[Clinical and laboratory aspects of the Aspirin-like defect as hereditary thrombocytopathy].

UNLABELLED The Aspirin-like defect (ALD) is caused by defects in the intraplatelet arachidonic acid (AA)-metabolism. We here present the characteristics of a larger cohort in a single centre. PATIENTS, METHODS Based on 17 ALD index patients bleeding symptoms, agonist-induced platelet aggregation and closure times in the PFA-100 test were analysed in a family cohort of altogether 52 individuals from 17 families. Absent aggregation to AA (maximal aggregation or=1 bleeding symptoms. CONCLUSION In case of a bleeding tendency diagnostic procedures should rule out primary haemostatic defects. Hereditary platelet function defects including ALD are an important differential diagnosis. Family studies are reasonable.