7521 Unmasking of PCOS after Microprolactinoma Treatment

Abstract Disclosure: F. Erenler: None. B. Aydogan Mathyk: None. Background: PCOS and prolactinomas are two of the leading causes of secondary amenorrhea. Hirsutism is a common finding for both diagnosis and can be the presenting symptom. We are presenting a case of secondary amenorrhea, initially diagnosed with microprolactinoma without signs of hyperandrogenism, which progressed to overt PCOS after prolactinoma treatment. Case: A 22-year-old female with history of Hashimoto’s hypothyroidism presented with secondary amenorrhea. Patient was on combined oral contraception pills (COC) for menstrual regulation and discontinued them with a desire of natural cycles. After the discontinuation of COC, her menstrual cycles did not return for four months and patient was subsequently found to have a microprolactinoma with prolactin (PRL) level 70.6 ng/mL - high (nl: 2.8-29.2 ng/mL), LH 6.1 mIU/mL (follicular phase: 1.9-12.5 mIU/mL), FSH 2.4 mIU/mL - low (follicular phase: 2.5-10.2 mIU/mL), androstenedione 132 ng/mL (follicular phase: 51-213 ng/mL), testosterone 36 ng/mL (nl: 2-45 ng/mL), AMH 33 ng/mL - high (nl: 1.02-14.63 ng/mL), DHEA-S 241 mcg/dL (nl: 44-286 mcg/dL), HCG neg. MR Sella showed a 0.5 cm hypoenchancing pituitary lesion, confirming the diagnosis of prolactinoma. Patient was started treatment with cabergoline 0.25 mg twice a week and PRL level trended down to 3.9 ng/mL. With normalization of PRL, patient started complaining of new onset hirsutism without return of her menses. Ferriman Gallway score was 8. Further workup showed elevated androgen markers: LH 25.7 mIU/mL - high (follicular phase: 1.9-12.5 mIU/mL), FSH 5.0 mIU/mL (follicular phase: 2.5-10.2 mIU/mL), PRL 4.7 ng/mL -low (nl: 4.8-23.2 ng/mL), androstenedione 341 ng/mL -high (41-262 ng/mL), E2 63.4 pg/mL (nl: 12.5-160 pg/mL), AMH 22.3 ng/mL – high (nl: 1.23-11.61 ng/mL), testosterone 94.7 ng/mL - high (nl: 10-55 ng/mL), DHEA-S 261 mcg/dL (nl:110-431.7 mcg/dL). ACTH stimulation test pursued to rule out NCAH and17-OH progesterone levels were within normal range after stimulation. Pelvis US obtained due to high suspicion for PCOS and was consistent with polycystic ovaries. The diagnosis of PCOS confirmed by Rotterdam criteria. Patient has phenotype A PCOS by the definition of NIH 2012 consensus. Conclusion: Hyperprolactinemia and pituitary adenomas can cause secondary amenorrhea. In our case, the treatment of hyperprolactinemia with cabergoline unmasked the underlying PCOS. The clinical and biochemical manifestation of PCOS became apparent following the removal of prolactin’s suppressive effect on GnRH. Presentation: 6/2/2024