ISSN No. 1606-7754                   Vol.14 No.1  April 2006

Platelet aggregation in diabetic Nigerians
GC Onyemelukwe1, AG Bakari1, EC Mba2
Department of Medicine1, Department of Haematology2, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria


The prevalence of macrovascular thrombosis among African diabetic patients has been shown to be lower than in Caucasians. Differences in platelet aggregation may be responsible for this observation. There has been no previous study of platelet aggregation among type-2 diabetic Nigerians. The aim of this study was to investigate platelet aggregation among diabetic Nigerian patients. Platelets from 34 diabetic patients (24 males, 10 females) and 35 control subjects were studied for aggregation in response to adenosine, ADP, and adrenaline. The intensity of the aggregation was categorized as excellent (>80%), moderate (30% - 79%), and poor (<30%). Diabetic and control subjects were of similar age, and had similar platelet counts and serum antithrombin III levels. Similarly, both diabetic patients and control subjects demonstrated lower platelet aggregation to collagen, ADP and adrenaline. However, while all control subjects exhibited spontaneous disaggregation with ADP, this was not seen in 14% of the diabetic patients (P<0.05). In diabetic Nigerians, although there is increased tendency to impaired platelet disaggregation, platelet hyper-aggregability is uncommon and this may be one of the reasons for the observed low incidence of large vessel disease, especially coronary artery disease, in our patients. ( Int J Diab Metab14: 33-37, 2006)

Key words: diabetes mellitus, platelet aggregation, large vessel disease, Nigerians


There are wide geographical and racial differences in the incidence of atherosclerosis and reports from Africa in the seventies1-4 demonstrated that it was rare. Williams5 had observed that Europeans living in Africa showed an eight-fold greater risk of pulmonary thromboembolism when compared with age- and sex-matched Africans. These differences were thought to be due to differences in the pattern of serum lipids and apolipoproteins, platelet reactivity and fibrinolytic activities. Dupuy and others6 compared healthy Europeans and Nigerians living in Zaria, Nigeria, while Bertrand7 and co-workers compared healthy Ivorians and Europeans living in Cote dí Ivoire. Both studies suggested that reduced incidence of thrombosis in Africans may be due to relative thrombocytopenia, rapid disaggregation of platelets after aggregation with ADP and reduced ristocetin-induced aggregation in black Africans when compared to Europeans. When flowing blood is exposed to subendothelial collagen after atherosclerotic rupture or deep arterial injury, platelets interact with collagen and adhere via adhesive glycoproteins such as fibronectin, Von-Willebrand factor, and thrombospondin. Platelets are activated to release adenosine diphosphate (ADP) and thromboxane A2 and through complex reactions in which coagulation factors and platelets are recruited and aggregated. These events have led to the in vitro use of collagen, ristocetin, adrenaline and ADP in testing platelet aggregation. No previous study of platelet aggregation has been carried out in Nigerian diabetic patients.

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