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Submitted on July 15, 2004
Accepted on September 23, 2004
Massachusetts General Hospital Program in Nutritional Metabolism (P.K., B.C. and S.G.) and Neuroendocrine Unit, Harvard Medical School, Boston, MA, 02114, General Clinical Research Center (J.B.), Massachusetts Institute of Technology, Cambridge, MA 02139
* To whom correspondence should be addressed.
Steven Grinspoon, E-mail: sgrinspoon{at}partners.org
Prior studies suggest reduced overnight growth hormone (GH) secretion in association with excess visceral adiposity among patients with HIV lipodystrophy. We now investigate GH responses to standardized GHRH-arginine in HIV infected patients with fat redistribution (LIPO, n = 39) in comparison to BMI and age-matched control groups [HIV without fat distribution (NONLIPO, n = 17)] and healthy control subjects (C, n = 16). IGF-I [242 ± 17, 345 ± 38, 291 ± 27 ng/mL, (P < 0.05 vs. NONLIPO) was lowest in the LIPO group. Our data demonstrate failure rates of 18% in the LIPO group vs. 5.9% for the NONLIPO group and 0% for the C group using a stringent criterion of 3.3 ng/mL for peak GH response to GHRH-arginine (P < 0.05 LIPO vs. C). Using less stringent cut-offs, the failure rate in the LIPO group rises to 38.5% at 7.5 ng/mL. Among the lipodystrophic patients, the peak GH response to GHRH-arginine was significantly predicted by VAT (P = 0.008), free fatty acid (P = 0.04) and insulin level (P = 0.007) in regression modeling controlling for age, BMI, sc fat area and triglyceride level. These data demonstrate increased failure rates to standardized stimulation testing with GHRH-arginine in HIV patients with fat redistribution, in association with increased visceral adiposity. The effects of low dose GH should be assessed in the large subset of patients with HIV lipodystrophy and abnormal GH stimulation testing.
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