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Primary aldosteronism
Trends in Cardiovascular Medicine ( IF 9.3 ) Pub Date : 2021-03-26 , DOI: 10.1016/j.tcm.2021.03.005
John Funder 1
Affiliation  

In 1955 Dr Jerome Conn first documented primary aldosteronism (PA). Since then, screening, diagnosis and treatment have developed, in the process both refining and complicating management. Currently, screening requires 4–6 weeks of lead-up, including major changes in antihypertensive therapy, followed by a blood draw for plasma aldosterone concentration (PAC) and plasma renin activity (PRA) or concentration (PRC). Screening is considered indicative of PA on the basis of the PAC and the aldosterone to renin ratio (ARR). This is then followed by one or more of 6 confirmatory/exclusion tests. Three things have changed. First is now incontrovertible evidence that a single spot PAC is a deeply flawed index of true aldosterone status, so that many referred patients with PA fall at the first hurdle. A valid index of aldosterone status is an integrated value, measured as urinary aldosterone excretion (UEA) over 24 h. On the basis of the UEA, the prevalence of PA appears to be 3–5 times higher than the currently accepted figure of 5–10% of hypertensives. The second is the recognition that inadequately treated PA has a cardiovascular risk profile ~threefold that of matched essential hypertensives. Third is the realization that <1% of hypertensives are ever screened for PA, who are thus in double jeopardy for the risks of untreated PA on top of those for hypertension per se. Taken together, this a major if occult public health issue; if it is to be addressed, radical changes in management are needed. Some are in screening, which needs to be simply done on all newly-presenting hypertensives; others are major simplifications of screening in established hypertension. The front-line actors need to be Internists/Primary Care Providers; the costs will be significant, but much less than those of increased morbidity/premature mortality in unrecognized PA. Possible suggestions as to how best to address this constitute the final chapter of this article.



中文翻译:

原发性醛固酮增多症

1955 年 Jerome Conn 博士首次记录了原发性醛固酮增多症 (PA)。从那时起,筛查、诊断和治疗得到了发展,在这个过程中,管理既精细化又复杂化。目前,筛查需要 4-6 周的引导期,包括抗高血压治疗的重大变化,然后抽血检查血浆醛固酮浓度 (PAC) 和血浆肾素活性 (PRA) 或浓度 (PRC)。根据 PAC 和醛固酮与肾素比 (ARR),筛查被认为是 PA 的指征。然后进行 6 项确认/排除测试中的一项或多项。三件事发生了变化。首先,现在无可争议的证据表明,单点 PAC 是真实醛固酮状态的一个存在严重缺陷的指标,因此许多转诊的 PA 患者在第一关就跌倒了。醛固酮状态的有效指标是一个积分值,以 24 小时内的尿醛固酮排泄量 (UEA) 来衡量。根据 UEA,PA 的患病率似乎比目前接受的 5-10% 的高血压数字高 3-5 倍。第二个是认识到治疗不充分的 PA 的心血管风险约为匹配的原发性高血压的三倍。第三是认识到只有不到 1% 的高血压患者接受了 PA 筛查,因此与高血压本身相比,他们面临未经治疗的 PA 风险的双重危险。总而言之,这是一个重大而神秘的公共卫生问题;如果要解决这个问题,就需要彻底改变管理。有些正在筛查中,只需对所有新出现的高血压患者进行筛查;其他是已确定的高血压筛查的主要简化。一线演员需要是内科医生/初级保健提供者;成本将是巨大的,但远低于在未被承认的 PA 中增加发病率/过早死亡率的成本。关于如何最好地解决这个问题的可能建议构成了本文的最后一章。

更新日期:2021-03-26
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