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Subclinical Primary Aldosteronism
Annals of Internal Medicine ( IF 39.2 ) Pub Date : 2017-10-10 , DOI: 10.7326/m17-2237
E. Victor Adlin 1
Affiliation  

The prevalence of primary aldosteronism (PA) in patients with hypertension has been widely disputed since the syndrome was first described by Jerome W. Conn in 1956. It was originally believed to be rare, but in 1964 Dr. Conn noted that 2 hallmarks of PA, low plasma renin activity (PRA) and adrenal adenomas, were present in many hypertensive persons. He suggested that the prevalence of PA, rather than less than 1%, might be as high as 20% (1).
Within the next few years, low PRA levels were indeed noted in hypertensive patients (2). Increased mineralocorticoid activity was suspected in these patients because of low salivary sodium–potassium ratios, a marker of mineralocorticoid excess (3), and an exaggerated decrease in blood pressure after treatment with aminoglutethimide, a blocker of adrenal steroid hormone production (4), and with spironolactone, an inhibitor of the mineralocorticoid receptor (5). But urinary aldosterone excretion was normal in these patients, so researchers postulated that the suspected mineralocorticoid excess was caused by an unknown mineralocorticoid or by aldosterone, despite its normal levels.


中文翻译:

亚临床原发性醛固酮增多症

自1956年杰罗姆·W·康恩(Jerome W. Conn)首次描述高血压综合征以来,原发性醛固酮增多症(PA)的患病率一直受到广泛争议。最初被认为是罕见的,但1964年,康恩博士指出,PA的两个特点高血压患者中存在血浆肾素活性低(PRA)和肾上腺腺瘤。他建议PA的患病率可能会高达20%(而不是少于1%)(1)。
在接下来的几年内,确实在高血压患者中发现PRA水平较低(2)。这些患者怀疑盐皮质激素活性增加是由于唾液钠钾比率低,盐皮质激素过量的标志物(3)以及用氨基谷氨酰胺治疗,肾上腺类固醇激素产生的阻滞剂后血压的过分降低(4)和螺内酯是盐皮质激素受体的抑制剂(5)。但是这些患者的尿中醛固酮排泄是正常的,因此研究人员推测,尽管盐皮质激素水平正常,但怀疑的盐皮质激素过量是由未知的盐皮质激素或醛固酮引起的。
更新日期:2017-10-10
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