Mechanisms of response to treatment in autoimmune thrombocytopenic purpura

Article Abstract:

The authors explored the biological mechanisms of the increase in platelets which occur following treatment for autoimmune thrombocytopenia. [A platelets is a small segment of cell membrane derived from very large multinuclear cells of the bone marrow (megakaryocytes). Platelets are the smallest component of the blood and are and integral part of clot formation. In this disease, the number of platelets is drastically reduced and the normal clotting mechanism of the blood is affected. The cause of autoimmune thrombocytopenia is the patients' abnormal production of an antibody against their own platelets, resulting in the destruction of platelets. The authors studied the rate of production, survival times of platelets and the level of antibody against platelets (immunoglobulin) before and after treatment with a steroid, prednisone, or splenectomy (removal of the spleen) in 19 afflicted patients. Eleven of 12 patients (92 percent) responded to drug therapy with a 300 percent increase in platelet count; the survival rate of these platelets was unaffected. Following splenectomy, six of ten patients had an average four-fold increase in platelet count that correlated with increased platelet survival; platelet production was unchanged. Other measurements of platelet physiology were made concerning both the spleen and the liver. The authors conclude that prednisone improves platelet count primarily by increasing platelet production; splenectomy affects circulation platelet count by decreasing the rate of destruction and removal i.e., prolonging platelet survival. Base-line measurements of platelet turnover and platelet localization in the liver may also be helpful in predicting the response of these patients to either prednisone or splenectomy.

Analysis, Case studies, Prednisone, Physiology, Splenectomy, Radioactive tracers in physiology, Radioactive tracers

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Kinetic studies of the mechanism of thrombocytopenia in patients with human immunodeficiency virus infection

Article Abstract:

HIV-associated thrombocytopenia appears to result from reduced platelet production and not autoimmune destruction of platelets. Thrombocytopenia is a reduction in the number of blood platelets. Survival of radioactively-labelled platelets was compared among 24 patients with HIV-associated thrombocytopenia, 20 HIV patients with normal platelet counts and 12 healthy subjects. Of the 24 with thrombocytopenia, 16 were not treated and 8 took zidovudine, and of the 20 with no thrombocytopenia, 10 took nothing and 10 took zidovudine. Platelet survival was lowest among patients with thrombocytopenia, both the treated and non-treated. HIV patients with normal platelet counts also had significantly reduced platelet survival compared with healthy subjects. More importantly though, all HIV patients, even those with normal counts, had diminished platelet production. Among patients taking zidovudine, however, platelet production increased. HIV may directly infect the cells that develop into blood platelets.

Complications and side effects, HIV infection, HIV infections, Thrombocytopenia

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Immune thrombocytopenic purpura - the changing therapeutic landscape

Article Abstract:

The different treatment procedures used for treating immune thrombocytopenic purpura (ITP) in adults, a chronic disease in which a low platelet count often causes mucocutaneous bleeding, are discussed. Corticosteroids, intravenous globulin and [Rh.sub.0](D) immune globulin for patients who are Rh-positive, are some of the effective initial treatments and thrombopoietic agents have represented a promising new therapeutic strategy for ITP that is refractory to second- and third-time therapies.

United States, Health aspects, Causes of, Risk factors, Disease/Disorder overview

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