关键词: 11-hydroxysteroid dehydrogenase hypertension hypokalemia licorice pseudohyperaldosteronism

Mesh : Humans Glycyrrhiza / adverse effects Female Male Middle Aged Hyperaldosteronism Glycyrrhetinic Acid / pharmacology Adult Hypokalemia / chemically induced 11-beta-Hydroxysteroid Dehydrogenase Type 2 / metabolism Aged Hypertension Aldosterone / metabolism blood Renin / blood metabolism

来  源:   DOI:10.3390/ijms25137454   PDF(Pubmed)

Abstract:
Pseudohyperaldosteronism (PHA) is characterized by hypertension, hypokalemia, and a decrease in plasma renin and aldosterone levels. It can be caused by several causes, but the most frequent is due to excess intake of licorice. The effect is mediated by the active metabolite of licorice, glycyrrhetinic acid (GA), which acts by blocking the 11-hydroxysteroid dehydrogenase type 2 and binding to the mineralocorticoid receptor (MR) as an agonist. The management of licorice-induced PHA depends on several individual factors, such as age, gender, comorbidities, duration and amount of licorice intake, and metabolism. The clinical picture usually reverts upon licorice withdrawal, but sometimes mineralocorticoid-like effects can be critical and persist for several weeks, requiring treatment with MR blockers and potassium supplements. Through this case series of licorice-induced PHA, we aim to increase awareness about exogenous PHA, and the possible risk associated with excess intake of licorice. An accurate history is mandatory in patients with hypertension and hypokalemia to avoid unnecessary testing. GA is a component of several products, such as candies, breath fresheners, beverages, tobacco, cosmetics, and laxatives. In recent years, the mechanisms of action of licorice and its active compounds have been better elucidated, suggesting its benefits in several clinical settings. Nevertheless, licorice should still be consumed with caution, considering that licorice-induced PHA is still an underestimated condition, and its intake should be avoided in patients with increased risk of licorice toxicity due to concomitant comorbidities or interfering drugs.
摘要:
假性醛固酮增多症(PHA)的特征是高血压,低钾血症,血浆肾素和醛固酮水平下降。它可能是由几个原因引起的,但最常见的是由于过量摄入甘草。这种作用是由甘草的活性代谢产物介导的,甘草次酸(GA),它通过阻断11-羟基类固醇脱氢酶2型并作为激动剂与盐皮质激素受体(MR)结合而起作用。甘草诱导的PHA的管理取决于几个个体因素,比如年龄,性别,合并症,甘草摄入量的持续时间和数量,和新陈代谢。临床情况通常在甘草戒断后恢复,但有时盐皮质激素样作用可能很关键,并持续数周,需要用MR阻滞剂和钾补充剂治疗。通过这一系列甘草诱导的PHA,我们的目标是提高对外源性PHA的认识,以及过量摄入甘草可能带来的风险。高血压和低钾血症患者必须有准确的病史,以避免不必要的检查。GA是几个产品的组成部分,如糖果,呼吸清新剂,饮料,烟草,化妆品,和泻药。近年来,甘草及其活性化合物的作用机制得到了更好的阐明,表明它在几种临床环境中的益处。然而,甘草仍应谨慎食用,考虑到甘草引起的PHA仍然是一个被低估的情况,由于伴随的合并症或干扰药物,甘草毒性风险增加的患者应避免其摄入。
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