MON-468 - Functional Contralateral Adrenal Disease: A Spectrum of Hypercortisolism and Hyperaldosteronism

Background

Adrenal adenomas represent the most frequently encountered adrenal incidentalomas and are identified in ~3–7% of adults undergoing abdominal imaging, with prevalence rising to ~10% in individuals older than 70 years. The majority of these lesions are nonfunctioning (80–85% of cases), while 15–20% demonstrate hormonal activity. Evaluation of adrenal adenomas prior to surgical intervention includes biochemical testing to identify autonomous hormone secretion and radiographic assessment to estimate malignancy risk.

Case

A 59-year-old woman with a medical history including Ehlers-Danlos syndrome, papillary thyroid carcinoma status post total thyroidectomy, postsurgical hypothyroidism, hyperparathyroidism status post parathyroid adenoma resection, obesity, Type 2 diabetes mellitus, and hypertension, was referred for endocrine evaluation of a right adrenal mass (2.5cm). Biochemical testing showed failure of a 1-mg overnight dexamethasone suppression test cortisol of 4.58 µg/dL ( < 1.8 µg/dL), elevated late-night salivary cortisol level 0.239 µg/dL ( < 0.010–0.090), and normal 24-hour urinary free cortisol 26 ug/24hr (6-42 ug/24hr). Morning ACTH level was low, 2.8 pg/mL (7.2-63.3 pg/mL), as was DHEA-S 26 µg/dL (70-188 µg/dL), supporting a diagnosis of ACTH-independent Cushing’s syndrome. The patient also had primary hyperaldosteronism, with low renin 0.208 ng/mL/hr (0.167-5.380 ng/mL/hr) and aldosterone 6.8 ng/dL (5-30 ng/dL) with aldosterone-to-renin ratio of 32.7 ( < 20).

The adrenal mass was monitored radiographically for four years during which it enlarged to 4.2cm. A laparoscopic right adrenalectomy was performed to exclude malignancy. Pathology confirmed a benign adrenal adenoma. Postoperatively, her morning ACTH level corrected to 65.7 pg/mL, with a cortisol of 15.7 µg/dL. A follow up 1-mg overnight dexamethasone suppression test cortisol was 0.7 µg/dL, indicating normal suppression. Spironolactone therapy was initiated to control hypertension and normalize renin.

Discussion

Postoperative ACTH rise and normalization of dexamethasone suppression confirmed the right adrenal adenoma as the primary source of cortisol excess. In cases of dual cortisol and aldosterone excess, surgical management should be prioritized to resolve Cushing’s syndrome while preserving residual adrenal function, and medical therapy reserved for the treatment of persistent hyperaldosteronism.

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