Endocrine Abstracts

Background: Hypogonadotropic hypogonadism (HH) is one of the few treatable causes of male infertility; spermatogenesis induction can be achieved with gonadotrophins or pulsatile GnRH. Treatment protocols are normally long, and outcome varies according to the underlying aetiology, age of onset and history of undescended testes. Regular follow-ups are needed to assess the response and monitor for adverse effects of therapy that could make the management challenging.

Case presentation: A 39-year-old male was reviewed in the clinic for fertility management. He had normal childhood growth and development but had no secondary sexual characteristics up to his late teenage years. There was no evidence of other pituitary hormone deficiencies and the pituitary MRI had been normal. There was no history of recreational drugs including opioid or anabolic steroid use. The diagnosis of normosmic congenital HH had been made. He had been initially treated with testosterone injections. He has two children aged 13 and 8 years following successful sperm induction with gonadotrophins. Since then, he had been taking testosterone undecanoate injections every 12 weeks. His partner is 34 years old and has no fertility problems. This time he presented seeking fertility treatment. He had small-volume testes (Prader orchidometer: 6 ml) with otherwise normal secondary sexual characteristics. He occasionally smoked and was at low risk for obstructive sleep apnoea. His weight was 100 kg and his height was 190 cm (BMI: 27.7 kg/m²). Blood results revealed a raised haematocrit, testosterone, and suppressed LH and FSH (<0.1U/l) consistent with testosterone therapy. He was azoospermic. Testosterone replacement was withheld, and he was started on subcutaneous injections of human chorionic gonadotrophin 2500 IU twice weekly. Since he remained azoospermic after one year of treatment, subcutaneous menotropin 75 IU twice weekly was added. There was a spermatogenic response, but haematocrit increased again (Table 1)

Conclusions: Response to gonadotrophins in male HH is variable with the need for prolonged and intensive treatment in some; yet, adverse effects could limit treatment intensification.