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The Influence of Glycyrrhetinic Acid on Plasma Cortisol and Cortisone in Healthy Young Volunteers

Department of Medicine, Division of Endocrinology (M.A.M., P.W.C.K.) Nijmegen, The Netherlands
The Departments of Geriatric Medicine (W.H.L.H., R. W.M.M.J.) and Experimental and Chemical Endocrinology (T.J.B.), University Hospital Nijmegen, The Netherlands

Address all correspondence and requests for reprints to: M. A MacKenzie, M.D., Department of Medicine, Division of Endocrinology, University Hospital, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands.

Based on studies in laboratory animals and on measurements of the urinary metabolites (allo)tetrahydrocortisol and tetrahydrocortisone in human volunteers it has been claimed that liquorice-induced mineralocorticoid excess is caused by a unique defect in the conversion of cortisol to cortisone. To further evaluate this hypothesis we have investigated the influence of glycyrrhetinic acid (GA), the mineralocorticoid-active constituent of liquorice, on plasma cortisol and cortisone in 10 healthy young normotensive volunteers.

Pure GA (500 mg/day), administered orally from days 3-10 of the study, exerted pronounced mineralocorticoid activity. Ingestion of GA resulted in an elevated urinary excretion of free cortisol and virtually unchanged plasma cortisol levels in the presence of markedly decreased levels of both plasma cortisone and urinary free cortisone.

These results provide direct clinical support for the hypothesis that GA induces an inhibition of the activity of 11β-dehydrogenase, resulting in a blockade in the conversion of cortisol to cortisone.

Received November 21, 1989.

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