Department of Internal Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Barbra Streisand Women's Heart Center, Cedars-Sinai Medical Center, Smidt Heart Institute, Los Angeles, California, USA.
J Womens Health (Larchmt). 2021 Jul;30(7):1047-1051. doi: 10.1089/jwh.2020.8548. Epub 2020 Sep 29.
Androgen-producing tumors in women are rare neoplasms that can cause secondary virilizing characteristics. Of patients presenting with symptoms of hyperandrogenism, these tumors are found in ∼0.2% of cases. Androgen-producing tumors can arise from the ovary or the adrenal gland. Those arising from the ovary are rare, accounting for <5% of all ovarian tumors. This case presents a hilar Leydig cell tumor of the ovary, which resulted in secondary virilization of a 45-year-old female 2 months after cessation of combined oral contraceptives (COC). Laboratory findings showed markedly elevated total and free testosterone concentrations with normal dehydroepiandrosterone sulfate, however neither pelvic ultrasound nor magnetic resonance imaging demonstrated any masses. Venous sampling under fluoroscopy revealed supraphysiologic testosterone concentrations from the right ovarian vein suggesting the source. The patient underwent bilateral salpingo-oophorectomy revealing a 1.3 cm hilar cell tumor of the right ovary. This article reviews the clinical features, diagnosis, and treatment of hilar Leydig cell tumors and describes the long-term complications of supraphysiologic testosterone levels. As the tumor presented after cessation of COC, we also review the mechanisms by which COC might suppress supraphysiologic androgen levels and mask the secondary virilizing effects of androgen-producing tumors.
女性产生雄激素的肿瘤是罕见的肿瘤,可导致继发性男性化特征。在出现高雄激素血症症状的患者中,这些肿瘤约占 0.2%。产生雄激素的肿瘤可起源于卵巢或肾上腺。起源于卵巢的肿瘤很少见,占所有卵巢肿瘤的<5%。本病例介绍了一例卵巢门部的勒迪厄细胞瘤,导致一名 45 岁女性在停用复方口服避孕药(COC)后 2 个月出现继发性男性化。实验室检查显示总睾酮和游离睾酮浓度显著升高,脱氢表雄酮硫酸酯正常,但盆腔超声和磁共振成像均未发现任何肿块。透视下静脉取样显示右侧卵巢静脉的睾酮浓度高于生理水平,提示其来源。患者接受了双侧输卵管卵巢切除术,显示右侧卵巢有 1.3cm 的门部细胞肿瘤。本文回顾了门部勒迪厄细胞瘤的临床特征、诊断和治疗,并描述了高生理水平睾酮的长期并发症。由于肿瘤在 COC 停药后出现,我们还回顾了 COC 抑制高生理雄激素水平并掩盖产生雄激素的肿瘤的继发性男性化作用的机制。