Current evidence points to a significant interdependence of the neuroendocrine axis and the cytokine mediator systems. For example, the exogenous administration of tumor necrosis factor elicits increased secretion of ACTH, cortisol, catecholamines, and growth hormone. These interdependent mediator systems also exhibit negative feedback. For example, glucocorticoids reduce tumor necrosis factor and IL-1 transcription. The cytokines may also serve to attenuate the magnitude of the postinjury metabolic response by direct influences upon hypothalamic and pituitary hormone production. This is suggested by the thyroid hormonal profile commonly observed in critically ill patients which may serve to limit the degree of catabolic processes in the seriously ill. If this challenge is of a modest reparable degree and of limited duration, the initial counter-regulatory hormone and cytokine responses promote the mobilization of energy stores and the maintenance of substrate availability for critical organ function. In contrast, the hormonal response to prolonged insult erodes metabolic reserves and potentially limits recovery from life-threatening illness.
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