Page Stephanie T, Kalhorn Thomas F, Bremner William J, Anawalt Bradley D, Matsumoto Alvin M, Amory John K
Department of Medicine, University of Washington, Seattle,Washington, USA.
J Androl. 2007 Sep-Oct;28(5):734-41. doi: 10.2164/jandrol.107.002790. Epub 2007 May 9.
Male hormonal contraceptive regimens function by suppressing gonadotropin secretion, resulting in a dramatic decrease in testicular androgen biosynthesis and spermatogenesis. Animal studies suggest that persistent intratesticular (iT)-androgen production has a stimulatory effect on spermatogenesis in the setting of gonadotropin suppression. We hypothesized that men with incompletely suppressed spermatogenesis (>1,000,000 sperm/mL) during male hormonal contraceptive treatment would have higher iT-androgen concentrations than men who achieved severe oligospermia (<or=1,000,000 sperm/mL). Twenty healthy men ages 18-55 years enrolled in a 6-month male contraceptive study of transdermal testosterone (T) gel (100 mg/d) plus depomedroxyprogesterone acetate (300 mg intramuscularly every 12 weeks) with or without the gonadotropin releasing hormone (GnRH) antagonist acyline (300 microg/kg subcutaneously every 2 weeks for 12 weeks) were studied. During the 24th week of treatment, subjects underwent fine needle aspirations of the testes and iT-T and iT-dihydrotestosterone (iT-DHT) were measured in testicular fluid by liquid chromatography-tandem mass spectrometry. All men dramatically suppressed spermatogenesis; 15 of 20 men were severely oligospermic, and 5 of 20 suppressed to 1.5 million-3.2 million sperm per milliliter. In all subjects, mean iT-T and iT-DHT concentrations were 35 +/- 8 and 5.1 +/- 0.8 nmol/L. IT-androgen concentrations did not significantly differ in men who did and did not achieve severe oligospermia (P = .41 for iT-T; P = .18 for iT-DHT). Furthermore, there was no significant correlation between iT-T or iT-DHT and sperm concentration after 24 weeks of treatment. In this study of prolonged gonadotropin suppression induced by male hormonal contraceptive treatment, differences in iT-androgens did not explain differences in spermatogenesis. Additional studies to identify factors involved in persistent spermatogenesis despite gonadotropin suppression are warranted.
男性激素避孕方案通过抑制促性腺激素分泌起作用，导致睾丸雄激素生物合成和精子发生显著减少。动物研究表明，在促性腺激素抑制的情况下，睾丸内持续产生雄激素对精子发生有刺激作用。我们假设，在男性激素避孕治疗期间精子发生未被完全抑制（>100万精子/毫升）的男性，其睾丸内雄激素浓度会高于达到严重少精子症（≤100万精子/毫升）的男性。20名年龄在18 - 55岁的健康男性参与了一项为期6个月的男性避孕研究，该研究使用经皮睾酮（T）凝胶（100毫克/天）加醋酸甲羟孕酮（每12周肌肉注射300毫克），部分受试者还联合使用促性腺激素释放激素（GnRH）拮抗剂阿西立肽（每2周皮下注射300微克/千克，共12周）。在治疗的第24周，受试者接受睾丸细针穿刺，通过液相色谱 - 串联质谱法测量睾丸液中的睾丸内睾酮（iT - T）和睾丸内双氢睾酮（iT - DHT）。所有男性的精子发生均受到显著抑制；20名男性中有15名严重少精子，20名中有5名精子抑制到每毫升150万 - 320万。在所有受试者中，平均iT - T和iT - DHT浓度分别为35±8和5.1±0.8纳摩尔/升。达到和未达到严重少精子症的男性，其睾丸内雄激素浓度无显著差异（iT - T的P = 0.41；iT - DHT的P = 0.18）。此外，治疗24周后，iT - T或iT - DHT与精子浓度之间无显著相关性。在这项关于男性激素避孕治疗诱导的长期促性腺激素抑制的研究中，睾丸内雄激素的差异并不能解释精子发生的差异。有必要进行更多研究以确定在促性腺激素抑制情况下仍持续精子发生的相关因素。
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