In-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria
To investigate in vivo platelet function in acute falciparum malaria plasma concentrations of βthromboglobulin (βTG), platelet factor 4 (PF4) and thrombospondin (TSP) were determined in 10 severely-ill Thai patients and 11 healthy volunteers. 8 patients recovered. At presentation, the platelet count...
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th-mahidol.224992018-08-10T15:49:49Z In-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria W. Supanaranond T. M.E. Davis J. Dawes K. Silamut N. Vilaiwanna N. J. White Mahidol University John Radcliffe Hospital Heart Research Institute Australia Paholpolpayuhasena Hospital Medicine To investigate in vivo platelet function in acute falciparum malaria plasma concentrations of βthromboglobulin (βTG), platelet factor 4 (PF4) and thrombospondin (TSP) were determined in 10 severely-ill Thai patients and 11 healthy volunteers. 8 patients recovered. At presentation, the platelet counts of the 10 patients were significantly lower (p < 0.025) than those of the controls, and a slight but significant increase (p < 0.05) in βTG/PF4 ratios in the patients suggested low-grade platelet activation. Presentation plasma βTG and PF4 concentrations did not differ from control values, probably due to the opposing effects of decreased circulating platelet mass and increased activation. By contrast, admission concentrations of TSP in the surviving patients were markedly lower (p < 0.001) than those of the controls; βTG/PF4 ratios, but not TSP levels, returned to normal during treatment. Hepatic dysfunction and oliguric renal failure probably contributed to a sustained increase in plasma β - TG and TSP in the 2 fatally ill patients, but associated elevated PF4 levels indicated concomitant platelet activation. Our results support the suggestion that in vivo platelet activation, which appears to be rapidly controlled by treatment, occurs in patients with severe, non-fatal falciparum malaria. TSP production, apparently from non-platelet sources, was decreased and/or its consumption was increased in these patients, perhaps by factors such as cytoadherence of infected erythrocytes and consequent endothelial damage. © 1992 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted. 2018-08-10T08:49:49Z 2018-08-10T08:49:49Z 1992-01-01 Article Platelets. Vol.3, No.4 (1992), 195-200 10.3109/09537109209013183 09537104 2-s2.0-0026459765 https://repository.li.mahidol.ac.th/handle/123456789/22499 Mahidol University SCOPUS https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0026459765&origin=inward |
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Medicine W. Supanaranond T. M.E. Davis J. Dawes K. Silamut N. Vilaiwanna N. J. White In-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria |
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To investigate in vivo platelet function in acute falciparum malaria plasma concentrations of βthromboglobulin (βTG), platelet factor 4 (PF4) and thrombospondin (TSP) were determined in 10 severely-ill Thai patients and 11 healthy volunteers. 8 patients recovered. At presentation, the platelet counts of the 10 patients were significantly lower (p < 0.025) than those of the controls, and a slight but significant increase (p < 0.05) in βTG/PF4 ratios in the patients suggested low-grade platelet activation. Presentation plasma βTG and PF4 concentrations did not differ from control values, probably due to the opposing effects of decreased circulating platelet mass and increased activation. By contrast, admission concentrations of TSP in the surviving patients were markedly lower (p < 0.001) than those of the controls; βTG/PF4 ratios, but not TSP levels, returned to normal during treatment. Hepatic dysfunction and oliguric renal failure probably contributed to a sustained increase in plasma β - TG and TSP in the 2 fatally ill patients, but associated elevated PF4 levels indicated concomitant platelet activation. Our results support the suggestion that in vivo platelet activation, which appears to be rapidly controlled by treatment, occurs in patients with severe, non-fatal falciparum malaria. TSP production, apparently from non-platelet sources, was decreased and/or its consumption was increased in these patients, perhaps by factors such as cytoadherence of infected erythrocytes and consequent endothelial damage. © 1992 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted. |
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Mahidol University W. Supanaranond T. M.E. Davis J. Dawes K. Silamut N. Vilaiwanna N. J. White |
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Article |
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W. Supanaranond T. M.E. Davis J. Dawes K. Silamut N. Vilaiwanna N. J. White |
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W. Supanaranond |
title |
In-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria |
title_short |
In-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria |
title_full |
In-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria |
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In-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria |
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In-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria |
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in-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria |
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2018 |
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https://repository.li.mahidol.ac.th/handle/123456789/22499 |
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1763495841621868544 |