SAT-159 - A Rare Case of Postmenopausal Hyperandrogenism Due to Bilateral Ovarian Leydig Cell Hyperplasia.

Background:
Postmenopausal hyperandrogenism is uncommon and warrants evaluation for a pathologic androgen source. Non-neoplastic ovarian causes, such as Leydig cell hyperplasia, are exceedingly rare and diagnostically challenging, as imaging often fails to identify ovarian pathology despite severe biochemical and clinical hyperandrogenism.

Case Presentation:
A 69-year-old postmenopausal woman with hypertension, type 2 diabetes mellitus, and hyperlipidemia was referred for evaluation of progressive hyperandrogenic symptoms. Over four years, she developed worsening androgen-dependent hair growth involving the face, chest, and trunk, progressing from fine to coarse terminal hair, along with androgenic alopecia over the vertex scalp and voice deepening. She had underwent hysterectomy with ovarian preservation at age 24. Physical examination revealed excessive terminal hair growth over the face, chest, and extremities with scalp hair thinning and temporal recession. There were no clinical features of hypercortisolism such as central obesity, facial rounding, dorsocervical fat pad, wide striae and easy bruising. Laboratory evaluation showed marked hyperandrogenemia with total testosterone of 150 ng/dL (ref. 0–41ng/dL), confirmed by LC–MS at 125 ng/dL (ref. 8–60 ng/dL), and elevated free testosterone 3.88 ng/dL; ref. < 0.13–0.84 ng/dL). Sex hormone–binding globulin was normal. Gonadotropins were in the postmenopausal range LH 40.8 mIU/mL, FSH 65.0 mIU/mL. DHEA sulfate, 17-hydroxyprogesterone, and midnight salivary cortisol levels were normal. Transvaginal ultrasound failed to visualize ovaries, MRI of the abdomen and pelvis showed no adrenal or ovarian mass. Given progressive symptoms and biochemical findings consistent with an ovarian source, she underwent laparoscopic bilateral salpingo-oophorectomy. Ovarian histopathology revealed bilateral nodular Leydig cell hyperplasia. Postoperatively, testosterone normalized within three months total testosterone level of 6 ng/dL , free testosterone of 0.9 ng/dL , and spironolactone was discontinued.

Discussion:
The differential diagnosis of postmenopausal hyperandrogenism includes adrenal or ovarian neoplasms, ovarian hyperthecosis, congenital adrenal hyperplasia, hypercortisolism, and rare non-neoplastic ovarian disorders such as Leydig cell hyperplasia. Leydig cell hyperplasia is a benign condition characterized by diffuse or microscopic proliferation of androgen-producing Leydig cells, often without ovarian enlargement, rendering imaging frequently nondiagnostic. Biochemical localization is therefore critical; markedly elevated testosterone with normal DHEA sulfate strongly suggests an ovarian source. In symptomatic postmenopausal women with concordant biochemical findings, bilateral salpingo-oophorectomy is both diagnostic and curative, even when imaging is unrevealing.

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