MON-275 Non concordant side in concomitant Mild Autonomous Cortisol Secretion and Primary Aldosteronism: How should we prioritize treatment?

Abstract Disclosure: N.E. Fretes Oviedo: None. M. Eldib: None. R. Perez-Soto: None. P. Rao: None. Introduction: Secondary hypertension is often caused by renovascular abnormalities or endocrine disorders. Among endocrine causes, primary aldosteronism (PA) is the most common but often undiagnosed. Other causes include pheochromocytoma, Cushing's syndrome, and hyperthyroidism. Definitive etiology can remain elusive and complicate management strategies. Case Presentation: A 69-year-old male with a history of PA, multiple hospitalizations for hypertensive urgency, one leading to non-ST elevation myocardial infarction, heart failure with preserved ejection fraction, and a left adrenal nodule, presented for evaluation of resistant hypertension. His medication regimen included Nifedipine XL 90 mg daily, Carvedilol 12.5 mg twice daily, Doxazosin 2 mg daily, Clonidine 0.1 mg daily, Eplerenone 100 mg twice daily, Losartan 50 mg daily, and Potassium 60 mEq daily. He denied fatigue, proximal muscle weakness, stretch marks, easy bruising, weight changes, or fractures. No prediabetes or impaired fasting glucose. A 1 mg-dexamethasone suppression (DST) test revealed an elevated cortisol level (6.6 mcg/dL) and an appropriate dexamethasone level (255 ng/dL), consistent with Mild Autonomous Cortisol Secretion (MACS). His ACTH was low-normal (7 pg/mL), and DHEA-S was 81 mcg/dL. Late- night salivary free cortisol and 24-hour urine free cortisol were normal. A CT scan of the adrenal glands showed bilateral thickening, with a 2.6 x 3.5 cm left adrenal nodule of 3 Hounsfield units (H.U.), suggestive of adenoma. Adrenal vein sampling with cosyntropin stimulation revealed a Lateralization Index (LI) of 4.2:1 with the excess secretion from the normal appearing right adrenal gland. The source of MACS was likely the adenoma on the left. The case was discussed at the adrenal tumor board. Given patient's multiple hospitalizations for hypertensive urgency, PA was considered to have the greatest impact on his health, and a right adrenalectomy was performed. Post-surgery AM cortisol was elevated at 24.1 mcg/dL. Discussion: Aldosterone and cortisol excess can independently increase cardiovascular mortality, fragility fractures, and overall mortality. Few studies address the coexistence of these conditions. Hormone excess is usually thought to come from the same nodule, though in this case, it was likely from separate sources, we need to repeat the DST at least three months after surgery to confirm this. Our patient's resistant hypertension may have resulted from the combination of both endocrine disorders. Conclusion: While surgical adrenalectomy may reverse cardiac remodeling in patients with PA and concurrent MACS, there is limited guidance on how to prioritize treatment when hormone excess originates from different adrenal glands. In such cases, clinical judgment and an individualized approach are essential, along with optimal medical management to mitigate long-term complications and risks. Presentation: Monday, July 14, 2025