Platelet functional defects in thrombocytopenic purpura.

With the technical assistance of \Iiss MAuIIEEN JENNER T HERE IS now considerable evidence to suggest that the hemorrhagic manifestations of thrombocytopenic purpura and certain other disorders are probably due largely to deranged platelet function rather than to a reduction in platelet numbers. It is, of course, true that associated vascular changes also play an important role in thrombocytopenic purpura. Wald and McAuley,’ St-efanini et al.,2 Cronkite et al.3 and Hirsch and Dameshek4 have all demonstrated a dissociation between platelet numbers and the consumption of prothrombin. Wald and McAuley’ showed that a rapid improvement in prothrombin consumption occurred without a coincidental rise in platelet numbers immedi-