Objective: Resistant hypertension in the absence of overt Cushingoid features can mask autonomous cortisol secretion (ACS), a frequently overlooked secondary cause that contributes to persistent blood pressure elevation and increased cardiovascular risk. This study aims to present the diagnostic pathway and therapeutic impact of identifying ACTH-independent cortisol excess in a patient with long-standing hypertension and progressive proximal muscle weakness.Design and method: A 56-year-old woman with hypertension and hypercholesterolaemia presented with progressive proximal muscle weakness and uncontrolled blood pressure despite multidrug therapy (perindopril, amlodipine, indapamide, doxazosin). Routine labs were unremarkable. Endocrine evaluation included plasma renin activity, aldosterone, potassium, ACTH, DHEA-S, 24-hour urinary free cortisol, and 1 mg overnight dexamethasone suppression test. Imaging consisted of abdominal CT to assess adrenal morphology. Based on hormonal and radiological findings, unilateral adrenalectomy was performed, and postoperative hormonal response and blood pressure outcomes were evaluated. Results: Renin was suppressed (0.49 ng/mL/h) with normal aldosterone and potassium, excluding primary aldosteronism. Urinary free cortisol remained within normal limits; however, dexamethasone suppression was inadequate (5.8 μg/dL). ACTH was low-normal and DHEA-S markedly reduced, consistent with ACTH-independent cortisol secretion. CT revealed a 35-mm left adrenal adenoma. Laparoscopic adrenalectomy confirmed a benign adrenocortical tumour. Postoperatively, cortisol decreased to 1.2 μg/dL, necessitating glucocorticoid replacement. At 3-month follow-up, blood pressure normalised with reduction in antihypertensive therapy, and muscle strength significantly improved. Conclusions: Autonomous cortisol secretion should be suspected in patients with resistant hypertension and subtle catabolic features, even without overt Cushingoid appearance. Early identification of ACS enables curative intervention, improves blood pressure control, and prevents long-term cardiovascular consequences of chronic cortisol excess. This case highlights the importance of systematic endocrine evaluation in difficult-to-treat hypertension.
Ebeoğlu et al. (Fri,) studied this question.