Patients with sickle cell disease have increased tendency to develop vaso-occlusive crisis. Although red blood cell sickling is the primary initiating event, extension of the vaso-occlusive process can occur as a result of other factors. Evidence is accumulating that platelets may have some role in vasoocclusive process. For example, increased circulating platelet aggregates (1), Pthromboglobulin (2) and shortened platelet survival (3) have been demonstrated during acute vaso-occlusion. However, decreased platelet aggregation (4) has been shown in patients with sickle cell disease, attributed to a state of exhaustion. Certain arachidonic acid metabolites mainly platelet-derived thromboxane Az (TXA,) and vessel wall-derived prostacyclin (PGIJ may be important in maintaining platelet homeostasis. An increase in TXA2 (vaso-constrictor and pro-aggregant) and/or a decrease in PG12 (vaso-dilator and antiaggregant) may cause platelet activation and formation of thrombus. The goal of this study was to measure plasma concentrations of TXAz and PGI, metabolites to detect if an abnormality of these prostaglandins occurs in sickle cell disease. Platelet TXA2 generation in vitro was also qualified to determine a primary platelet hyperactivity.