Dexamethasone effect on prostanoid formation in healthy man

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Abstract
Dexamethasone was administered to 6 healthy female volunteers for 4 d, resulting in plasma levels of 4.8 .+-. 1.4 .times. 10-8 mol/l. Urinary excretions of 6 prostanoids as well as colagen-induced platelet thromboxane formation and aggregation were determined before, during and 1 mo. after administration of dexamethasone. Dexamethasone had no effect on urinary thromboxane B2 (77 .+-. 22 ng/d vs. 63 .+-. 16 ng/d during dexamethasone), dinor-thromboxane B2, the major urinary metabolite of thromboxane B2 (406 .+-. 84 ng/d vs. 380 .+-. 90 ng/d), dinor-6-keto-prostaglandin F1.alpha., the major urinary metabolite of prostacyclin (199 .+-. 41 ng/d vs. 237 .+-. 53 ng/d), tetranor-5,11-diketo-7.alpha.-hydroxy-prostane-1,16-diolic acid, the major urinary metabolite of prostaglandins E1 and E2 (7712 .+-. 1677 ng/d vs. 7886 .+-. 2565 ng/d) 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. (14394 .+-. 2053 ng/d vs. 18288 .+-. 2251 ng/d). Prostaglandin E2 excretion slightly but significantly increased from 217 .+-. 48 ng/d to 294 .+-. 55 ng/d. Collagen-induced platelet thromboxane formation and aggregation were not altered. Glucocorticoids apparently do not regulate renal, platelet or total body prostanoid formation in healthy man.