Transient non-thrombocytopenic purpura in hookworm infestation.

The transient purpura in 3 young men with marked eosinophilia and hookworm infestation was found to be caused by a qualitative platelet defect which manifested as a failure of platelets to aggregate with collagen and an absence of the secondary phase aggregation with epinephrine. These aggregation abnormalities could not be normalized with normal plasma, nor did patient plasma inhibit normal platelets, implying that the dysfunction was not caused by an abnormality in the plasma but was an intrinsic platelet defect. Arachidonic acid induced enhanced aggregation and a mutual correction of the absent secondary epinephrine-induced aggregation was observed when patient and aspirin-treated platelets were mixed together, suggesting that the defect was unlikely to be related to the platelet prostaglandin synthesis pathway. We propose that the acquired platelet dysfunction was caused by impaired ADP release due possibly to a transient platelet storage pool abnormality.