Rodriguez-Rigau L J, Weiss D B, Zukerman Z, Grotjan H E, Smith K D, Steinberger E
Fertil Steril. 1978 Nov;30(5):577-85. doi: 10.1016/s0015-0282(16)43641-1.
Seminiferous epithelium histology, Leydig cell density, and in vitro testosterone synthesis were quantitated in bilateral testicular biopsies from men with varying degrees of unilateral or bilateral varicoceles. Results were correlated with plasma levels of gonadotropins (follicle-stimulating hormone [FSH], luteinizing hormone [LH]) and testosterone (T), as well as with semen quality. In patients with bilateral varicoceles, spermatogenesis, Leydig cell density, plasma T levels, and in vitro T synthesis were significantly lower than in patients with unilateral varicoceles. Varicoceles appeared to affect maximally the latest stages of spermatogenesis. A negative correlation between FSH and LH levels and spermatogenesis was observed; however, a dissociation between the two gonadotropins occurred when spermatogenesis declined. Plasma T levels were within the normal range in all patients. The T:LH ratio was significantly correlated with spermatogenesis and sperm motility. Leydig cell density was abnormally low in oligospermic patients, and it was significantly correlated with in vitro T synthesis, spermatogenesis, sperm motility, and semen volume. Sperm count and motility were significantly correlated in this group of patients, suggesting a common pathophysiology for the effect of varicocele on spermatogenesis and sperm motility. This common pathophysiology appears to be disturbed Leydig cell function resulting in decreased testicular androgen production, in turn causing inadequate spermatogenesis and epididymal function.
对患有不同程度单侧或双侧精索静脉曲张的男性进行双侧睾丸活检,对生精上皮组织学、睾丸间质细胞密度和体外睾酮合成进行定量分析。结果与促性腺激素(卵泡刺激素[FSH]、黄体生成素[LH])和睾酮(T)的血浆水平以及精液质量相关。双侧精索静脉曲张患者的精子发生、睾丸间质细胞密度、血浆T水平和体外T合成均显著低于单侧精索静脉曲张患者。精索静脉曲张似乎对精子发生的最晚阶段影响最大。观察到FSH和LH水平与精子发生呈负相关;然而,当精子发生下降时,两种促性腺激素之间出现分离。所有患者的血浆T水平均在正常范围内。T:LH比值与精子发生和精子活力显著相关。少精子症患者的睾丸间质细胞密度异常低,且与体外T合成、精子发生、精子活力和精液量显著相关。该组患者的精子计数和活力显著相关,提示精索静脉曲张对精子发生和精子活力的影响存在共同的病理生理学机制。这种共同的病理生理学机制似乎是睾丸间质细胞功能紊乱,导致睾丸雄激素分泌减少,进而导致精子发生和附睾功能不足。