Abstract 34
It has been recently shown that IGF-1 is a metabolic signal capable of activating the GnRH/LH releasing system at the time of puberty in rats. In addition, studies in adult female transgenic mice, expressing the hGH gene, indicate that the endogenous production of hGH increases pituitary secretion of LH. The present study examines the role of hGH treatment (1 IU/kg.bw.week during at least 1 y) on the hypothalamic-pituitary-gonadal axis in 13 patients with TS during pubertal age, i.e., equal or older than 9 ys. Mean ± SD chronological age (CA) of the hGH treated TS group (Gr) was 13.2 ± 2.51 ys and bone age (BA) was 10.0 ± 1.78 ys. Serum levels of LH, FSH and estradiol (E2) were determined before and after two SC injections of 100 µg GnRHa (Buserelin acetate) separated by 24 hs. Sampling was as follows: 24 hs after the first injection and 4,6 and 24 hs after the second one. Serum E2 response was considered to be positive (i.e., functional ovarian tissue), when a value equal or greater than 55 pmol/L was obtained in any of the post injection samples. A control (C) untreated Gr of 10 TS patients (CA: 14.2 ± 1.72 ys, BA: 11.2 ± 1.78 ys) was also studied. To analyze serum gonadotropin responses, the hGH Gr and the C Gr, were subdivided according to the serum E2 response to the test in 6 (+) and 7 neg (-) responders in the former and in 3 (+) and 7(-) responders in the latter Gr. The two serum E2 responses were similar (hGH Gr 81.4 ± 37.4 and C Gr 69 ± 13.4 pmol/L). Basal serum LH and serum FSH levels were similar in hGH Gr and in C Gr in E2 (+) as well as in E2 (-) responders (LH, hGH E2 (+) 20.8 ± 20.1 hGH E2 (-) 15.3 ± 19.1, C E2 (+) 54.6 ± 58.2, C E2 (-) 20 ± 17 U/L; FSH: hGH E2 (+) 98 ± 88, hGH E2 (-) 52.1 ± 45.8, C E2 (+) 89 ± 54.6, C E2 (-) 125 ± 39.4 U/L) After Buserelin, in the hGH Gr, serum LH and FSH were significantly higher in the E2 (+) subgroup (124 ± 51.6 and 171 ± 102, respectively) than in the E2 (-) one (49.3 ± 35.7 ± and 76.9 ± 41.2, p<0.01 and -<0.05 respectively). On the contrary, in the C Gr, serum LH and FSH were significantly lower in the E2 (+) subgroup (65.1 ± 39.5 and 146 ± 95.3, respectively) than in the E2 (-) one (217 ± 82.1 and 240 ± 92.3, p<0.02 and p<0.05, respectively). In conclusion, hGH treatment modified the gonadotropin release pattern in the presence of functional ovarian tissue. This is an additional evidence of the influence of GH on the regulation of the GnRH-gonadotropin axis.
