Exp Clin Endocrinol Diabetes 1998; 106(5): 410-414
DOI: 10.1055/s-0029-1212007
Original

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Quantification of cortisol inactivation in cirrhosis of the liver

M. Vogeser1 , G. Fischer2 , K. Jacob1
  • 1Institute of Clinical Chemistry, Klinikum Großhadern, Ludwig-Maximilians-Universität Munich, Germany
  • 2Department of Internal Medicine II, Klinikum Großhadern, Ludwig-Maximilians-Universität Munich, Germany
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Publikationsverlauf

Publikationsdatum:
14. Juli 2009 (online)

Summary

Impaired cortisol inactivation in patients with cirrhosis of the liver has been described, but precise data are limited and the pathophysiological significance of this finding has to be elucidated. Therefore, we assessed the main urinary cortisol metabolites using capillary gas chromatography and urinary free cortisol using an enzyme immunoassay in 20 consecutive patients with cirrhosis of the liver and in 28 healthy controls; ratios of cortisol inactivation were calculated (cortisol metabolites/cortisone metabolites, and sum of tetrahydrogenated cortisol metabolites/free urinary cortisol). In patients with cirrhosis free urinary cortisol was normal, whereas the sum of cortisol metabolites was significantly reduced; therefore, cortisol synthesis seems to be adequately adapted to the decreased hepatic inactivation (conjugation, ring A-reduction). A significantly reduced ratio of cortisol metabolites to cortisone metabolites indicating impaired renal 11 β-hydroxysteroid dehydrogenase activity was only found in a subgroup of patients with as-cites.