title: Reversal of idiopathic hypogonadotropic hypogonadism: a cohort study in Chinese patients.
abstract: Although idiopathic hypogonadotropic hypogonadism (IHH) has traditionally been viewed as a life-long disease caused by a deficiency of gonadotropin-releasing hormone neurons, a portion of patients may gradually regain normal reproductive axis function during hormonal replacement therapy. The predictive factors for potential IHH reversal are largely unknown. The aim of our study was to investigate the incidence and clinical features of IHH male patients who had reversed reproductive axis function. In this retrospective cohort study, male IHH patients were classified into a reversal group (n = 18) and a nonreversal group (n = 336). Concentration of gonadotropins and testosterone, as well as testicle sizes and sperm counts, were determined. Of 354 IHH patients, 18 (5.1%) acquired normal reproductive function during treatment. The median age for reversal was 24 years old (range 21-34 years). Compared with the nonreversal group, the reversible group had higher basal luteinizing hormone (LH) (1.0 ± 0.7 IU l -[1] vs 0.4 ± 0.4 IU l-1 , P< 0.05) and stimulated LH (28.3 ± 22.6 IU l-1 vs 1.9 ± 1.1 IU l-1 , P< 0.01) levels, as well as larger testicle size (5.1 ± 2.6 ml vs 1.5 ± 0.3 ml, P< 0.01), at the initial visit. In summary, larger testicle size and higher stimulated LH concentrations are favorite parameters for reversal. Our finding suggests that reversible patients may retain partially active reproductive axis function at initial diagnosis.
authors.forename: Jiang-Feng
authors.initials: JF
authors.lastname: Mao
authors.forename: Hong-Li
authors.initials: HL
authors.lastname: Xu
authors.forename: Jin
authors.initials: J
authors.lastname: Duan
authors.forename: Rong-Rong
authors.initials: RR
authors.lastname: Chen
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Bin
authors.initials: B
authors.lastname: Li
authors.forename: Min
authors.initials: M
authors.lastname: Nie
authors.forename: Le
authors.initials: L
authors.lastname: Min
authors.forename: Hong-Bing
authors.initials: HB
authors.lastname: Zhang
authors.affiliation: Department of Endocrinology, Peking Union Medical College Hospital, Key Laboratory of Endocrinology, Ministry of Health, Beijing 100730, China.
authors.forename: Xue-Yan
authors.initials: XY
authors.lastname: Wu
mesh_terms: D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000097:blood; D015331:Cohort Studies; D005640:Follicle Stimulating Hormone / Q000097:blood; D005500:Follow-Up Studies; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists; D020249:Hormone Replacement Therapy; D006801:Humans; D007006:Hypogonadism / Q000097:blood / Q000188:drug therapy* / Q000473:pathology*; D007986:Luteinizing Hormone / Q000097:blood*; D008297:Male; D009929:Organ Size / Q000187:drug effects; D011237:Predictive Value of Tests; D012189:Retrospective Studies; D013737:Testis / Q000187:drug effects / Q000473:pathology*; D013739:Testosterone / Q000494:pharmacology / Q000627:therapeutic use*; D016896:Treatment Outcome; D017329:Triptorelin Pamoate / Q000494:pharmacology; D055815:Young Adult
chemical_list: D015415:Biomarkers; D017329:Triptorelin Pamoate; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone