Endocrine Abstracts

JOINT398

A 69-year-old male was referred to the Endocrinology clinic for evaluation of adrenal-origin hypertension. Despite being on optimized doses of four antihypertensive drugs, including two diuretics (amlodipine 10 mg, losartan 100 mg, chlorthalidone 50 mg, hydralazine 100 mg, and spironolactone 300 mg), his blood pressure remained poorly controlled. His history revealed resistant hypertension since age 32, raising suspicion of a secondary cause. In 2021, clinical and cardiological evaluations were undertaken ahead of surgery for a left-sided cervical tumor, initially suspected to be a schwannoma with pheochromocytoma. During surgery, the tumor was identified as a benign fusocellular neoplasm affecting the vagus nerve. Despite this, his hypertension and hypokalemia persisted, prompting further investigation. Initial laboratory tests revealed elevated serum aldosterone levels (39.8 ng/dL), suppressed plasma renin activity (0.1 ng/mL/h), and recurring hypokalemia (ranging between 2.9–3.6 mEq/l). Two assessments of urinary metanephrines showed normal levels, renal function was preserved, and sleep apnea was excluded as a contributing factor. An MRI identified bilateral adrenal nodules, raising the suspicion of an endocrine etiology for his refractory hypertension. By 2023, his persistent hypertension and refractory hypokalemia prompted repeated evaluations, confirming elevated aldosterone levels, suppressed renin, and a high aldosterone-to-renin ratio. Imaging showed stable bilateral adrenal nodules, with the most notable being a 2.2 × 1.8 cm lesion in the left adrenal gland’s posterior limb. Adrenal vein sampling revealed markedly increased aldosterone secretion from the left adrenal gland, confirming unilateral primary hyperaldosteronism. In April 2024, the patient underwent successful left adrenalectomy. Histological analysis confirmed a benign corticomedullary adenoma. Postoperatively, blood pressure monitoring in May 2024 demonstrated normalized systolic and diastolic readings throughout the day. Spironolactone was discontinued, and the patient maintained control with atenolol, losartan, and a reduced dose of amlodipine (5 mg). Three months later, all biochemical markers, including creatinine, aldosterone, potassium, and renin levels, were within normal limits. This case underscores the critical need to investigate secondary causes of hypertension, especially in patients with resistant or early-onset disease. Early diagnosis and appropriate treatment of primary hyperaldosteronism not only optimize blood pressure control but also correct electrolyte imbalances and significantly reduce long-term cardiovascular risks. A multidisciplinary approach remains essential for achieving the best outcomes.