Endocrinology and Metabolism

Original Article

Clinical Study
Changes in Glucose Metabolism after Adrenalectomy or Treatment with a Mineralocorticoid Receptor Antagonist for Primary Aldosteronism: Yu-Fang Lin, Kang-Yung Peng, Chia-Hui Chang, Ya-Hui Hu, Vin-Cent Wu, Shiu-Dong Chung, Taiwan Primary Aldosteronism Investigation (TAIPAI) Study Group; Endocrinol Metab. 2020;35(4):838-846. Published online December 2, 2020; DOI: https://doi.org/10.3803/EnM.2020.797

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Background
Data on the effects of excess aldosterone on glucose metabolism are inconsistent. This study compared the changes in glucose metabolism in patients with primary aldosteronism (PA) after adrenalectomy or treatment with a mineralocorticoid receptor antagonist (MRA).
Methods
Overall, 241 patients were enrolled; 153 underwent adrenalectomy and 88 received an MRA. Fasting glucose, homeostatic model assessment of insulin resistance (HOMA-IR), and homeostatic model assessment of β-cell function (HOMA-β) were compared between the treatment groups after 1 year. Plasma aldosterone concentration (PAC) and factors determining HOMA-IR and PAC were evaluated.
Results
No baseline differences were observed between the groups. Fasting insulin, HOMA-IR, and HOMA-β increased in both groups and there were no significant differences in fasting glucose following treatment. Multiple regression analysis showed associations between PAC and HOMA-IR (β=0.172, P=0.017) after treatment. Treatment with spironolactone was the only risk factor associated with PAC >30 ng/dL (odds ratio, 5.2; 95% confidence interval [CI], 2.7 to 10; P<0.001) and conferred a 2.48-fold risk of insulin resistance after 1 year compared with surgery (95% CI, 1.3 to 4.8; P=0.007).
Conclusion
Spironolactone treatment might increase insulin resistance in patients with PA. This strengthened the current recommendation that adrenalectomy is the preferred strategy for patient with positive lateralization test. Achieving a post-treatment PAC of <30 ng/dL for improved insulin sensitivity may be appropriate.

Citations

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Review Article

CTNNB1 Mutation in Aldosterone Producing Adenoma: Jian-Jhong Wang, Kang-Yung Peng, Vin-Cent Wu, Fen-Yu Tseng, Kwan-Dun Wu; Endocrinol Metab. 2017;32(3):332-338. Published online September 18, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.3.332

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Abstract PDF PubReader

Discoveries of somatic mutations permit the recognition of subtypes of aldosterone-producing adenomas (APAs) with distinct clinical presentations and pathological features. Catenin β1 (CTNNB1) mutation in APAs has been recently described and discussed in the literature. However, significant knowledge gaps still remain regarding the prevalence, clinical characteristics, pathophysiology, and outcomes in APA patients harboring CTNNB1 mutations. Aberrant activation of the Wnt/β-catenin signaling pathway will further modulate tumorigenesis. We also discuss the recent knowledge of CTNNB1 mutation in adrenal adenomas.

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