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Submitted on September 20, 2005
Accepted on July 19, 2006
Department of Intensive Care Medicine, Catholic University of Leuven, Leuven, Belgium (I.V., S.V.P., P.J.W., G.V.d.B.), Department of Internal Medicine, Erasmus University Medical Center, Rotterdam, The Netherlands (R.P.P.), Laboratory for Experimental Medicine and Endocrinology, Catholic University of Leuven, Leuven, Belgium (I.J., R.B.), Department of Clinical Biochemistry, Statens Serum Institut, Copenhagen, Denmark (K.S.), NANEA, Department of Epidemiology and Social Medicine, Aarhus University, Aarhus, Denmark (K.S.), and Immunoendocrine Research Unit, Medical Department M, Aarhus University Hospital, Aarhus, Denmark (T.K.H.)
* To whom correspondence should be addressed. E-mail: greta.vandenberghe{at}med.kuleuven.be.
Context: Both excessive and insufficient activation of the hypothalamic-pituitary-adrenal axis in response to critical illness are associated with increased mortality.
Objective: To study the effect of intensive insulin therapy, recently shown to reduce mortality and morbidity of critically ill patients, on the cortisol response to critical illness.
Design: Pre-planned subanalysis of a large randomized controlled study measuring serum total cortisol, cortisol-binding globulin (CBG) and albumin, and calculating free cortisol levels.
Setting: University hospital surgical intensive care unit.
Patients: 451 critically ill patients dependent on intensive care for more than 5 days and 45 control subjects matched for gender, age, height and weight.
Intervention: Strict blood glucose control to normoglycemia with insulin.
Results: Total and calculated free cortisol levels were equally elevated upon admission in both patient groups, and thereafter were lower in intensive insulin-treated patients. Lower cortisol levels statistically related to the outcome benefit of intensive insulin therapy. CBG levels and structure were affected by critical illness, but not by insulin therapy, neither were albumin levels. Administration of hydrocortisone in so-called "replacement dose" resulted in several fold higher total and free cortisol levels, indicating that re-evaluation of the doses used is warranted.
Conclusion: Lower serum cortisol levels in critically ill patients receiving intensive insulin therapy statistically related to improved outcome with this intervention. The lower cortisol levels were not related to altered cortisol-binding capacity.
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