelosuppressive effects of zidovudine, trimethoprim/sulfamethoxazole, ganciclovir, and, in the case of GM-CSF, alpha-interferon, and cancer chemotherapies. Erythropoietin has been successfully used to ameliorate the anemia associated with HIV infection and zidovudine therapy. Treatment with these hematopoietic stimulants is very well tolerated with minimal toxicity. Of the granulocyte stimulants, G-CSF appears to induce fewer side effects than GM-CSF in trials conducted to date. Future trials demonstrating that the amelioration of hematopoietic suppression by the colony-stimulating factors results in increased clinical response rates and improved survival are necessary to fully assess the value of this approach in the care of HIV-infected patients.
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PMID:The use of hematopoietic hormones in HIV infection and AIDS-related malignancies. 202 93

The possible mechanisms of neutropenia associated with both human immunodeficiency virus (HIV) infection and drug treatment in adults are examined, and the current and investigational strategies for managing neutropenia are reviewed. Neutropenia associated with HIV arises from diverse mechanisms, including cellular immune dysfunction, direct effects on progenitor cells, humoral immune dysfunction, and vitamin deficiencies. Drug-induced neutropenia may be related to direct cytotoxic effects, immunologic mediators, and the effects of vitamin depletion on the bone marrow. Bone marrow toxicity in patients receiving zidovudine appears to be more frequent in those patients with advanced disease, low CD4 cell counts, a pretreatment anemia, low serum vitamin B12 levels, and low or low normal serum folic acid levels. Patients with AIDS also are at increased risk for adverse events associated with folate antagonists and sulfonamides compared with other patient populations. Lithium therapy has improved neutrophil counts in patients receiving zidovudine; however, the toxicities associated with use of lithium, combined with the lower dosages of zidovudine now recommended, may obviate its use. The use of colony-stimulating factors appears promising for increasing the number and function of circulating neutrophils. Although concomitant use of interferon alfa and zidovudine may result in a strong synergistic anti-HIV effect, dose-limiting neutropenia has been reported in patients receiving the combination. There are currently no controlled data assessing the effectiveness of intravenous immune globulin in the treatment of HIV-related or drug-related neutropenia. In evaluating neutropenia, the clinician must attempt to discern whether the neutropenia is more likely related to disease state(s) or drug therapies. Potential management strategies include modulation of the disease state, discontinuation or dose reduction of the offending agent, or administration of exogenous immune enhancer.
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PMID:Neutropenia in patients infected with human immunodeficiency virus. 203 44

A 31-year-old female developed severe aplastic anemia following acute non-A non-B hepatitis. Because of the impossibility of bone marrow transplantation, bolus methylprednisolone therapy was done. Soon after the therapy, pancytopenia improved. She has since taken mepitiostane and no longer needs blood transfusions. Good response to the immunosuppressive therapy suggests that the pathogenesis of this anemia is related to the immune system. In vitro culture demonstrated that the patient's serum contained a factor which suppressed hematopoietic activity, possibly gamma-interferon.
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PMID:Successful treatment of a patient with posthepatitic severe aplastic anemia with bolus methylprednisolone. 212 50

A 59 years old woman, born in Fukuoka Prefecture, was admitted to our hospital in Aug, 1988 because of diarrhea, fever and skin eruption. Physical examination revealed systemic lymphadenopathy and hepatosplenomegaly. The white blood cell count was 11,200/microliters with 28% atypical lymphocytes with convoluted nuclei. Mild anemia, thrombocytopenia and hypercalcemia were also observed. Antibody against the adult T-cell leukemia (ATL) associated antigen in serum was positive. OKT 4/8 ratio was high. A diagnosis of ATL was made. Because of the complications of pneumonia and herpes simplex, systemic chemotherapy was not given, and interferon (IFN)-alpha-2b was intramuscularly injected daily from Oct, 1988, resulting in the disappearance of atypical lymphocytes and improvement of skin lesions. The effect of IFN therapy lasted for three months, followed by increase of atypical lymphocytes. Although the patient became refractory to systemic IFN therapy, local injection of IFN into a buccal tumor infiltrated with atypical lymphocytes resulted in its regression of size. In spite of continued administration of IFN, the patient died of pneumonia in Jan, 1989.
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PMID:[Successful treatment of adult T-cell leukemia with interferon-alpha-2b by systemic and local administration]. 224 35

We have previously shown that the combination of 5-fluorouracil (5-FUra) and recombinant alpha-2a-interferon (rIFN-alpha-2a) produced objective responses in 23 of 32 (63%) previously untreated patients with advanced colorectal carcinoma. Because in vitro data suggest that rIFN-alpha-2a modulates the cytotoxic effects of 5FUra in a concentration-dependent manner, a phase I clinical trial was initiated to determine the maximum tolerated dose of rIFN-alpha 2a when administered in combination with 5FUra. A total of 27 patients with advanced colorectal carcinoma were enrolled. The median age was 64 years, and the median performance status was 1. A total of 18 patients had no prior chemotherapy and 19 no prior 5FUra. 5FUra was administered at 750 mg/m2/day by continuous i.v. infusion for 5 days, followed by weekly bolus therapy. rIFN-alpha 2a was administered at 6, 9, 12, 15, or 18 x 10(6) units s.c. beginning on day 1. The dose-limiting toxicity of this regimen was fatigue, resulting in a decrease in performance status, and this was the only toxicity that correlated with increasing dose of rIFN-alpha 2a. Eastern Cooperative Oncology Group grade 3-4 toxicities included leukopenia (6), thrombocytopenia (2), anemia (4), stomatitis (4), diarrhea (4), neurological (2), infection (2), and allergy (2). Three quarters of the patients required interruption of therapy or dose reductions of either 5FUra or rIFN-alpha 2a for toxicity. Among the patients with measurable disease who were previously untreated with 5FUra, 5 of 9 at the lowest dose levels achieved an objective response, including one pathological complete responder, whereas 0 of 9 at the three highest dose levels responded. Among patients previously treated with 5FUra, only 1 achieved an objective response. We conclude that the maximum tolerated dose of rIFN-alpha 2a, when administered with 5FUra as above, is 15-18 x 10(6) units; however, the efficacy of this regimen does not appear to be related to the dose intensity of rIFN-alpha 2a, and future regimens should employ a lower dose, intermittent schedule of rIFN-alpha 2a, which may be better tolerated.
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PMID:Phase I trial of 5-fluorouracil and recombinant alpha 2a-interferon in patients with advanced colorectal carcinoma. 231 95

The occurrence of autoimmune disease in patients receiving alpha-interferon (alpha-IFN) therapy has been reported in several studies; these include autoimmune thyroiditis, thrombocytopenia, anemia, exacerbation of psoriasis, and the occurrence of sarcoidosis. The primary mechanism presumably is the emergence of autoantibodies to various structural proteins or receptors. Two studies have recently shown that a significant percentage of patients treated with recombinant alpha-interferon (r alpha-IFN) do form autoantibodies. The authors report six additional cases of development or exacerbation of autoimmune phenomena in patients receiving alpha-IFN therapy. Five of these patients developed symmetric polyarthropathies and the sixth had thyroiditis. The presence of a history of underlying autoimmune disease or baseline serologic abnormalities in five of these patients, including the patient who developed thyroiditis, suggests that alpha-IFN treatment can lead to the exacerbation of an underlying subclinical autoimmune process.
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PMID:Exacerbation of symptoms of autoimmune disease in patients receiving alpha-interferon therapy. 234 7

We describe the clinical and laboratory features of 17 adult patients with a variant form of hairy cell leukemia (HCL-V) studied over the last 7 years. The main findings were: splenomegaly, moderate anemia, thrombocytopenia, and a raised white blood cell count (median 116 x 10(9)/L; range 15 to 482). The circulating lymphoid cells had abundant villous cytoplasm and a round, occasionally bilobed nucleus, with a prominent nucleolus. Monocytopenia, a feature of typical HCL, was not seen; neither was tartrate-resistant acid phosphatase demonstrated in eight cases tested. HCL-V cells had a mature B-cell phenotype: CD19+, CD20+, CD22+, FMC7+, CD11c+, CD10-, CD5-, with light chain isotope restriction in 15 cases. In contrast to typical hairy cells, HCL-V cells were negative with the monoclonal antibodies anti-HC2 and anti-TAC (CD25). Immunoglobulin (Ig) was not detected in two cases and IgG was expressed in the cell membrane of 73% of cases. Bone marrow histology was different from HCL, showing interstitial infiltration by cells clumped together and a moderate amount of reticulin, but the spleen showed the typical red pulp expansion of HCL. HCL-V patients did not respond to splenectomy (5 of 7) or alpha-interferon (7 of 7); 2 of 3 patients had a partial response to 2'deoxycoformycin. The clinical course was benign with 15 patients alive with a median survival greater than 4 years. We confirm that HCL-V is a distinct clinico-pathologic entity with intermediate features between HCL and B-prolymphocytic leukemia.
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PMID:A variant form of hairy cell leukemia resistant to alpha-interferon: clinical and phenotypic characteristics of 17 patients. 236 67

In a 59-year-old man with multiple myeloma (kappa-light chain paraproteinaemia) in stage IIIB, bone marrow infiltration with atypical plasma cells was reduced by five cytostatic treatment courses with vincristine, melphalan, cyclophosphamide and prednisone (VMCP protocol), but anaemia requiring blood transfusion persisted (haemoglobin concentration 5.3 g/dl). Even administration of interferon alpha-2b (5 million units s.c. every other day) failed to alter this. Only a combination of interferon and erythropoietin (150 U/kg i.v. every other day) achieved lasting regression of the anaemia (haemoglobin concentration up to 14 g/dl). In four other anaemic patients with multiple myeloma, stage III, treated according to the VMCP protocol but without additional interferon, erythropoietin did not improve erythropoiesis.
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PMID:[Erythropoietin in multiple myeloma]. 237 40


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