Licorice-induced hypermineralocorticoidism
Article Abstract:
Licorice, ingested in excess, can cause retention of sodium and water, hypertension, decreased levels of potassium in the blood (hypokalemia), and suppression of the renin-aldosterone system, which helps regulate water and sodium balance and blood pressure. To learn more about the physiology of these effects, a 70-year-old patient was studied who had developed weakness, mental slowness, and weight loss during the previous year. The patient had been eating between 60 and 100 grams of licorice daily in the form of candy for several years. This amount of licorice is approximately 0.3 percent glycyrrhizic acid, the active ingredient that is converted to glycyrrhetinic acid in the body. The patient was evaluated in the hospital to determine his levels of sodium, potassium, and the hormones that regulate these substances. He was studied both with, and without, continued ingestion of licorice. He had the syndrome of mineralocorticoid excess, characterized by low potassium levels, hypertension, and suppression of the renin-angiotensin system. When the patient resumed eating licorice in the hospital after a brief interruption, his levels of aldosterone (which promotes sodium retention and potassium loss) and renin (a hypertensive substance whose levels affect the synthesis of aldosterone) fell and remained low for several weeks. Metabolic studies revealed that licorice caused the suppression of two enzyme systems, but at different rates: 11-beta-hydroxysteroid dehydrogenase (which normally converts cortisol to cortisone in the glucocorticoid pathway), and the renin-aldosterone system. Suppression in the former case was reversed more quickly after licorice was reinstated, whereas the activity of the renin-aldosterone system remained low for several months. Such prolonged suppression explains why licorice can be toxic, and may also be one cause of hypertension in cases where renin is low. A discussion is presented of the physiological effects of licorice on the renin-aldosterone system. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1991
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Lessons from licorice
Article Abstract:
Licorice, a very sweet substance used medically in Chinese medicines, can produce a syndrome of mineralocorticoid excess (elevated levels of aldosterone, a hormone secreted by the adrenal gland that affects water balance and sodium excretion) when ingested in large quantities. A study in the October 24, 1991 issue of The New England Journal of Medicine presents results that throw light on the mechanism of licorice's physiological effects. An enzyme defect has been shown to cause 'apparent' mineralocorticoid excess in the absence of increases in mineralocorticoid hormones (such as aldosterone) or excess sodium retention. The defect results in impaired metabolism of 11-alpha-cortisol, causing a build-up of cortisol and excess production of other metabolites of cortisol besides cortisone. On the basis of a previous report on this syndrome in an adult, it seems that the physiological effects of excess licorice consumption, and of apparent mineralocorticoid excess, could be due to inhibition of 11-beta-hydroxysteroid dehydrogenase. Although licorice was found to inhibit the conversion of cortisol to cortisone in normal subjects, the effects of chronic licorice abuse had not been detailed until the research article under discussion. The patient described in the article had a long history of ingesting excess licorice, which had induced a deficiency of 11-beta-hydroxysteroid dehydrogenase. This enzyme normally protects mineralocorticoid receptors, and can, as well, affect the access of cortisol to glucocorticoid receptors. It may be deficient in common conditions not associated with lack mineralocorticoid excess, such as chronic renal failure, hypothyroidism (insufficient thyroid hormone), and some forms of hypertension. The licorice article has helped illuminate the system that regulates the effects of cortisol on both mineralocorticoid and glucocorticoid receptors. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1991
User Contributions:
Comment about this article or add new information about this topic:
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