• J E Price, P S Klimiuk, and M I Jayson.
• Rheumatic Diseases Centre, University of Manchester, Hope Hospital, Salford.
• Ann. Rheum. Dis. 1991 Aug 1; 50 (8): 567-71.

AbstractSystemic sclerosis is characterised by vascular endothelial damage. Platelets adhering to the exposed subendothelium may contribute to the inflammatory changes found in the vessel wall. Increased in vitro platelet aggregability in systemic sclerosis has been reported. In vitro platelet aggregation of platelet rich plasma obtained from patients with systemic sclerosis (CREST (calcinosis, Raynaud's phenomenon oesophageal dysmotility, sclerodactyly, telangiectasia) variant) and from controls matched for age and sex was compared. Collagen, ADP, and platelet activating factor were used as aggregating agents. The actions of a platelet activating factor antagonist, BN52063, were also examined. Each agonist caused dose dependent platelet aggregation; there was no difference in either rate of primary aggregation or maximum percentage aggregation between platelets derived from patients with systemic sclerosis and from the control group (analysis of variance). BN52063 was shown to be a dose dependent, competitive antagonist of platelet aggregation induced by platelet activating factor; there was no difference in its action on platelets derived from patients with systemic sclerosis or controls. These results do not support the hypothesis that platelets from patients with systemic sclerosis are hyperactive and may explain the disappointing results obtained with antiplatelet drugs in systemic sclerosis.

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