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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Main Authors: W. Supanaranond, T. M.E. Davis, J. Dawes, K. Silamut, N. Vilaiwanna, N. J. White
Other Authors: Mahidol University
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Published: 2018
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Online Access:https://repository.li.mahidol.ac.th/handle/123456789/22499
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spelling 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
institution Mahidol University
building Mahidol University Library
continent Asia
country Thailand
Thailand
content_provider Mahidol University Library
collection Mahidol University Institutional Repository
topic Medicine
spellingShingle 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
description 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.
author2 Mahidol University
author_facet Mahidol University
W. Supanaranond
T. M.E. Davis
J. Dawes
K. Silamut
N. Vilaiwanna
N. J. White
format Article
author W. Supanaranond
T. M.E. Davis
J. Dawes
K. Silamut
N. Vilaiwanna
N. J. White
author_sort 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
title_fullStr In-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria
title_full_unstemmed In-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria
title_sort in-vivo platelet activation and anomalous thrombospondin levels in severe falciparum malaria
publishDate 2018
url https://repository.li.mahidol.ac.th/handle/123456789/22499
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