ATP2B3-Mutated Aldosterone-Producing Lesions Linked to Higher Biochemical Cure Rates

An international observational study published in Hypertension compared clinical and biochemical phenotypes of aldosterone-producing lesions harboring ATP1A1 and ATP2B3 mutations. Investigators at 16 centers collected medical-record data for 300 patients with primary aldosteronism: 204 with ATP1A1 mutations and 96 with ATP2B3 mutations. Mean age was 57±11 years, and 85% were men. Histopathology and peripheral and adrenal-vein steroid profiles were compared where available.

ATP2B3 mutations were associated with lower serum potassium, higher lateralization indices, and stronger contralateral suppression. Postoperative biochemical cure occurred in 96% of the ATP2B3 group versus 83% of the ATP1A1 group (P=0.02). Multiple CYP11B2-positive lesions were observed in 27% versus 47%, respectively (P=0.03). Among 126 patients with baseline peripheral steroid profiling, median aldosterone was 31 ng/dL (interquartile range, 20–43) with ATP2B3 mutations versus 23 ng/dL (11–38) with ATP1A1 mutations (P=0.03).

The findings suggest that these two mutation groups have distinct phenotypes and postoperative biochemical outcomes despite often being grouped together as ATPase mutations. Interpretation is limited by the observational design and incomplete availability of histopathology and steroid profiling. The abstract does not provide postoperative outcome denominators or follow-up duration, and biochemical cure should not be equated with resolution of hypertension.