SUN-101 “Ovaries Gone Rogue”: Hyperandrogenism Secondary to Ovarian Steroid Cell Tumor

Abstract Disclosure: A.M. Aviles Melendez: None. O. Onwudiwe: None. L.F. Chavez: None. Hyperandrogenism in females, presenting as virilization, calls for evaluation of adrenal versus ovarian source. Differential diagnosis includes polycystic ovarian syndrome, non-classical congenital adrenal hyperplasia, medications, hypercortisolism, and androgen producing tumors, seen in ∼0.2% cases. Less than 5% of androgen producing tumors derive from ovaries, with steroid cell tumors comprising less than 0.1% of ovarian tumors. We present a case of a postmenopausal female with rapidly progressive hirsutism in the setting of ovarian steroid cell tumor and concomitant mild autonomous cortisol secretion (MACS). A 75-year-old female with history of hypothyroidism, type 2 diabetes mellitus, obesity, hypertension, breast cancer, and chronic kidney disease presenting for evaluation of hirsutism, frontal balding, clitoromegaly, voice deepening, weight gain, rapidly developing and worsening over the previous 6 months, and an incidentally discovered right-sided adrenal mass. Uterine fibroids led to total hysterectomy at age 37, with intact ovaries. Denied androgenic steroid or minoxidil use. Physical examination pertinent for obesity, frontal balding, and facial, abdominal, back, and extremity hirsutism. Abdominal CT scan and MRI both showed a 1.6 cm right-sided adrenal adenoma. Transvaginal ultrasound failed to show reproductive organs. Laboratory values remarkable for elevated levels of total and free testosterone levels, at 482 ng/dL (N: 8-60 ng/dL), and 17.1 ng/dL (N: <0.13-0.79 ng/dL), respectively, elevated androstenedione: 5.21 ng/mL (N: 0.130-0.820 ng/mL), and 17-hydroxyprogesterone. Normal plasma metanephrines, renin, aldosterone, salivary and urinary cortisol. Low levels of DHEA-S: 11 ug/dL (N: 26-460 ug/dL), and ACTH: 11 pg/mL (N: 0-46 pg/mL). Dexamethasone-androgen 48-hour suppression test (DST) did not suppress testosterone levels, indicating ovarian source of hyperandrogenism, for which referred for surgery. Underwent bilateral salpingo-oophorectomy, finding a 2.7cm steroid cell tumor confined to the right ovary with benign features, and stromal hyperthecosis on the left ovary. Total and free testosterone levels postoperatively decreased to 11ng/dL and 0.21ng/dL, respectively. Cortisol decreased but not suppressed with initial DST. Test repeated without suppression, establishing concomitant MACS diagnosis. Referred for adrenalectomy.This case highlights the importance of detailed biochemical investigation of hyperandrogenism, as imaging may fail to show abnormalities. Steroid cell tumors, usually seen on reproductive age females, are rarely encountered, making our postmenopausal patient an even more uncommon case. Clinical and biochemical improvement of hyperandrogenism was seen after oophorectomy, but in the setting of concomitant MACS due to adrenal adenoma, adrenalectomy will be essential in achieving resolution. Presentation: Sunday, July 13, 2025