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Critical illness elicits a major stress response that activates the hypothalamic–pituitary–adrenal (HPA) axis. Furthermore, the administration of corticotropin stimulates cortisol secretion and causes structural changes in the adrenal gland that include adrenal-cell hypertrophy and hyperplasia.1 Adrenal glands that are obtained on autopsy from patients who have died after a prolonged critical illness2 are relatively heavy, and progressively compact lipid-depleted cells replace lipid-laden fasciculata cells.2 The symptoms of patients with critical illness vary: many have hypotension and are receiving inotropes or vasopressors, whereas others have sepsis, and many have the systemic inflammatory response syndrome (SIRS).3 Subsequent adrenal failure in critically ill . . .
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Celso E. Gómez-Sánchez (2013) studied this question.
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