Testosterone undecanoate supplementation together with human chorionic gonadotropin does not impair spermatogenesis in males with isolated hypogonadotropic hypogonadism:a retrospective study

Gon adotropin therapy is comm only used to in duce virilizati on and spermatoge nesis in male isolated hypog on adotropic hypog on adism (IHH) patients. In clinical practice, 5.6%-15.0% of male IHH patients show poor responses to gonadotropin treatment;therefore, testosterone (T) suppleme ntation can serve as an alter native therapy to no rmalize serum T levels and promote virilization. However, treatment with exogenous T impairs spermatogenesis and suppresses intratesticular T levels. This retrospective study aimed to determine whether oral testosterone undeca noate (TU) suppleme ntation together with human chorionic gonadotropin (hCG) would negatively affect spermatogenesis in IHH patients compared with hCG alone. One hundred and seven IHH patients were included in our study. Fifty-four patients received intramuscular hCG and oral TU, and 53 patients received intramuscular hCG alone. The median follow-up time was 29 (range: 12-72) mon ths in both groups. Compared with the hCG group, the hCG/TU group required a shorter median time to normalize serum T levels (P < 0.001) and achieve Tanner stage (III and V) of pubic hair and genital development (P < 0.05). However, there were no significant differences in the rate of seminal spermatozoa appearance, sperm concentration, or median time to achieve different sperm concentration thresholds between the groups. In addition, there were no significant differences in side effects, such as acne and gynecomastia, observed in both groups. This study indicates that oral TU supplementation together with hCG does not impair spermatogenesis in treated IHH patients compared with hCG alone, and it shortens the time to normalize serum T levels and promote virilization.

Trio-based genome sequencing identifies candidate causal genes in lifelong premature ejaculation

Dear Editor,Premature ejaculation(PE)is the most common sexual dysfunction with prevalence rates of 20%-30%.1Unfortunately,there are limited treatment options as a result of the lack of knowledge about the pathophysiology of PE.2Although the exact etiology of PE is not clear,it is known that PE is etiologcally heterogeneous,with both genetic and environmental factors playing a role.3Schapiro and Waldinger's study suggested that PE ran in families,with a higher morbidity in the family members of PE patients than that in unafected individuals.4,5.The results of Jern's study indicated that PE is moderately heritable,with an inheritability ratio of 28%in a cohort of 3946 pairs of twins.