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Platelet function, factor VIII, fibrinogen, and fibrinolysis in Nigerians and Europeans in relation to atheroma and thrombosis
  1. Evelyne Dupuy,
  2. A. F. Fleming1,
  3. J. P. Caen
  1. Department of Haemostasis and Experimental Thrombosis, Hôpital Lariboisière, 2, rue Ambroise Paré, 75475 PARIS CEDEX 10, France
  2. Department of Haematology, Ahamdu Bello University, Zaria, Nigeria

    Abstract

    Platelet function, factor VIII, fibrinogen levels, and fibrinolysis were studied in Europeans and in two groups of Nigerians living in Zaria, northern Nigeria, in order to see whether differences could help to explain the low incidence of atheroma and thrombosis in Nigerians. We confirmed the relative thrombocytopenia and observed a rapid disaggregation after ADP-induced platelet aggregation in Nigerians. The most striking difference was a reduced or absent ristocetin-induced platelet aggregation in Nigerian platelet-rich plasma, probably due to a plasma component interacting with the von Willebrand activity (VWF), since factor VIII coagulant activity, factor VIII related antigen, and isolated VWF were normal or high by European standards. Group II (rural population), but not group I (senior university staff in Zaria) of the Nigerians, tended to have high serum fibrinogen concentrations. Spontaneous fibrinolytic activity was enhanced in most Nigerians compared to the Europeans and was normally increased after venostasis in proportion to the initial activity. Fibrinolysis and ristocetin-induced platelet aggregation values for the Nigerians in group I were intermediate between European and Nigerian in the group II values, suggesting that differences were due more to environmental than to genetic factors.

    Relative thrombocytopenia, disaggregation after ADP-induced aggregation, inhibition of ristocetin-induced platelet aggregation, and active fibrinolysis help to explain the infrequency of thrombotic disease in Africans. Also the low incidence of atheroma may follow from less platelet adherence and less platelet release of mitogenic factors, which cause intimal hyperplasia.

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