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Abstract

Volume 22, Issue 4 (July 2020) 22, 390–395; 10.4103/aja.aja_88_19

Gonadotropin treatment for male partial congenital hypogonadotropic hypogonadism in Chinese patients

Ming Hao1,2, Min Nie1, Bing-Qing Yu1, Yin-Jie Gao1, Xi Wang1, Wan-Lu Ma1, Qi-Bin Huang1, Rui Zhang1, Jiang-Feng Mao1, Xue-Yan Wu1

1 NHC Key laboratory of Endocrinolog, Peking Union Medical College Hospital; Department of Endocrinology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China
2 Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, China

Correspondence: Dr. JF Mao (maojiangfeng88@sina.com) or Dr. XY Wu (wsheyan@vip.sina.com)

Date of Submission 23-Mar-2019 Date of Acceptance 20-Jun-2019 Date of Web Publication 23-Aug-2019

Abstract

Partial congenital hypogonadotropic hypogonadism (PCHH) is caused by an insufficiency in, but not a complete lack of, gonadotropin secretion. This leads to reduced testosterone production, mild testicular enlargement, and partial pubertal development. No studies have shown the productivity of spermatogenesis in patients with PCHH. We compared the outcomes of gonadotropin-induced spermatogenesis between patients with PCHH and those with complete congenital hypogonadotropic hypogonadism (CCHH). This retrospective study included 587 patients with CHH who were treated in Peking Union Medical College Hospital (Beijing, China) from January 2008 to September 2016. A total of 465 cases were excluded from data analysis for testosterone or gonadotropin-releasing hormone treatment, cryptorchidism, poor compliance, or incomplete medical data. We defined male patients with PCHH as those with a testicular volume of ≥4 ml and patients with a testicular volume of <4 ml as CCHH. A total of 122 compliant, noncryptorchid patients with PCHH or CCHH received combined human chorionic gonadotropin and human menopausal gonadotropin and were monitored for 24 months. Testicular size, serum luteinizing hormone levels, follicle-stimulating hormone levels, serum total testosterone levels, and sperm count were recorded at each visit. After gonadotropin therapy, patients with PCHH had a higher spermatogenesis rate (92.3%) than did patients with CCHH (74.7%). During 24-month combined gonadotropin treatment, the PCHH group took significantly less time to begin producing sperm compared with the CCHH group (median time: 11.7 vs 17.8 months, P < 0.05). In conclusion, after combined gonadotropin treatment, patients with PCHH have a higher spermatogenesis success rate and sperm concentrations and require shorter treatment periods for sperm production.

Keywords: gonadotropin treatment; partial congenital hypogonadotropic hypogonadism; spermatogenesis

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