Wu et al. (1981) studied a 3-generation family in which many members had a bleeding disorder due to a primary release defect of platelets. The hereditary defect resembles the acquired one produced by aspirin. Patients were all females ... Wu et al. (1981) studied a 3-generation family in which many members had a bleeding disorder due to a primary release defect of platelets. The hereditary defect resembles the acquired one produced by aspirin. Patients were all females with easy bruising, recurrent epistaxes, and hypermenorrhea; no male-to-male transmission was observed. Wu et al. (1980) found low platelet membrane sialyltransferase activity both basally and in response to stimulation by collagen or sodium arachidonate. This appeared to be the first reported instance of a primary defect in the platelet release reaction. The authors postulated either reduced thromboxane A2 production because of thromboxane synthetase deficiency (614158) or a platelet membrane abnormality that rendered platelets unresponsive to thromboxane A2. (see 601399).