Kendra Frey, MD: No financial relationships to disclose
Introduction Adrenal incidentalomas are detected in ~5% of patients. In contrast, bilateral adrenal masses are less common, accounting for ~14% of all adrenal incidentalomas. Adenomas are the most common cause of bilateral nodules and may be nonfunctioning or functioning. Functioning adenomas usually secrete cortisol, as either overt Cushing syndrome or mild autonomous cortisol secretion (MACS). Less frequently, they secrete aldosterone, co-secrete hormones, or rarely, produce androgens. Hormone excess with bilateral masses presents significant diagnostic and therapeutic challenges. Hypersecretion may be unilateral or bilateral, and distinguishing these is crucial for management. Diagnostic complexity is compounded by hormonal co-secretion, and therapy must be individualized.
Case Description A 67-year-old female with HTN, T2DM, obesity, and CKD3 was hospitalized for abdominal pain and emesis due to norovirus infection. On admission she had severe hypertension and hypokalemia, and CT abdomen revealed bilateral 2.5-2.9cm lipid rich adrenal nodules. After discharge, biochemical evaluation was initiated to assess for functioning adenomas.
Two separate 1mg dexamethasone suppression tests were consistent with MACS (baseline DHEA-S and ACTH confirmed diagnosis). Bone density scan to assess comorbidities revealed osteopenia.
Initial ARR was not suggestive of PA, but clinical suspicion remained high due to hypokalemia and severe HTN. After stopping MRA and ARB, ARR of 6.8 revealed PA (aldosterone 14.2 ng/dL by LC-MS, DRC 2.1 pg/mL).
AVS for cortisol lateralization was completed due to presence of T2DM, obesity, osteopenia and HTN. No lateralization was found.
Medical management of MACS and PA is being initiated with levoketoconazole and spironolactone.
Discussion This case highlights complexity inherent in evaluation and management of bilateral adrenal masses, particularly when hormonal co-secretion is present. While excess cortisol and aldosterone can each be addressed surgically or medically, coexisting MACS and PA complicates diagnosis and therapeutic decisions.
In this patient, consideration of surgery was necessary due to presence of multiple comorbidities associated with MACS which may improve with adrenalectomy. In contrast, probability of aldosterone lateralization was deemed intermediate by clinical, biochemical, and imaging features. As a result, AVS assessed cortisol rather than aldosterone lateralization.
Importantly, coexisting PA limited applicability of traditional AVS cortisol-to-aldosterone ratio to assess cortisol lateralization. Instead, AVS relied on cortisol-to-metanephrine ratio, per established protocols, to account for confounding aldosterone hypersecretion. In absence of clear lateralization, medical therapy was favored over surgery. This management reflects a personalized approach and shared decision making.
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