Platelet Dysfunction — Differentiation of a Newly Recognized Primary Type from That Produced by Aspirin

A recently described hemorrhagic disorder characterized by defective platelet aggregation induced by collagen and epinephrine appears to be caused, in part, by the same abnormality induced by aspirin ingestion — that is, inhibition of release of intrinsic platelet adenosine diphosphate (ADP). In contrast to the aspirin-induced defect, bleeding time was greatly prolonged, platelet adhesiveness was markedly impaired, adhesion of platelets to collagen fibrils was deficient, and aggregation of platelets by serotonin and glass beads was impaired. Both phases of epinephrine-induced platelet aggregation were blocked, whereas with aspirin only the second phase was absent. There was rapid disaggregation after low-molar ADP whereas with aspirin the rate was only slightly increased. As with the aspirin-induced platelet abnormality aggregation of platelets by trypsin, collagen and centrifugation was blocked, but aggregation by high-molar ADP and thrombin was normal. Platelet transfusions temporarily corrected most of the defects.