Hirsutism and virilism in women.

M A Kirschner
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Abstract

Hirsutism in women may be defined as excessive thick (terminal) hair growth in facial and body regions. It is one of the early manifestations of virilization that correlate closely with elevated testosterone production. Testosterone production rates in normal women average 0.2 mg/day, with 25% secreted by the ovaries, 25% by the adrenals, and 50% arising from the peripheral metabolism of prehormones, notably androstenedione. Increased testosterone from adrenal and/or ovarian sources induces 5 alpha-reductase activity within the susceptible hair follicle. This results in the local production of dihydrotestosterone, the potent androgen that is likely responsible for the growth and stimulation of the hair follicle that leads to hirsutism. Activation of the hair follicle by androgens provides a secondary pathway for testosterone metabolism, unfortunately at the expense of undesirable hair growth. Although virilization in women may be caused by exogenous androgens, it occurs primarily from diseases of the adrenals or ovaries. Androgen-producing tumors of the adrenals cause virilization in association with excessive production of a wide variety of C19 androgens. In contrast, ovarian tumors tend to secrete a narrower range of androgens and their presence may be more occult. The most common causes of hirsutism in women arise from nontumorous states, chiefly ovarian in origin. The androgenized ovary syndrome represents a spectrum of abnormalities ranging from idiopathic hirsutism to the polycystic ovary syndrome to ovarian hyperthecosis. These states are associated with mild to severe abnormalities of androgen production and concomitant mild to severe abnormalities of ovarian histology. The pathogenesis of these abnormalities is still speculative, but appears to be related to increased pulsatile and tonic secretion of LH with ovarian hyperstimulation. Of the various laboratory tests to evaluate hirsutism, simple measurements of plasma testosterone, free testosterone, and most recently androstanediol glucuronide seem to provide the best chemical evidence of androgen abnormalities. Treatment of hirsutism/virilism in women is difficult and frequently unsatisfactory. At present, treatment schemes include local methods, suppression of androgens via glucocorticoids or oral contraceptives, and antiandrogens.

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女性的多毛症和男子气概。
女性多毛症可以定义为面部和身体区域毛发生长过度厚(末端)。这是男性化的早期表现之一,与睾丸激素分泌升高密切相关。正常女性的睾酮分泌率平均为0.2毫克/天,其中25%由卵巢分泌,25%由肾上腺分泌,50%来自外周代谢的前激素,尤其是雄烯二酮。肾上腺和/或卵巢来源的睾酮增加可诱导易感毛囊内的5 - α还原酶活性。这导致局部产生双氢睾酮,这种强效雄激素可能负责毛囊的生长和刺激,导致多毛症。雄激素激活毛囊为睾酮代谢提供了第二途径,不幸的是,这是以不受欢迎的头发生长为代价的。尽管女性男性化可能是由外源性雄激素引起的,但它主要是由肾上腺或卵巢疾病引起的。肾上腺产生雄激素的肿瘤与多种C19雄激素的过量产生有关,可引起男性化。相比之下,卵巢肿瘤分泌的雄激素范围更窄,它们的存在可能更隐蔽。女性多毛症最常见的原因来自非肿瘤状态,主要来自卵巢。雄激素化卵巢综合征代表了一系列异常,从特发性多毛症到多囊卵巢综合征再到卵巢囊肿。这些状态与雄激素产生的轻度至重度异常以及伴随的卵巢组织学轻度至重度异常有关。这些异常的发病机制仍是推测性的,但似乎与卵巢过度刺激时LH的搏动性和滋补性分泌增加有关。在评估多毛症的各种实验室测试中,血浆睾酮、游离睾酮和最近的雄甾二醇葡萄糖醛酸盐的简单测量似乎提供了雄激素异常的最佳化学证据。治疗女性多毛症/阳刚症是困难的,而且常常不令人满意。目前,治疗方案包括局部方法,通过糖皮质激素或口服避孕药抑制雄激素,以及抗雄激素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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