Growth hormone (GH) resistance is defined biochemically by the finding of high GH and low IGF-I levels. It may be primary, as in Laron's syndrome (GH receptor mutations), or acquired (Table 1) (1). Acquired resistance is found in conditions that have in common malnutrition and net protein catabolism. There is evidence to suggest that GH resistance is permissive to protein catabolism and that its reversal may improve the nutritional state of some patients. In this review we discuss the clinical problem, its molecular basis and the possibility of therapeutic intervention with GH and/or IGF-I.
The clinical problem
Trauma, sepsis, surgery and organ failure are all associated with an increased catabolic rate. When prolonged, this results in malnutrition, muscle weakness, delayed wound healing and immunosuppression (2). Loss of body protein still occurs in these patients groups despite intense nutritional support (3). In many patients nutritional state is the most important predictor