Rohayem Julia, Luberto Alessandra, Nieschlag Eberhard, Zitzmann Michael, Kliesch Sabine
Center of Reproductive Medicine and Andrology, Department of Clinical Andrology, University of Muenster, Albert-Schweitzer-Campus 1, Building D11, D-48149, Muenster, Germany.
Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Via Università, 4, 41121, Modena, MO, Italy.
Endocrine. 2017 Mar;55(3):914-924. doi: 10.1007/s12020-016-1178-0. Epub 2017 Jan 9.
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.
To evaluate the impact of age at treatment of undescended testes on endocrine and spermatogenic testicular function in middle-aged men.
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.
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.
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.
出生时睾丸未降可能是由于胎儿发育期间睾酮缺乏所致。目前尚不清楚睾丸下降失败的过程是否会导致永久性内分泌损害。
评估睾丸未降患者的治疗年龄对中年男性内分泌和生精睾丸功能的影响。
对357例既往有睾丸未降的男性的生殖激素和精液数据进行评估，分析睾丸位置矫正时的年龄，并与709例出生时睾丸位置正常且精液正常的对照者的数据进行比较。
与对照组相比，睾丸未降的男性促黄体生成素平均水平较高（p < 0.0001），睾酮平均水平较低（p = 0.003）。他们的双侧睾丸体积也较小，促卵泡生成素水平较高，精子浓度较低（所有p < 0.0001）。双侧睾丸未降的受试者精子平均浓度最低。21%的病例精子浓度正常（单侧睾丸未降的男性中为27%，双侧睾丸未降的男性中为12%），44%被诊断为少精子症，35%为无精子症（单侧睾丸未降的为28%，双侧睾丸未降的为46%）。精液质量下降的受试者促性腺激素水平高于精液正常者。矫正年龄（中位数：6岁（1 - 39岁））与双侧睾丸体积和精子浓度呈负相关，与促卵泡生成素和促黄体生成素呈正相关，但与血清睾酮无关。
除了不育和睾丸癌外，潜在的、很少失代偿的性腺功能减退是睾丸未降的潜在长期后果，优先影响睾丸位置矫正延迟或失败的受试者。睾丸间质细胞功能受损可能导致生育能力受损。这些观察结果支持在婴儿早期矫正隐睾症。
