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原发性醛固酮增多症与阻塞性睡眠呼吸暂停:偶然关联还是病理生理联系?

Primary Aldosteronism and Obstructive Sleep Apnea: Casual Association or Pathophysiological Link?

机构信息

Division of Internal Medicine 4 and Hypertension Unit, Department of Medical Sciences, University of Torino, Torino, Italy.

出版信息

Horm Metab Res. 2020 Jun;52(6):366-372. doi: 10.1055/a-1133-7255. Epub 2020 Mar 27.

Abstract

The coexistence of aldosterone oversecretion and obstructive sleep apnea is frequently observed, especially in patients with resistant hypertension, obesity, and metabolic syndrome. Since aldosterone excess and sleep apnea are both independently associated with an increased risk of cardiovascular disease, to investigate whether their coexistence might be attributed to common predisposing conditions, such as metabolic disorders, or to an actual pathophysiological interconnection appears of great importance. Fluid overload and metabolic abnormalities relating to aldosterone oversecretion may be implicated in obstructive sleep apnea development. Nocturnal intermittent hypoxia may in turn exacerbate renin-angiotensin-aldosterone system activity, thus leading to hyperaldosteronism. Furthermore, fat tissue excess and adipocyte secretory products might predispose to both sleep apnea and aldosterone oversecretion in subjects with obesity. Consistent with these evidences, obstructive sleep apnea frequently affects patients with primary aldosteronism. Conversely, whether primary aldosteronism is more prevalent in individuals affected by obstructive sleep apnea compared to the general population remains controversial.

摘要

醛固酮分泌过多和阻塞性睡眠呼吸暂停经常同时存在,尤其是在难治性高血压、肥胖和代谢综合征患者中。由于醛固酮过多和睡眠呼吸暂停均独立与心血管疾病风险增加相关,因此研究这两种情况同时存在是否归因于共同的易患条件,如代谢紊乱,或归因于实际的病理生理关联显得尤为重要。醛固酮分泌过多相关的液体超负荷和代谢异常可能与阻塞性睡眠呼吸暂停的发生有关。反过来,夜间间歇性低氧可能会加重肾素-血管紧张素-醛固酮系统的活性,从而导致醛固酮增多症。此外,肥胖患者的脂肪组织过多和脂肪细胞分泌产物可能使睡眠呼吸暂停和醛固酮分泌过多的易患性增加。这些证据表明,阻塞性睡眠呼吸暂停常影响原发性醛固酮增多症患者。相反,原发性醛固酮增多症在阻塞性睡眠呼吸暂停患者中的患病率是否高于普通人群仍存在争议。

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