Until recently, interest in the role of platelets in inflamma-tory bowel disease (IBD) was confined to an awareness of thrombocytosis as a marker of disease activity,'and as a possible predisposing factor to systemic thromboembolism. Two recent conceptual advances suggest that platelets may contribute to the pathogenesis of IBD at the mucosal level. Firstly, it is now recognised that platelets themselves participate in the inflammatory response by acting as a potent source of inflammatory mediators and modulating the activity of other inflammatory cells. 2 Secondly, multifocal microinfarction in the mesenteric vasculature has been proposed as an early event in the pathogenesis of Crohn's disease3; this hypothesis has drawn attention again to earlier speculation about a vascular origin for ulcerative colitis. 4 5 We discuss here the evidence for a pathogenic role for platelets in IBD, and possible therapeutic implications of this.

Platelets as inflammatory celis Platelets are capable of directly eliciting an inflammatory response. Injection of extracts of platelets into the skin of healthy volunteers produces a strong inflammatory reaction-rubor, dolor, calor, and turgor-which persists for several hours. 6 Extracts of neutrophils and basophils fail to produce this reaction and eosinophils give only an early histamine-like response. Over the last two decades, the proinflammatory properties of platelets have gradually been elucidated2; those which may be important in IBD are described.