GH will not adversely affect the HPTA.
There is some support that GH will help testes function.
Balducci R, Toscano V, Mangiantini A, Bianchi P, Guglielmi R, Boscherini B. The effect of growth hormone administration on testicular response during gonadotropin therapy in subjects with combined gonadotropin and growth hormone deficiencies. Acta Endocrinologica 1993;128(1):19-23. http://www.eje-online.org/content/128/1/19.abstract
To evaluate the effect of growth hormone on testicular response to human chorionic gonadotropins (hCG) in vivo in humans, we selected patients with combined deficits of GH and gonadotropins who were in substitution treatment with both GH (from the time of diagnosis) and gonadotropins (from the time of induction of puberty). Testicular response to gonadotropin therapy was then evaluated during and six months after the cessation of GH treatment. Blood samples were collected before and 2, 4 and 6 days after hCG administration. hCG responses were calculated and expressed as the areas under the response curve. We studied four hypogonadotropic patients (aged 18–19 years) with associated GH deficiency. Their gonadotropin treatment consisted of hCG 1500IU every six days, and FSH 75 IU every three days. The GH therapy replacement consisted of 4 IU thrice weekly. Testosterone, androstenedione, 17α-hydroxyprogesterone and estradiol were measured. In all subjects the testosterone area during GH treatment was significantly higher compared to the testosterone area obtained without GH administration (2993±1091 vs 2310±751; M±SD; p<0.04). The androstenedione area followed a similar pattern (708±377 vs 402±248; M±SD; p<0.05). The 17α-hydroxyprogesterone area, on the contrary, was significantly higher during GH withdrawal (542±307 vs 235±190; M±SD; p<0.05). As far as the estradiol area is concerned, no significant differences were found (22860±10082 vs 25697±13640; M±SD). In conclusion, GH administration seems to improve testosterone production induced by human chorionic gonadotropins. The finding of the inverse response pattern of 17α-hydroxyprogesterone with respect to testosterone led us to suppose that the increased testosterone area during GH treatment may be due to an increased activity of C17,20-lyase enzyme.
Carani C, Granata AR, De Rosa M, et al. The effect of chronic treatment with GH on gonadal function in men with isolated GH deficiency. Eur J Endocrinol 1999;140(3):224-30. http://eje-online.org/content/140/3/224.abstract
Eleven adult males, previously submitted to neurosurgery because of a pituitary lesion (three with craniopharyngioma, three with clinically non-functioning adenoma and five with macroprolactinoma) were treated with recombinant GH for 12 months after the diagnosis of GH deficiency was made. Circulating FSH, LH, prolactin, testosterone, 17 beta-estradiol (E2), dehyroepiandrosterone (DHEA-S), androstenedione. 17-OH-progesterone (17OHP), IFG-I, and steroid hormone-binding protein (SHBG) levels were assayed before and after CG test at study entry and 6 and 12 months after GH treatment.
A significant increase in plasma IGF-I levels was obtained after 6 and 12 months of GH treatment. In addition, CG-stimulated, but not baseline, testosterone levels showed a significant increase after 6 and 12 months of GH treatment when compared with study entry (9.6 +/- 0.5 and 9.9 +/- 0.5 vs 7.9 +/- 0.5 ng/ml; P < 0.05). Baseline, but not CG-stimulated, serum 17OHP levels were significantly increased only after 12 months of GH treatment (1.7 +/- 0.1 vs 1.4 +/- 0.1 ng/ml; P < 0.05). No significant difference was found as far as both basal and CG-stimulated E2, androstenedione, DHEA-S and SHBG were concerned. With regards to the semen analysis, only seminal plasma volume was significantly increased after 12 months of GH treatment (2.9 +/- 0.3 vs 1.7 +/- 0.3 ml; P < 0.05). No significant change in sperm count, motility and abnormal forms was observed.
These data show that GH treatment displays a clear-cut effect upon Leydig cell function and increases the production of seminal plasma volume in fertile adult males with isolated GH deficiency.