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δ1-睾酮内酯长期抑制芳香化酶对少精子症男性垂体-性腺功能的影响。

Effect of chronic aromatase inhibition by delta 1-testolactone on pituitary-gonadal function in oligozoospermic men.

作者信息

Dony J M, Smals A G, Rolland R, Fauser B C, Thomas C M

出版信息

Andrologia. 1986 Jan-Feb;18(1):69-78. doi: 10.1111/j.1439-0272.1986.tb01741.x.

Abstract

Aromatase inhibition by delta 1-testolactone (Teslac, 500 mg twice daily) for 6 months in 9 patients with idiopathic oligozoospermia lowered the levels of serum estradiol (E2) and thereby sex hormone binding globulin (SHBG) (rS = +0.40, p less than 0.025) to values -35 and -25%, respectively, below the pretreatment values (P less than 0.001 and less than 0.005). The E2 decrease was accompanied by a temporary increase (+50%) in the levels of follicle stimulating hormone (FSH), not of luteinizing hormone (LH), and of 17 alpha-hydroxyprogesterone (17 alpha-OHP), but less of testosterone (T) (+30%), which led to a transient rise in the 17 alpha-OHP/T ratio. The T/E2 ratio and "free T" index (T/SHBG) almost doubled until the end of the treatment period. During delta 1-testolactone treatment the mean sperm density gradually rose from 8.1 +/- 1.3 (SEM) before to 21.3 +/- 6.7 X 10(6)/ml after 6 months (P less than 0.01), whereas the total sperm count almost threefold increased (P less than 0.05). Sperm concentrations exceeding 20 X 10(6)/ml were achieved in 4 of the 9 patients. Two of these patients' wives became pregnant. Although the data point to a pivotal role of estrogens in the pathogenesis of the spermatogenic lesion in some patients with idiopathic oligozoospermia, the lack of a beneficial effect of estrogen lowering in others points to a multicausal nature of the disease entity.

摘要

9例特发性少精子症患者接受δ1-睾酮内酯(Teslac,每日2次,每次500mg)芳香化酶抑制治疗6个月,血清雌二醇(E2)水平降低,从而使性激素结合球蛋白(SHBG)水平分别比治疗前值降低了-35%和-25%(rS = +0.40,p < 0.025)(P < 0.001和< 0.005)。E2降低伴随着促卵泡生成素(FSH)水平暂时升高(+50%),促黄体生成素(LH)水平未升高,17α-羟孕酮(17α-OHP)水平升高,但睾酮(T)水平升高较少(+30%),这导致17α-OHP/T比值短暂升高。直到治疗期结束,T/E2比值和“游离T”指数(T/SHBG)几乎翻倍。在δ1-睾酮内酯治疗期间,平均精子密度从治疗前的8.1±1.3(SEM)逐渐升至6个月后的21.3±6.7×10⁶/ml(P < 0.01),而总精子数几乎增加了两倍(P < 0.05)。9例患者中有4例精子浓度超过20×10⁶/ml。其中2例患者的妻子怀孕。尽管数据表明雌激素在一些特发性少精子症患者生精损伤的发病机制中起关键作用,但在其他患者中降低雌激素水平缺乏有益效果,这表明该疾病实体具有多因素性质。

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