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Reduced nocturnal ACTH-driven cortisol secretion during critical illness
Eva Boonen1, Philippe Meersseman, Hilke Vervenne
1Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, and.
American Journal of Physiology. Endocrinology and Metabolism
|February 27, 2014
Summary
Critically ill patients exhibit reduced pulsatile secretion of adrenocorticotropic hormone (ACTH) and cortisol, despite higher overall cortisol levels. This suggests non-ACTH-driven mechanisms contribute to critical illness hypercortisolism.
Area of Science:
- Endocrinology
- Critical Care Medicine
- Physiology
Background:
- Reduced cortisol metabolism is observed in critical illness.
- This may lead to suppressed adrenocorticotropic hormone (ACTH) and cortisol secretion via feedback inhibition.
Purpose of the Study:
- To investigate the hypothesis that reduced cortisol breakdown suppresses pulsatile ACTH and cortisol secretion.
- To analyze nocturnal secretory profiles of ACTH and cortisol in critically ill patients versus healthy controls.
Main Methods:
- Deconvolution analysis of plasma concentration time series for ACTH and cortisol.
- Nocturnal blood sampling (2100–0600) every 10 min in 40 patients and 8 controls.
- Calculation of approximate entropy, cross-approximate entropy, and dose-response relationships.
Main Results:
- Critically ill patients had higher total and free plasma cortisol but suppressed pulsatile cortisol secretion (54% lower) and pulsatile ACTH secretion (31% lower).
- Reduced burst mass, not pulse frequency, explained the suppressed pulsatile secretion for both hormones.
- Increased ACTH and cortisol irregularity and asynchrony were observed in patients, with normal ACTH-cortisol dose-response.
Conclusions:
- Critical illness hypercortisolism is associated with suppressed pulsatile ACTH and cortisol secretion.
- Increased irregularity and asynchrony suggest non-ACTH-dependent mechanisms drive hypercortisolism in critical illness.
- Findings challenge traditional views of the hypothalamic-pituitary-adrenal axis in critical illness.
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