Administration of growth hormone to catabolic patients

Complex alterations in the growth hormone (GH)insulin-like growth factor (IGF) axis are thought to play an important role in the protein catabolism that complicates recovery from trauma, burns, sepsis and major surgical procedures. The response to such critical illness is biphasic, with an initial acute phase followed by a chronic phase. Although basal levels of GH are sometimes increased under these circumstances, GH oscillatory activity is frequently attenuated.1 Moreover, in prolonged critical illness, blunted GH secretion has been shown to consist of a large number of small secretory bursts superimposed on basal release, probably caused, in part, by changes at the hypothalamus. 2 This reduction in pulsatile GH secretion seems to contribute to the fall in circulating levels of IGF-I, IGF-II, their major binding protein (IGFBP-3) and its associated acid-labile subunit (ALS), which has been consistently described in critically ill patients. 3 These changes in the GH-IGF axis are associated with the induction of a protease that decreases the affinity of IGFBP-3 for IGF-I, 3 thereby reducing the amount of IGF-I carried in a relatively inert state in the IGFBP-3ALS-IGF-I high molecular weight complex (see also Van den Berghe, page 77). Circulating levels of the GHindependent binding protein, IGFBP-1, which has a lower molecular weight than IGFBP-3 and a relatively short half-life, increase in response to traumatic or surgical injury, 4 and the normal inverse relationship between insulin and IGFBP-1 levels is lost (see also