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Licorice induced hypokalemia, edema, and thrombocytopenia.
Hum Exp Toxicol
December 2012
Department of Internal Medicine, Faculty of Medicine, Mustafa Kemal University, Hatay, Turkey.
Licorice originates from the root of Glycyrrhiza glabra, which has a herbal ingredient, glycyrrhizic acid, and has a mineralocorticoid-like effect. Chronic intake of licorice induces a syndrome similar to that found in primary hyperaldosteronism. Excessive intake of licorice may cause a hypermineralocorticoidism-like syndrome characterized by sodium and water retention, hypertension, hypokalemia, metabolic alkalosis, low-renin activity, and hypoaldosteronism.
View Article and Find Full Text PDFThe role of 11 beta-hydroxysteroid dehydrogenase in the pathogenesis of hypertension.
Cardiovasc Res
April 1998
Department of Medicine, St. Radboud University Hospital, University of Nijmegen, Netherlands.
The two 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) isozymes catalyze the interconversion of cortisol and cortisone. Type 1 11 beta-HSD (11 beta-HSD1) has bidirectional activity, while type 2 11 beta-HSD (11 beta-HSD2) mainly converts cortisol into cortisone. Of these two hormones only cortisol has affinity to mineralocorticoid receptors (MRs) and thus induces mineralocorticoid effects.
View Article and Find Full Text PDFLicorice-induced hypermineralocorticoidism.
N Engl J Med
October 1991
General Clinical Research Center, San Francisco General Hospital Medical Center.
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