Department of Endocrinology, Newcastle-upon-Tyne Hospitals, Newcastle Upon Tyne, UK.
Steroid Laboratory, Kings College Hospital, London, UK.
Clin Endocrinol (Oxf). 2018 Jan;88(1):13-20. doi: 10.1111/cen.13492. Epub 2017 Nov 7.
Postmenopausal hyperandrogenism can be tumour- or non-tumour-related, with pathology residing either in the ovary or adrenal gland(s). The tempo of investigation is determined by the clinical severity of hyperandrogenism (presence/absence of actual virilisation) and degree of serum testosterone elevation. When clinical or biochemical hyperandrogenism is severe, rapidly developing, or associated with hypercortisolism, screening for adrenocortical or ovarian carcinoma with cross-sectional imaging should be prioritised over detailed biochemical evaluation. Adrenal hyperandrogenism is readily characterised, both biochemically and radiologically. By contrast, even a combination of high-resolution imaging with laboratory evaluation, including dynamic endocrine testing, often cannot distinguish between ovarian hyperthecosis (OH) and virilising ovarian tumour (VOT); a definitive diagnosis usually emerging only after histological examination of excised ovaries. VOTs are typically below the resolution-limit of current imaging modalities and exhibit suppression of gonadotropin-dependent androgen secretion with GnRH-analogue therapy. Thus, for well-characterised ovarian hyperandrogenism, laparoscopic bilateral salpingo-oophorectomy may serve both as a diagnostic and therapeutic procedure. Nevertheless, women unable or unwilling to undergo ovarian surgery can be reassured that malignant VOTs are exceedingly rare and that long-term medical therapy with oral antiandrogens or GnRH-analogues is safe and well-tolerated. OH is strongly associated with insulin-resistance, with hyperinsulinaemia acting synergistically with raised gonadotropin levels to stimulate thecal cell hyperplasia and androgen secretion by the postmenopausal ovary, which lacks granulosa cell aromatase activity and thus cannot convert testosterone to 17 beta estradiol. Thus, features of metabolic syndrome may indicate OH, and significant reductions in androgens can thereby potentially be achieved with lifestyle measures and/or insulin-sensitising drugs.
绝经后高雄激素血症可与肿瘤或非肿瘤相关，其病理学表现为卵巢或肾上腺（多个）。调查的节奏取决于高雄激素血症的临床严重程度（是否存在实际的男性化）和血清睾酮升高的程度。当临床或生化高雄激素血症严重、快速发展或与皮质醇增多症相关时，应优先进行肾上腺或卵巢癌的横断面成像筛查，而不是进行详细的生化评估。肾上腺高雄激素血症在生化和影像学上均易于识别。相比之下，即使结合高分辨率成像和实验室评估，包括动态内分泌测试，也常常无法区分卵巢性多毛症（OH）和高雄激素性卵巢肿瘤（VOT）；通常只有在切除的卵巢组织学检查后才能明确诊断。VOT 通常低于当前成像方式的分辨率限制，并表现为促性腺激素依赖性雄激素分泌抑制与 GnRH 类似物治疗。因此，对于特征明确的卵巢高雄激素血症，腹腔镜双侧输卵管卵巢切除术既可以作为诊断方法，也可以作为治疗方法。然而，无法或不愿意接受卵巢手术的女性可以放心，恶性 VOT 极为罕见，并且长期口服抗雄激素或 GnRH 类似物治疗是安全且耐受良好的。OH 与胰岛素抵抗密切相关，高胰岛素血症与升高的促性腺激素水平协同作用，刺激绝经后卵巢的间质细胞增生和雄激素分泌，而卵巢缺乏颗粒细胞芳香化酶活性，因此不能将睾酮转化为 17β雌二醇。因此，代谢综合征的特征可能提示 OH，并且生活方式改变和/或胰岛素增敏药物可能显著降低雄激素。
