The acute injury response, which generally occurs in the absence of feeding, is characterized by the catabolism of body stores of protein, carbohydrate and fat to provide substrates needed to meet increased energy demands and to supply the metabolic intermediates necessary for gluconeogenesis and protein synthesis during this period. Severe, prolonged or recurrent metabolic demands of stress eventually overwhelm the ability of the critically-ill patient to supply adequate amounts of these endogenous substrates and is associated with increased mortality and morbidity in the intensive care setting. Although the timely provision of exogenous nutrients can benefit acutely stressed patients by supporting the injury response, it is clear that nutritional therapy alone can not overcome the catabolic effects caused by severe injury and sepsis to allow net anabolism. Over the past several decades, increasing interest in hormonal manipulation to promote anabolic metabolism and blunt endogenous catabolism has led to investigations involving the use of growth hormone (GH) in states of coexisting nutritional depletion an acute metabolic stress. Though clinical studies have demonstrated promising results in metabolically stressed adults and older children, investigations of this sort in acutely ill infants are virtually non-existent.
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