To examine the possibility that prostaglandin metabolism is pathophysiologically important in Raynaud's phenomenon, peripheral venous 6-keto prostaglandin Fla (6-keto PGF1α) and thromboxane B2 (TXB2) concentrations were measured in 45 patients with severe Raynaud's phenomenon. Patients with Raynaud's phenomenon had a significantly higher plasma concentration of 6-keto PGF1α compared to controls (p < .001), although their plasma TXB2 concentration was not statistically different from control patients. Subgroup analysis revealed that only patients with progressive systemic sclerosis (PSS) had an elevated plasma 6-keto PGF1α concentration. To gauge the functional significance of the 6-keto PGF1α elevations, seven patients with Raynaud's phenomenon were chronically administered indomethacin (50 mg P.O. b.i.d.); six of the seven patients noted no improvement in their Raynaud's phenomenon. Three of the patients developed pedal edema shortly after starting indomethacin. This study suggests that the increased plasma 6-keto PGF1α concentration in Raynaud's phenomenon may be due to a compensatory release of prostacyclin and that the pathophysiologic defect does not involve the thromboxane mechanism.
All Science Journal Classification (ASJC) codes