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Exp Clin Endocrinol Diabetes. 1999;107(8):539-46.

Cortisol metabolism in the postoperative period after cardiac surgery.

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Institute of Clinical Chemistry, Klinikum Grosshadern, Ludwig-Maximilians-University Munich, Germany.


Relative 11beta-hydroxysteroid dehydrogenase deficiency has been shown previously to arise from endogenous hypercortisolism in diseases of the hypothalamic/pituitary/adrenocortical system; whether stress induced hypercortisolism may also result in substrate overload of 11beta-hydroxysteroid dehydrogenase has not yet been studied. We therefore studied the characteristics of cortisol metabolisation during the postoperative period of cardiac surgery, representing a well standardized surgical procedure. In a prospective, observational, consecutive case study, 14 patients undergoing cardiac surgery were investigated. During the first two days after cardiac surgery urine was collected from the patients during two 10 hour overnight periods (8 p.m. (day of surgery) until 6 a.m., and during the following night). Using capillary gas-chromatography, main urinary cortisol metabolites were quantified (tetrahydrocortisone, tetrahydrocortisol, allo-tetrahydrocortisol, cortolones, cortols as sum of cortisol metabolites (CM)). Free urinary cortisol (FUC) was determined by an automated immunoassay after extraction. The ratio of cortisol metabolites (tetrahydrocortisol, allo-tetrahydrocortisol, cortols) to cortisone metabolites (tetrahydrocortisone, cortolones) was calculated to characterize the overall activity of 11beta-hydroxysteroid dehydrogenase, an enzyme system catalyzing the conversion of cortisol to inactive cortisone (CMR, cortisol metabolisation ratio). Total cortisol metabolisation (including hepatic ring A-reduction and conjugation) was estimated by a cortisol turnover quotient (CM/FUC). In all urinary samples the ratio of cortisol to cortisone metabolites was markedly elevated compared to controls (patients: median 1.9, interquartile range 1.5-2.4, absolute range 1.0-3.2; controls: median 0.45, interquartile range 0.36-0.52); this ratio was positively correlated to FUC (r2 = 0.30; p = 0.003). The cortisol turnover quotient was markedly reduced (patients: median 38.0, interquartile range 20.0-103.9, absolute range 8.3-211.9; controls: median 259, interquartile range 176-415) and inversely correlated to FUC (r2 = 0.64, p < 0.001). It is concluded that major surgical trauma results in a marked relative reduction of cortisol inactivation probably consequent to substrate overload of the metabolizing enzymes; as the activity of these enzymes (mainly 11beta-hydroxysteroid dehydrogenase) is crucial for the modulation of cortisol receptor access, tissue corticoid sensitivity in the postoperative period may vary substantially from physiological conditions.

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