Objective: To determine whether inhibin B levels are reflective of the etiology of gonadal dysfunction.
Design: Institutional study.
Setting: A tertiary care university-affiliated infertility clinic.
Patient(s): Forty-four men: 16 with primary testicular failure, 10 with partial idiopathic hypogonadotropic hypogonadism (IHH), 8 with primary germ cell failure, one with iatrogenic hypogonadotropic hypogonadism, one with untreated Kallmann's syndrome, and 8 healthy fertile controls.
Intervention(s): Three individuals (one each with IHH, hypogonadotropic hypogonadism [HH], and Kallmann's syndrome) underwent treatment with human chorionic gonadotropin.
Main outcome measure(s): Baseline serum inhibin B, FSH, LH, total testosterone and estradiol levels, and sperm concentrations were measured.
Result(s): Serum inhibin B concentrations were significantly higher in fertile controls (255 +/- 59 pg/mL) than in men presenting with primary testicular failure (75 +/- 46 pg/mL, P<.0001) or in those presenting with primary germ cell failure (73 +/- 31 pg/mL, P<.0001). Inhibin B levels were also lower in males with partial IHH (187 +/- 112 pg/mL, P<.05). The patient with iatrogenic HH had a level of 184 pg/mL, whereas the patient with Kallmann's syndrome had nondetectable levels (<10 pg/mL). Serum inhibin B levels correlated positively with sperm concentration (P=.0001), and negatively with FSH levels (P=.01) and LH levels (P<.05). Human chorionic gonadotropin therapy altered inhibin B levels.
Conclusion(s): Inhibin B plays an important role as an endocrine regulator of FSH secretion, whereas gonadotropins are involved in the regulation of inhibin B secretion.