Case Report: Primary aldosteronism coexisting with adrenal insufficiency in a 73-year-old woman with paradoxical hyponatremia

Introduction Primary aldosteronism (PA) and autoimmune polyglandular syndrome type 2 (APS-2) represent opposing ends of adrenal pathology—hyperfunction versus hypofunction. Their coexistence is exceptionally rare and diagnostically challenging. Case presentation A 73-year-old woman with a 30-year history of refractory hypertension and recent hyponatremia was diagnosed with PA (aldosterone-to-renin ratio 29.11, positive captopril challenge, left adrenal hyperplasia). Spironolactone controlled blood pressure but paradoxically worsened hyponatremia. Two independent circadian cortisol profiles confirmed persistently low cortisol with preserved normal rhythm (first: 118.65/100.80/50.25 nmol/L; second: 133.34/71.62/39.12 nmol/L at 08:00/16:00/00:00). In contrast, plasma ACTH levels sent to an external laboratory showed no circadian variation (08:00 7.19 pmol/L, 16:00 1.21 pmol/L, 00:00 1.68 pmol/L; reference 1.60-13.90 pmol/L). This discordance-preserved cortisol rhythmicity with absent ACTH rhythm-raised the possibility of a preanalytical artifact rather than secondary adrenal insufficiency, although this inference could not be definitively proven. Physical examination revealed skin hyperpigmentation, and her history of Hashimoto’s thyroiditis supported a clinically probable diagnosis of APS-2 (clinically probable Addison’s disease with autoimmune thyroid disease), given the absence of confirmatory 21-hydroxylase antibody testing and ACTH-stimulation testing. Intervention and outcomes Prednisone 5 mg daily was added to her regimen of spironolactone and levothyroxine. Her symptoms resolved, and serum sodium normalized. Conclusion This report describes a rare case of primary aldosteronism occurring in the setting of clinically probable APS-2. The discordant cortisol-ACTH pattern serves as a critical reminder that ACTH is highly labile; clinicians must interpret results holistically, integrating clinical context and circadian patterns, and remain mindful of diagnostic uncertainty when confirmatory assays cannot be completed.