This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints, Permissions and Rights Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by MACKENZIE, M. A. Articles by KLOPPENBORG, P. W. C. Search for Related Content PubMed PubMed Citation Articles by MACKENZIE, M. A. Articles by KLOPPENBORG, P. W. C.

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.

This article has been cited by other articles:

				I. S. K. Harahap, N. Sasaki, Gunadi, S. Yusoff, M. J. Lee, S. Morikawa, N. Nishimura, T. Sasaki, S. Usuki, M. Hirai, et al. Herbal Medicine Containing Licorice May Be Contraindicated for a Patient With an HSD11B2 Mutation Evid. Based Complement. Altern. Med., December 9, 2009; (2009) nep211v1. [Abstract] [Full Text] [PDF]

				R T Netea-Maier, E J van Lindert, M den Heijer, A van der Eerden, G F F M Pieters, C G J Sweep, J A Grotenhuis, and A R M M Hermus Transsphenoidal pituitary surgery via the endoscopic technique: results in 35 consecutive patients with Cushing's disease. Eur. J. Endocrinol., May 1, 2006; 154(5): 675 - 684. [Abstract] [Full Text] [PDF]

				M. Boscaro, L. Barzon, and N. Sonino The Diagnosis of Cushing's Syndrome: Atypical Presentations and Laboratory Shortcomings Arch Intern Med, November 13, 2000; 160(20): 3045 - 3053. [Abstract] [Full Text] [PDF]

				M. B. Feinstein and R. P. Schleimer Regulation of the Action of Hydrocortisone in Airway Epithelial Cells by 11beta -Hydroxysteroid Dehydrogenase Am. J. Respir. Cell Mol. Biol., September 1, 1999; 21(3): 403 - 408. [Abstract] [Full Text]

				S. H.M. van Uum, A. R.M.M. Hermus, P. Smits, T. Thien, and J. W.M. Lenders The role of 11{beta}-hydroxysteroid dehydrogenase in the pathogenesis of hypertension Cardiovasc Res, April 1, 1998; 38(1): 16 - 24. [Abstract] [Full Text] [PDF]

				P. C. White, T. Mune, and A. K. Agarwal 11{beta}-Hydroxysteroid Dehydrogenase and the Syndrome of Apparent Mineralocorticoid Excess Endocr. Rev., February 1, 1997; 18(1): 135 - 156. [Abstract] [Full Text]