Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, Texas.
Department of Obstetrics and Gynecology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.
J Clin Endocrinol Metab. 2019 Jul 1;104(7):2796-2800. doi: 10.1210/jc.2018-02464.
Ovarian hyperandrogenism from polycystic ovary syndrome (PCOS) and hyperinsulinemia from insulin resistance are modulators of ovarian follicle development. We report on a woman with PCOS and hyperandrogenism and severe insulin resistance from metabolic syndrome who received long-term GnRH analogue therapy preceding bilateral salpingo-oophorectomy for massive ovarian enlargement. Ovarian histological examination showed proliferating granulosa cells within antral follicles coexistent with serous cystadenofibromas, demonstrating a unique link between hyperinsulinemia and granulosa cell mitogenesis.
A 30-year-old woman with PCOS with hyperandrogenism, severe insulin resistance from metabolic syndrome, and nonalcoholic steatohepatitis experienced abdominal pain from bilaterally enlarged ovaries. She had previously experienced a pulmonary embolism while taking oral contraceptives and hepatotoxicity from metformin and spironolactone therapies. Long-term GnRH analogue therapy to induce pituitary desensitization to GnRH successfully decreased gonadotropin-dependent steroidogenesis without improving insulin resistance. Despite GnRH analogue therapy, progressive ovarian enlargement in the presence of hyperinsulinemia from worsening metabolic function eventually required bilateral salpingo-oophorectomy for removal of massively enlarged ovaries. Histological examination showed both ovaries contained proliferating granulosa cells within antral follicles coexistent with serous cystadenofibromas.
In women with PCOS and hyperinsulinemia from severe insulin resistance due to metabolic syndrome, granulosa cell proliferation within antral follicles can occur despite long-term GnRH analogue therapy, implicating hyperinsulinemia as a granulosa cell mitogen in the absence of gonadotropin-dependent ovarian function.
多囊卵巢综合征（PCOS）导致的卵巢过度雄激素血症和胰岛素抵抗导致的高胰岛素血症是调节卵巢卵泡发育的因素。我们报告了一例患有 PCOS 和高雄激素血症以及代谢综合征严重胰岛素抵抗的女性，她在双侧输卵管卵巢切除术之前接受了长期 GnRH 类似物治疗，以治疗卵巢增大。卵巢组织学检查显示，在窦卵泡内有增生的颗粒细胞，同时存在浆液性囊腺瘤纤维瘤，表明高胰岛素血症与颗粒细胞有丝分裂之间存在独特的联系。
一名 30 岁患有 PCOS 的女性，表现为高雄激素血症、代谢综合征引起的严重胰岛素抵抗和非酒精性脂肪性肝炎，因双侧卵巢增大而出现腹痛。她之前在服用口服避孕药时曾发生肺栓塞，服用二甲双胍和螺内酯时曾发生肝毒性。长期 GnRH 类似物治疗以诱导垂体对 GnRH 的脱敏，成功地降低了促性腺激素依赖性类固醇生成，但并未改善胰岛素抵抗。尽管进行了 GnRH 类似物治疗，但由于代谢功能恶化导致的高胰岛素血症，卵巢仍在继续增大，最终需要进行双侧输卵管卵巢切除术以切除增大的卵巢。组织学检查显示，双侧卵巢的窦卵泡内都有增生的颗粒细胞，同时存在浆液性囊腺瘤纤维瘤。
在患有 PCOS 且由于代谢综合征导致严重胰岛素抵抗而出现高胰岛素血症的女性中，尽管进行了长期 GnRH 类似物治疗，窦卵泡内的颗粒细胞仍可能发生增殖，这表明高胰岛素血症是一种在没有促性腺激素依赖性卵巢功能的情况下促进颗粒细胞有丝分裂的物质。
