Delayed treatment of undescended testes may promote hypogonadism and infertility
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ORIGINAL ARTICLE
Delayed treatment of undescended testes may promote hypogonadism and infertility Julia Rohayem1 Alessandra Luberto1,2 Eberhard Nieschlag1 Michael Zitzmann1 Sabine Kliesch1 ●
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Received: 18 July 2016 / Accepted: 10 November 2016 © Springer Science+Business Media New York 2016
Abstract Context Undescended testes at birth may be caused by testosterone deficiency during fetal development. It is unclear whether the process of failed descent contributes to permanent endocrine impairment. Objectives To evaluate the impact of age at treatment of undescended testes on endocrine and spermatogenic testicular function in middle-aged men. Patients and methods Reproductive hormone and semen data of 357 men with previously undescended testes were evaluated with respect to age at correction of testicular position and compared to those of 709 controls with eutopic testes at birth and normozoospermia. Results Men with undescended testes had higher mean Luteinizing Hormone levels (p < 0.0001) and lower mean testosterone levels (p = 0.003) compared to controls. They also had lower bi-testicular volumes, higher Follicle Stimulating Hormone levels, and lower sperm concentrations (all p < 0.0001). Lowest mean sperm concentrations were found in subjects with bilateral undescended testes. Normal sperm concentrations were found in 21 % of cases (in 27 % of men with unilateral and in 12 % with bilateral
undescended testes), while oligozoospermia was diagnosed in 44 %, and azoospermia in 35 % (in 28 % with unilateral, 46 % with bilateral undescended testes). Subjects with reduced semen quality had higher gonadotropin levels than those with normozoospermia. Age at correction (median: 6 years (1–39)) was inversely correlated with bi-testicular volumes and sperm concentrations, and positively correlated with FSH and LH, but not with serum testosterone. Conclusion Latent, rarely decompensated hypogonadism is a potential long-term consequence of undescended testes, besides infertility and testicular cancer, preferentially affecting subjects with delayed or unsuccessful correction of testicular position. Impaired Leydig cell function is likely to contribute to compromised fertility. These observations support correction of cryptorchidism during early infancy. Keywords Cryptorchidism Undescended testes (UDT) Testicular function LH Testosterone ●
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Introduction Electronic supplementary material The online version of this article (doi:10.1007/s12020-016-1178-0) contains supplementary material, which is available to authorized users. * Sabine Kliesch [email protected] 1
Center of Reproductive Medicine and Andrology, Department of Clinical Andrology, University of Muenster, Albert-SchweitzerCampus 1, Building D11, D-48149 Muenster, Germany
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Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Università, 4, 41121 Modena, MO, Italy
Undescended testes (UDT) are found in 1–4 % full-term and up to 45 % pre-term male newborns [1, 2]. The
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