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Reduced Cortisol Metabolism during Critical Illness

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  • Eva Boonen
  • Hilke Vervenne
  • Philippe Meersseman
  • Ruth Andrew
  • Leen Mortier
  • Peter E. Declercq
  • Yoo-Mee Vanwijngaerden
  • Isabel Spriet
  • Pieter J. Wouters
  • Sarah Vander Perre
  • Lies Langouche
  • Ilse Vanhorebeek
  • Brian R. Walker
  • Greet Van den Berghe

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http://www.nejm.org/doi/full/10.1056/NEJMoa1214969
Original languageEnglish
Pages (from-to)1477-1488
Number of pages12
JournalNew England Journal of Medicine
Volume368
Issue number16
DOIs
Publication statusPublished - 18 Apr 2013

Abstract

BACKGROUND

Critical illness is often accompanied by hypercortisolemia, which has been attributed to stress-induced activation of the hypothalamic-pituitary-adrenal axis. However, low corticotropin levels have also been reported in critically ill patients, which may be due to reduced cortisol metabolism.

METHODS

In a total of 158 patients in the intensive care unit and 64 matched controls, we tested five aspects of cortisol metabolism: daily levels of corticotropin and cortisol; plasma cortisol clearance, metabolism, and production during infusion of deuterium-labeled steroid hormones as tracers; plasma clearance of 100 mg of hydrocortisone; levels of urinary cortisol metabolites; and levels of messenger RNA and protein in liver and adipose tissue, to assess major cortisol-metabolizing enzymes.

RESULTS

Total and free circulating cortisol levels were consistently higher in the patients than in controls, whereas corticotropin levels were lower (P

CONCLUSIONS

During critical illness, reduced cortisol breakdown, related to suppressed expression and activity of cortisol-metabolizing enzymes, contributed to hypercortisolemia and hence corticotropin suppression. The diagnostic and therapeutic implications for critically ill patients are unknown. (Funded by the Belgian Fund for Scientific Research and others; ClinicalTrials.gov numbers, NCT00512122 and NCT00115479; and Current Controlled Trials numbers, ISRCTN49433936, ISRCTN49306926, and ISRCTN08083905.)

    Research areas

  • BILE-ACIDS, HUMANS, ADRENOCORTICOTROPIN, BETA-HYDROXYSTEROID DEHYDROGENASE, ADRENAL AXIS, SEPTIC SHOCK, 11-BETA-HYDROXYSTEROID DEHYDROGENASE, ADIPOSE-TISSUE, IN-VIVO, APPARENT MINERALOCORTICOID EXCESS

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