Antimullerian hormone in patients with hypogonadotropic hypogonadism

Antimullerian hormone (AMH) is produced by immature Sertoli cells until pub ertal maturation. At puberty, elevation of serum testosterone correlates wi th a decrease in serum AMH. To further investigate the hormonal control of AMH secretion, serum AMH levels were measured in 20 normal men (20-60 yr) i n 12 patients (19-30 yr) with congenital hypogonadotropic hypogonadism (CHH ), and in 18 patients (19-65 yr) with acquired hypogonadotropic hypogonadis m (AHH) either untreated or during testosterone or human chorionic gonadotr opin (hCG) therapy. Mean serum AMH levels in normal adult men were low (20 +/- 4.9 pmol/L). In untreated CHH patients, mean serum AMH levels were sign ificantly higher than in normal men (292 +/- 86 pmol/L, P < 0.001) and were similar to those previously reported in prepubertal boys. In men with AHH, mean serum AMH levels were also significantly increased (107 +/- 50 pmol/L ; P < 0.01) when compared with healthy men but were less than in men with C HH. In addition, in 10 patients treated for prostate cancer, a modest but s ignificant increase of serum AMH (from 11.4 +/- 5.7 pmol/L to 49 +/- 9.9 pm ol/L; P < 0.01)was observed 12 months after suppression of the gonadal axis with the GnRH agonist Triptorelin (3.75 mg IM once a month). Plasma testosterone (T) and serum AMH levels were measured at baseline and at 3 and 6 months in 10 HH patients (6 CHH and 4 AHH) treated with bCG (150 0 IU/twice weekly for 6 months) and in 8 HH (4 CHH and 4 AHH) patients trea ted with T (T enanthate 250 mg/3 weeks for 6 months). hCG treatment induced an increase of plasma T (from 1.0 +/- 0.7 to 11 +/- 2.4 and 19 +/- 4.8 nmo l/L, at 3 and 6 months respectively) associated with a dramatic decrease of serum AMH (from 314 +/- 93 to 56 +/- 30 and 17 +/- 4,3 pmol/L). The simila r increase in plasma T levels (from 1.4 +/- 1.0 to 15.6 +/- 4.2 and 23 +/- 6.2 ng/mL) obtained with exogenous T induced a lesser decrease of serum AMH (from 221 +/- 107 pmol/L to 114 +/- 50 and 66 +/- 17 pmol/L, at 3 and 6 mo nths respectively). In conclusion, high plasma AMH levels in CHH patients are related to the ab sence of pubertal maturation of Sertoli cells. The high AMH levels in AHH a nd its increase after Triptorelin-induced gonadotropin deficiency suggest t hat the suppression of AMH is a reversible phenomenon. Finally, the inhibit ion of AMH production by Sertoli cells is induced by intratesticular T.