Editorial: The Rational Use of Growth Hormone in HIV-Infected Patients

Extract

GH secretion and action is affected by nutritional status and changes in body composition. Acquired resistance to the action of GH is common in severe undernutrition as a result of impaired GH receptor and postreceptor signaling of IGF-I in the liver. In contrast, reduced GH secretion occurs in generalized obesity (1), most likely through inhibition by somatostatin. It is, therefore, not surprising that HIV disease is characterized by a number of abnormalities in the GH–IGF-I axis. In patients with AIDS wasting and loss of significant weight and muscle mass, a pattern of acquired GH resistance is seen, with increased GH and simultaneously decreased concentrations of IGF-I (2). In such patients, the expected GH-induced increase in IGF-binding protein-3 is diminished (3). In addition, increased proteolysis of IGF-binding protein-3 is seen in HIV-infected children with growth failure, which may affect the tissue concentration of free IGF-I (4). In contrast, recent data suggest reduced GH concentrations in HIV-infected patients with fat redistribution receiving highly active antiretroviral therapy, characterized by excess abdominal visceral fat and loss of sc fat (5). Although the mechanisms of these changes in fat redistribution have not been elucidated, recent data suggest a strong inverse correlation between increased visceral fat and reduced GH concentrations, determined from overnight frequent sampling (5). Taken together, these data suggest adaptive responses in GH secretion depending on changes in nutritional status and body composition in HIV-infected patients. In contrast, normal GH secretion has been reported in otherwise healthy HIV-infected patients, without demonstrated wasting or lipodystrophy (6).