Endocrine dysfunction during sepsis—are changes in hormone levels a physiological adaptation or a therapeutic target?

During the acute phase of sepsis, defined as a life-threatening organ-dysfunction caused by a dysregulated host response to an infection, patients often show severe changes in hormones and metabolic markers. These include downregulation of hormones such as TSH, T3, testosterone and estrogen, and an upregulation of other hormones such as cortisol, vasopressin, insulin-like growth factor I (IGF-I) and insulin. Whether these endocrine changes during sepsis are part of a physiological response and have beneficial effects on clinical outcomes, or in contrast, further worsen the clinical course and need therapeutic modulation has important therapeutic implications. The objective of this review is to discuss the current pathophysiological concepts underlying hormonal changes that frequently occur in patients with sepsis and important modulation factors (e.g., acute vs. chronic illness, pre-existing illness among others).