New Insight into Cortisol's Role in Critical Illness


Although the healthcare community's understanding of the hypothalamic-pituitary-adrenal axis under stress is fairly good, one point has baffled researchers.

When a person feels stressed, the body’s internal networks quickly send signals to the hypothalamus to release corticotropin-releasing hormone (CRH), which triggers the anterior pituitary gland to release plasma adrenocorticotropic hormone (ACTH), thus producing cortisol.

This pathway is critical — especially during a life-threatening illness — because it activates the endocrine and metabolic processes necessary to respond to the stressor at the organ and tissue level. In fact, elevated plasma cortisol concentrations are common during critical illness and increase as a severe condition becomes more serious, according to previous research.

Although the healthcare community’s understanding of the hypothalamic-pituitary-adrenal (HPA) axis under stress is fairly good, one point has baffled researchers. While stress activates the HPA axis and increases cortisol production during critical illness, plasma ACTH levels are often normal or low, which have complicated the diagnosis of adrenal failure and raised questions concerning other factors that might contribute to elevated cortisol levels.

Thus, in the June 2014 issue of Current Opinion in Endocrinology & Diabetes, researchers from Belgium reviewed cortisol’s true role in critical illness.

Not too long ago, scientists learned that cortisol’s plasma clearance is markedly reduced during critical illness, which has been shown to suppress renal and hepatic expression, as well as the activity of key cortisol-metabolizing enzymes. Unable to be cleared efficiently, serum cortisol levels have been known to increase.

New research has also demonstrated that critically ill patients’ cortisol production rate is less than double that of matched healthy subjects — an increase considered only moderate in magnitude. Such research has also shown that patients with systemic inflammatory response syndrome (SIRS) have a non-ACTH-driven increase in cortisol.

Low plasma ACTH concentrations appear to be the result of feedback inhibition subsequent to elevated cortisol that suppresses ACTH. If that theory is proven true, the traditional 200 mg daily dose of hydrocortisone for critically ill patients would be incorrect, especially since the dosage is 6 times higher than the body’s normal production of cortisol and is based on the assumption that HPA axis activation increases cortisol production significantly during critical illness.

As the healthcare community looks for a reliable method of assessing critically ill patients’ HPA axis responses, more research will be needed on the topic. Nevertheless, the authors of the current study believed that, in the future, physicians will use lower hydrocortisone doses and taper as soon as possible to avoid drug-induced complications.

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