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20 April 2023 AperTO - Archivio Istituzionale Open Access dell'Università di Torino Original Citation: Diagnosis and treatment of primary aldosteronism Published version: DOI:10.1016/S2213-8587(21)00210-2 Terms of use: Open Access (Article begins on next page) Anyone can freely access the full text of works made available as "Open Access". Works made available under a Creative Commons license can be used according to the terms and conditions of said license. Use of all other works requires consent of the right holder (author or publisher) if not exempted from copyright protection by the applicable law. Availability: This is a pre print version of the following article: This version is available http://hdl.handle.net/2318/1863584 since 2022-06-06T17:37:44Z
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Diagnosis and treatment of primary aldosteronism

Apr 20, 2023

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Health & Medicine

Hiep Nguyen

Primary aldosteronism is a common cause of secondary hypertension associated with excess cardiovascular morbidities. Primary aldosteronism is underdiagnosed because it does not have a specific, easily identifiable feature and clinicians are poorly aware of the disease. The diagnostic workup is a multistep process of screening, confirmatory testing, and subtype differentiation of unilateral from bilateral forms for therapeutic management. Adrenal venous sampling is key for reliable subtype identification but may be bypassed in patients with specific characteristics.

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For unilateral disease, surgery offers the possibility of cure with total laparoscopic unilateral adrenalectomy the treatment of choice. Bilateral forms are mainly treated with mineralocorticoid receptor antagonists. Prompt diagnosis of primary aldosteronism and implementation of targeted treatment strategies mitigate aldosteronespecific target organ damage, and outcomes are excellent with appropriate patient management. Advances in molecular histopathology challenge the traditional concept of primary aldosteronism as a binary disease, in which unilateral aldosterone-producing adenoma is juxtaposed with bilateral adrenal hyperplasia. Somatic mutations drive autonomous aldosterone production in most adenomas.