Summary
In 25 normal controls (Group I) and in 23 patients (Groups II and III) platelet malonyldialdehyde formation in the presence of N-ethyl maleimide (NEM) or thrombin was evaluated as an indicator of enhanced platelet function. 12 patients (Group III) with diabetes mellitus, nephrotic syndrome, or acute lymphatic leukemia in remission either exhibited spontaneous platelet aggregation (6/12), or enhanced platelet aggregation to minimal concentrations of ADP and Epinephrine (6/12). In these same Group III patients platelet malonyldialdehyde formation was markedly increased (p <0.0005) when compared to the values in the Group I normal controls. Studies in the 12 abnormal subjects later revealed normal aggregation patterns in 6/12 on follow-up evaluation. Concomitant estimation of platelet malonyldialdehyde at this time revealed a decrease into the normal range for platelet malonyldialdehyde values in the presence of thrombin in these 6 patients. Although significantly decreased from initial levels, (p <0.0005) malonyldialdehyde estimation in the presence of NEM was still slightly above the normal range. In 11 patients (Group II) both platelet aggregation tracings and malonyldialdehyde formation was normal and similar to values in the control population. Platelet malonyldialdehyde is a byproduct of the platelet endoperoxides which are intermediaries in the sequence of platelet prostaglandin synthesis. These results, therefore, suggest that part of the phenomenon of platelet hyperaggregability is intrinsic to the platelet and may involve platelet prostaglandin synthesis. The estimation of platelet malonyldialdehyde is a simple technique which appears to detect platelet hyperfunction.
