MON-179 - Persistent Hyperandrogenism Despite Prolactin Normalization: A Case of Coexisting Microprolactinoma, PCOS, and Functional Adrenal Hyperandrogenism

Background: Hyperprolactinemia occurs in 12% of women with polycystic ovary syndrome (PCOS), with microprolactinomas accounting for approximately 25% of these cases. Adrenal hyperandrogenism (HA) affects 20-30% of women with PCOS. Coexistence of these conditions presents diagnostic challenges, as hyperprolactinemia can independently elevate adrenal androgens and mimic PCOS findings.

Clinical

Case: A 38-year-old G1P0 woman presented with oligomenorrhea, male-pattern alopecia, galactorrhea, weight gain, and progressive hirsutism. Initial laboratory evaluation showed: prolactin (PRL) 90.68 ng/mL, total testosterone 15 ng/dL, free testosterone 2.4 pg/mL, androstenedione 66 ng/dL, DHEA-S 292 mcg/dL, 17-hydroxyprogesterone (17-OHP) 16 ng/dL, LH 2.55 mIU/mL, and FSH 3.66 mIU/mL. ACTH, IGF-1, and morning cortisol, and 1 mg dexamethasone suppression test were normal. Pituitary MRI identified a 7 mm microadenoma. Pelvic ultrasound revealed a 2.2 cm simple ovarian cyst, and abdominal MRI excluded adrenal tumor.

She was diagnosed with micro-prolactinoma and started bromocriptine with improvement in galactorrhea and menstrual regularity. Due to intolerance, she was transitioned to cabergoline. Despite PRL normalization, hirsutism persisted. In 2021, androstenedione was 87 ng/dL and DHEA-S 376 mcg/dL. In 2023, ACTH-stimulated 17-OHP was normal at 230 ng/dL and stimulated DHEA-S was 279 mcg/dL, excluding non-classic congenital adrenal hyperplasia (NCAH). The microadenoma was stable on follow up MRI. She was diagnosed with PCOS, adrenal HA, and hyperprolactinemia secondary to pituitary microadenoma, and continued on cabergoline.

Discussion: This case illustrates diagnostic complexity when micro-prolactinoma coexists with PCOS and adrenal HA. Cabergoline reduces DHEA-S levels by ~ 30% at 1 year. However, persistent elevated DHEA-S and hirsutism despite prolactin normalization suggest an independent source of androgen excess rather than prolactin-mediated effects alone. Approximately 13% of patients with controlled prolactinomas demonstrate PCOS features, while 2.8-10% of PCOS patients have prolactinomas. The patient met Rotterdam criteria for PCOS (oligomenorrhea and hyperandrogenism), rendering ultrasound findings irrelevant for diagnosis. ACTH stimulation testing with normal 17-OHP response excluded NCAH, which can mimic PCOS. Elevated androstenedione with normal ACTH-stimulated 17-OHP, combined with persistently elevated DHEA-S despite cabergoline therapy, confirmed functional adrenal HA—a phenotype observed in up to 30% of PCOS patients.

This case demonstrates that persistent HA following prolactin normalization indicates coexisting PCOS with adrenal androgen excess rather than solely prolactin-mediated effects, requiring comprehensive evaluation to characterize the specific HA phenotype and guide appropriate long-term management.

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