Department of Endocrinology, Diabetes and Metabolism, Cleveland Clinic, Cleveland, Ohio, USA.
Endocr Pract. 2011 Mar-Apr;17(2):e21-5. doi: 10.4158/EP10138.CR.
To describe a postmenopausal woman with severe hyperandrogenism who responded dramatically to a gonadotropin-releasing hormone (GnRH) agonist.
Detailed clinical and laboratory findings are presented, and the pertinent literature is reviewed.
A 53-year-old postmenopausal woman with end-stage renal disease, who had undergone kidney transplantation, was referred because of high serum testosterone levels. She presented with worsening acne and hirsutism for the previous 2 years. Her medications included prednisone (7.5 mg every other day). On examination, mild facial acne and hirsutism but no virilizing features were noted. Laboratory results showed generous postmenopausal gonadotropin levels and markedly elevated total and free testosterone levels, which failed to suppress with a 2-day low-dose dexamethasone test. Transvaginal ultrasonography and a computed tomographic scan failed to identify an ovarian or adrenal abnormality. Administration of a GnRH agonist (Depo-Lupron) resulted in a dramatic decline in follicle-stimulating hormone, luteinizing hormone, and testosterone levels after 1 month, which persisted during the course of 11 months of therapy. The source of marked hyperandrogenism in postmenopausal women represents a diagnostic challenge. The absence of a tumor on diagnostic imaging and the inability to perform catheterization studies confound the problem. Androgen levels did not suppress with glucocorticoids. We reasoned that a clear response to a GnRH agonist would indicate a nontumorous ovarian source of hyperandrogenism. Regrettably, the literature has described cases of ovarian tumors and, rarely, adrenal adenomas that are responsive to gonadotropins.
The striking improvement in a postmenopausal woman with severe hyperandrogenism by means of GnRH agonist therapy demonstrates its potential use in poor surgical candidates without necessarily delineating the source of androgen excess.
描述一名绝经后妇女出现严重的高雄激素血症,对促性腺激素释放激素(GnRH)激动剂反应明显。
呈现详细的临床和实验室发现,并回顾相关文献。
一名 53 岁绝经后妇女,患有终末期肾病,已接受肾移植,因血清睾丸酮水平升高而转介。她因过去 2 年来痤疮和多毛症恶化而就诊。她的药物治疗包括泼尼松(隔日 7.5 毫克)。检查时,发现轻度面部痤疮和多毛症,但无男性化特征。实验室结果显示绝经后促性腺激素水平升高,总睾酮和游离睾酮水平显著升高,用 2 天低剂量地塞米松试验不能抑制。阴道超声和 CT 扫描未能发现卵巢或肾上腺异常。使用 GnRH 激动剂(Depo-Lupron)治疗 1 个月后,促卵泡激素、黄体生成素和睾酮水平显著下降,并在 11 个月的治疗过程中持续下降。绝经后妇女出现明显高雄激素血症的原因是一个诊断挑战。诊断影像学上无肿瘤,并且无法进行导管研究,使问题更加复杂。雄激素水平不能被糖皮质激素抑制。我们认为,对 GnRH 激动剂的明确反应表明卵巢来源的高雄激素血症是非肿瘤性的。遗憾的是,文献描述了卵巢肿瘤的病例,很少有肾上腺腺瘤对促性腺激素有反应。
GnRH 激动剂治疗绝经后严重高雄激素血症妇女的显著改善表明,在没有明确雄激素过多来源的情况下,它可能对手术不佳的患者有用。