Platelet production and platelet survival in polycythaemia vera with special reference to the spleen size.
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Biomedical subjects
Publications and source records attributed to J Kutti.
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Four adults, recently diagnosed, acute leukemic patients received 40 separate platelet transfusion treatments before, during, and after intravenous administration of amphotericin B. Fourteen of these platelet transfusions were administered while the patients also received amphotericin B; 26 platelet transfusions were given before or after amphotericin B therapy. The mean platelet increment for platelet transfusions administered while the patients were untreated with amphotericin B was 58 +/- 6 per cent. While the same patients were being treated with amphotericin B, the mean platelet increment was significantly decreased to 29 +/- 8 per cent (t = 3.1; p less than 0.005). In addition, when the patients were not being given amphotericin B, a highly significant negative relationship (r = -0.77; p less than 0.001) between the values for bleeding time and venous platelet count was present. In contrast, during amphotericin B treatment there was no correlation between the patients' bleeding times and venous platelet counts. We propose that amphotericin B therapy has a direct toxic effect on the function and circulation of transfused platelets. These toxic effects are quickly corrected by discontinuing this antifungal antibiotic.
Nineteen recently diagnosed patients with acute leukemias received prophylactic platelet transfusions when thrombocytopenic. Platelet concentrates were always transfused within eight hours of collection. The result of each transfusion was carefully monitored for the posttransfusion platelet increment. One patient died four days after admission to the present study. Seven patients died 1 to 14 months after the institution of antileukemic chemotherapy. Four patients received marrow transplants 1 to 2 months after starting chemotherapy and, therefore, were longer evaluated in this study. One patient was lost to follow-up after seven months of observation. The remaining six patients are alive and have been followed for 9 to 18 months. During the period of observation, none of the patients developed any evidence of refractoriness to platelet transfusion therapy. Although this series does not permit any firm conclusions to be made, it appears that the magnitude of the problem of alloimmunization to platelet transfusion therapy may be overemphasized.
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Chronic idiopathic thrombocytopenic purpura (ITP) is a consequence of rapid platelet destruction caused by circulating platelet antibodies. In this study we compared three methods for detecting serum platelet antibodies in a population of 65 patients with chronic ITP. In two of the techniques intact platelets were used as the antibody target, i.e. the whole platelet ELISA and the flow cytometric assay; in the third an antigen-specific modified antigen capture ELISA (MACE) was employed. By using the whole platelet ELISA and the flow cytometric assay 35% and 45% of the patients, respectively, displayed an antiplatelet antibody. In most cases (26 or 29 patients) IgG was the predominant antiplatelet immunoglobulin. As analysed using the MACE-technique glycoprotein (GP) Ib/IX-specific antibodies occurred with the same frequency as antibodies specific for GPIIb/IIIa. Moreover, there was a poor correlation between the MACE results on the one hand and results from the intact platelet-based techniques on the other, i.e. several patients were positive in one assay whereas they were negative in the other. We conclude that all three techniques have their merits and demerits; it appears reasonable that they should be used together in the evaluation of the autoimmune process of chronic ITP.
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