Outcome of Gonadotropin Therapy for Male Hypogonadotropic Hypogonadism at University Affiliated Male Infertility Centers: A 30-Year Retrospective Study

Abstract

Initial TV values provide insight into phenotypic variables such as time of onset and severity in patients with primary or secondary HH, and may predict sperm output in response to hCG/hMG therapy.

European Consensus Statement on congenital hypogonadotropic hypogonadism—pathogenesis, diagnosis and treatment

“…Spermatogenesis can be induced either by long-term pulsatile GnRH administration (pump) 193 or more commonly by subcutaneous gonadotropin injections (2-3 times weekly). [194][195][196][197][198] These therapies induce both testicular testosterone production by Leydig cells and spermatogenesis in the seminiferous tubules. [199][200][201][202] The majority of patients with CHH develop sperm in their ejaculate with longterm therapy.…”

“…First, cryptorchidism indicates a poor fertility prognosis. 193,195 Men with CHH who have cryptor chidism often require extended courses of treatment (18-24 months). 203,204 Prepubertal testicular volume (<4 ml) and/or low serum levels of inhibin B are also negative determinants of fertility outcome.…”

“…203,204 Prepubertal testicular volume (<4 ml) and/or low serum levels of inhibin B are also negative determinants of fertility outcome. [193][194][195][196][197] Clinicians should be aware that although ~75% of men will develop sperm, counts rarely reach the normal range with longterm therapy. A 2014 meta-analysis identified a mean sperm count of 5.9 × 10 6 /ml (range: 4.7-7.1 × 10 6 /ml) for gonadotropin therapy and 4.3 × 10 6 /ml (range: 1.8-6.7 × 10 6 /ml) for GnRH therapy.…”

“…Anovulation and ovarian reserve can be assessed via a combination of history of menstrual cycle abnormalities, laboratory examination and pelvic ultrasonography. Couples should be counselled appropriately on the basis of the identified predictors of CHH fertility-inducing treatment, [193][194][195][196][197][198]200 as well as the partner's reproductive status and age in order to develop realistic expectations regarding treatment outcome.…”

Management of Male Hypogonadotrophic Hypogonadism

“…A second wave of increased HPG axis activity then occurs during the early stages of puberty, with a second wave of Sertoli cell proliferation. This wave of proliferation is followed by terminal differentiation, and Leydig cells begin to secrete testosterone, allowing the normal development of puberty [4].A disruption in any of these events, from fetal to adult life, can lead to hypogonadism, and this can be manifested in a wide variety of clinical symptoms, according to the time of onset and the severity of the resulting hormone deficiency. In many cases, the symptoms may not be recognised before puberty.…”