• Greet Van den Berghe.
• Department of Intensive Care Medicine, University Hospital Gasthuisberg Catholic University of Leuven, B-3000 Leuven, Belgium. greta.vandenberghe@med.kuleuven.ac.be
• Endocrinol. Metab. Clin. North Am. 2003 Jun 1; 32 (2): 385-410.

AbstractProlonged critical illness has a high morbidity and mortality. The acute and chronic phases of critical illness are associated with distinct endocrine alterations. The acute neuroendocrine response to critical illness involves an activated anterior pituitary function. In prolonged critical illness, however, a reduced pulsatile secretion of anterior pituitary hormones and the so-called "wasting syndrome" occur. The impaired pulsatile secretion of GH, thyrotropin and gonadotropin can be re-amplified by relevant combinations of releasing factors, which also substantially increase circulating levels of IGF-1, GH-dependent IGFBPs, thyroxin, tri-iodothyronine and testosterone. Anabolism is clearly re-initiated at the time GH secretagogues, thyrotropin-releasing hormone and gonadotropin-releasing hormone are coadministered but the effect on survival remains unknown. A lethal outcome of critical illness is predicted by a high serum concentration of IGFBP-1, pointing to impaired insulin effect rather than pituitary function, and survival was recently shown to be dramatically improved by strict normalization of glycemia with exogenous insulin. In addition to the illness-induced endocrine alterations, patients may have pre-existing central or peripheral endocrine diseases, either previously diagnosed or unknown. Hence, endocrine function testing in a critically ill patient represents a major challenge and the issue of treatment remains controversial. The recent progress in knowledge of the neuroendocrine response to critical illness and its interrelation with peripheral hormonal and metabolic alterations during stress, allows for potential new therapeutic perspectives to safely reverse the wasting syndrome and improve survival.

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