ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2006) 11 P189

Recombinant hGH therapy in males with organic GHD: should we trust in total testosterone levels for diagnosis of central hypogonadism?

C Giavoli1, AG Lania1, E Ferrante1, F Ermetici2, S Bergamaschi1, CL Ronchi1, B Ambrosi2, A Spada1 & P Beck-Peccoz1

1Institute of Endocrine Sciences, University of Milan, Fondazione Ospedale Maggiore Policlinico IRCCS, Milan, Italy; 2Endocrinology Unit, University of Milan, Policlinico San Donato, Milan, Italy.

Previous evidences have suggested that in adults with organic hypopituitarism the condition of GH deficiency (GHD) could mask the presence of other pituitary deficits. In our experience, both central hypothyroidism and hypoadrenalism were unmasked during rhGH therapy in adults with GHD due to central organic lesions. Few and conflicting information are available about the relationship among GHD, rhGH therapy and gonadal function. Aim of the present study was to investigate the hypothalamic-pituitary-gonadal axis (HPG) in 12 adult males (mean age 47±8(S.D.) yrs) with organic GHD and normal HPG axis. The gonadal function was evaluated by measuring of serum testosterone, LH and FSH (basal and after GnRH challenge) and SHBG levels, before and during rhGH (mean dose 0.3±0.1 mg/day for 13±4 months). Careful clinical evaluation of symptoms of hypogonadism was also performed. To check the efficacy and adequacy of rhGH, serum IGF-I levels and percent of body fat (BF%) were measured too. Serum IGF-I levels normalized during rhGH and BF significantly decreased by 8%. Serum testosterone levels significantly decreased on rhGH (from 18.1±5.8 to 14.2±5.4 nmol/l, P=0.01), along with a parallel and significant decrease of SHBG (from 31.1±12.6 to 24.3±8.2 nmol/l, P<0.05). Thus, FAI (Free Androgen Index: Testosterone/SHBG) did not change (0.61±0.2 and 0.63±0.3 at baseline and during rhGH, respectively). No difference was found in either basal or stimulated gonadotropins levels. Notably, on rhGH 2 of 12 patients showed low total testosterone levels (9.7 and 6.7 nmol/l, n.v. 10-35) with neither change of FAI nor signs or symptoms of hypogonadism. In conclusion, re-evaluation of HPG axis during substitutive rhGH replacement showed a significant decrease in serum testosterone levels strictly related to variations of transport proteins and not accompanied by signs and symptoms of hypogonadism. Thus, during rhGH, the monitoring of HPG function cannot be based on the measurement of total testosterone levels, but should mainly rely on a careful clinical evaluation, in order to avoid unnecessary replacement therapy.

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