Dexamethasone effect on prostanoid formation in healthy man

1. Dexamethasone was administered to six healthy female volunteers for 4 days, resulting in plasma levels of 4.8 +/- 1.4 x 10(-8) mol/l. Urinary excretions of six prostanoids as well as collagen-induced platelet thromboxane formation and aggregation were determined before, during and 1 month after administration of dexamethasone. 2. Dexamethasone had no effect on urinary thromboxane B2 (77 +/- 22 ng/day vs 63 +/- 16 ng/day during dexamethasone), dinor-thromboxane B2, the major urinary metabolite of thromboxane B2 (406 +/- 84 ng/day vs 380 +/- 90 ng/day), dinor-6-keto-prostaglandin F1 alpha, the major urinary metabolite of prostacyclin (199 +/- 41 ng/day vs 237 +/- 53 ng/day), tetranor-5,11-diketo-7 alpha-hydroxy-prostane-1,16-dioic acid, the major urinary metabolite of prostaglandins E1 and E2 (7712 +/- 1677 ng/day vs 7886 +/- 2565 ng/day) and tetranor-11-keto-5 alpha,7 alpha-dihydroxy-prostane- 1,16-dioic acid, the major urinary metabolite of prostaglandins F1 alpha and F2 alpha (14,394 +/- 2053 ng/day vs 18,288 +/- 2251 ng/day). Prostaglandin E2 excretion slightly but significantly increased from 217 +/- 48 ng/day to 294 +/- 55 ng/day. Collagen-induced platelet thromboxane formation and aggregation were not altered. 3. These results suggest that glucocorticoids do not regulate renal, platelet or total body prostanoid formation in healthy man.