6444 The Cortisol Conundrum: A Case of Cushing’s Disease Masked by Cabergoline

Abstract Disclosure: A. Khan: None. T. Vedere: None. Introduction: The most common cause of endogenous hypercortisolism is Cushing’s disease (CD) accounting for 70% of the cases. We describe a case where the diagnosis of CD was delayed due to cabergoline (CBG) use. Case A 25-year-old male with history of OSA, multiple sclerosis, obesity, recurrent kidney stones, and a pituitary microadenoma, presumed to be a prolactinoma, presented with gynecomastia and erectile dysfunction (ED). He had developed gynecomastia in his teenage years. Workup showed elevated prolactin level (PRL) and MRI pituitary showed a 5mm pituitary adenoma. Patient was started on CBG 0.5 mg once a week and had been on it for 4 years at presentation. Most recent PRL had normalized to 13.7 (12.0-18.0) ng/ml and MRI pituitary showed stable size of the adenoma. He reported generalized weakness with proximal muscle weakness, weight gain, easy bruising, ED, decreased libido, and persistent gynecomastia for a few years. Interestingly, he had noted a 50 lb weight gain, low mood, and worsening striae when he was taken off CBG for 3 months in the past. Physical exam was significant for obese male with dorsocervical and supraclavicular fat pads, facial plethora, reduced motor power in proximal upper extremities and prominent wide purple striae on the abdomen. In the past, while on CBG, 24-hour urine free cortisol levels were 85.9 and 40.9 (4.0-50.0) mcg/24hrs in two collections. While briefly off CBG, 24-hour urine cortisol level was 254.2 mcg/24hrs. We obtained salivary cortisol levels which were elevated at 0.666 (<0.308) mcg/dL and 1.005 mcg/dL on two samples and ACTH was 67.6 (7.2-63.3) pg/ml while on CBG. IPSS results pointed to a pituitary source. Patient underwent transsphenoidal hypophysectomy and was discharged on hydrocortisone (HC). Pathology showed minute pituitary tissue, possible pituitary adenoma. Specimen was too small to perform staining for ACTH and PRL. Postoperatively, he has done well off HC with significant clinical improvement and normalization of salivary cortisol levels. Discussion Dopamine agonist such a CBG is the first line treatment of prolactinomas. The evidence for CBG use in CD has been controversial; some studies show almost a 40% decrease of cortisol levels. Given that CBG suppresses ACTH secretion by acting on dopamine receptor subtype 2, it would also mask CD by reducing cortisol levels in urine and serum. Our patient had equivocal results for 24-hour urine cortisol level for CD. While CBG adds to the armamentarium for these ACTH-PRL secreting pituitary adenomas, its use interferes with work up in patients with pituitary adenoma who are still undergoing diagnostic tests for pituitary function evaluation. Our case highlights a unique diagnostic challenge in the work up of CD. Presentation: 6/3/2024