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Effects of Testosterone Administration on Growth Hormone Pulse Dynamics in Human Immunodeficiency Virus-Infected Women

Neuroendocrine Unit and Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114

Address all correspondence and requests for reprints to: Dr. Steven Grinspoon, Program in Nutritional Metabolism, Longfellow 207, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114. E-mail: sgrinspoon{at}partners.org.

The effects of testosterone administration on the GH axis in androgen-deficient HIV-infected women are unknown. In this study, we determined the effects of transdermal testosterone administration on GH secretory dynamics and pulse characteristics in this population. GH-IGF-I parameters were determined in response to testosterone (4.1 mg/patch, twice a week; estimated delivery rate, 150 µg/d) vs. placebo over 6 months in 31 HIV-infected women. IGF-I increased significantly in the testosterone-treated compared with the placebo-treated patients [37 (–4, 73) vs. –30 (–98, 39) ng/ml, P = 0.01; 4.8 (–0.5, 9.6) vs. –3.9 (–12.8, 5.1) nmol/liter]. GH pulse frequency increased significantly in the testosterone-treated compared with the placebo-treated subjects [1.0 (1.0, 2.0) vs. 0.0 (–0.5, 1.5) peaks per 12 h, respectively; P = 0.02]. Before testosterone administration, overnight GH pulse amplitude was significantly related to IGF-I in univariate (r = 0.41, P = 0.03) and multivariate regression analysis; however, free testosterone, estradiol, and body mass index were not significantly correlated with baseline IGF-I. In contrast, after 6 months of treatment with testosterone, the change in IGF-I was significantly correlated to the change in free testosterone in univariate (r = 0.40, P = 0.04) and multivariate regression analysis. For each 1.0 pg/ml (3.5 pmol/liter) increase in free testosterone, IGF-I increased 19 ng/ml (2.5 nmol/liter), controlling for estradiol, body mass index, and GH pulse parameters (r² = 0.64). We demonstrate that IGF-I increases in response to physiologic, transdermal testosterone in HIV-infected women. The mechanism of this effect is unknown, but may involve a direct effect of testosterone on IGF-I, independent of changes in GH pulse dynamics.

This work was supported in part through National Institutes of Health Grants R01 DK54167 and M01 RR00088 and the Mary Fisher Clinical AIDS Research and Education Fund.

Abbreviations: ANCOVA, Analysis of covariance; BMI, body mass index; CV, coefficient of variation; IBW, ideal body weight; IGFBP, IGF binding protein; VAT, visceral adipose tissue.