Reversible inhibition of testicular steroidogenesis and spermatogenesis by a potent gonadotropin-releasing hormone agonist in normal men: an approach toward the development of a male contraceptive.

Reversible inhibition of testicular steroidogenesis and spermatogenesis by a potent gonadotropin-releasing hormone agonist in normal men: an approach toward the development of a male contraceptive.
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正常男性中有效的促性腺激素释放激素激动剂对睾丸类固醇生成和精子发生的可逆抑制:一种开发男性避孕药的方法。

DOI:
10.1056/nejm198109173051203
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发表时间:
1981
期刊:
The New England journal of medicine
影响因子:
--
通讯作者:
Rabin,D
Rabin,D
中科院分区:
--
文献类型:
--
作者:
Linde,R;Doelle,GC;Alexander,N;Kirchner,F;Vale,W;Rivier,J;Rabin,D

文献摘要

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我们研究了一种强有力的促性腺激素释放激素激动剂D-Trp6-Pro9-N-乙酰胺-LHRH(LHRHa)在8名正常男性身上的抗生育作用,他们每天接受6到10周的皮下注射。所有八个人的血浆睾丸素水平都大幅下降。血浆17-羟孕酮和血清雌二醇-17β水平与血睾酮水平呈正相关。5名男性在治疗的第六至第七周之间出现阳萎,每个病例在停止治疗后的两周内都得到了缓解。血清促性腺激素水平也在治疗期间下降,治疗结束时短暂反弹至基础水平以上。精子密度和活动率在治疗后第7周至第18周降至最低点。在6名受试者中,精子水平降至每毫升6X106精子或更少,在另外两名受试者中,精子水平分别比基础平均值低70%和86%。在10到14周的恢复期内,所有男性的精子密度恢复到治疗前的水平。这一结果与LHRHa诱导的垂体腺“脱敏”是一致的,但不排除LHRHa对睾丸类固醇生成和精子生成的直接抑制作用。(英国医学杂志)1981年;305:663-7。)
We studied the antifertility effects of a potent gonadotropin-releasing hormone agonist, D-Trp6-Pro9-N-ethylamide-LHRH (LHRHA) in eight normal men, who received daily subcutaneous injections for six to 10 weeks. Plasma testosterone levels fell substantially in all eight. Plasma 17-hydroxyprogesterone and serum estradiol-17β levels decreased concordantly with plasma testosterone. Impotence developed in five men between the sixth and seventh weeks of treatment, with resolution in each case within two weeks of stopping treatment. Serum gonadotropin levels also fell during treatment, briefly rebounding above basal levels when therapy ended. Sperm density and motility fell to a nadir during the seventh to 18th week after therapy. In six subjects sperm levels fell to 6X106sperm per milliliter or less, and in the other two they decreased 70 and 86 per cent below basal mean values. Sperm density returned to pretreatment levels in all men during the 10-to-14-week recovery period.These results are consistent with LHRHA-induced pituitary "desensitization" but do not exclude a direct inhibitory effect of LHRHAon testicular steroidogenesis and spermatogenesis. (N Engl J Med. 1981; 305:663–7.)