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Identification of glycyrrhizin metabolites in humans and of a potential biomarker of liquorice-induced pseudoaldosteronism: a multi-centre cross-sectional study.
Arch Toxicol
November 2019
Center for Kampo Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.
Article Synopsis
- Liquorice, primarily containing glycyrrhizin (GL), is utilized for its sweetness and medicinal properties, but can lead to pseudoaldosteronism, causing symptoms like edema, low potassium levels, and high blood pressure.
- A study was conducted to analyze GL metabolites in blood and urine from patients showing pseudoaldosteronism symptoms while consuming liquorice-containing herbal products, involving data collection from four hospitals over several years.
- The results identified certain metabolites like 18β-glycyrrhetinic acid and 18β-glycyrrhetyl-3-O-sulfate but did not find a significant link between these metabolites and the observed symptoms of high blood pressure or edema.
Syndromes that Mimic an Excess of Mineralocorticoids.
High Blood Press Cardiovasc Prev
September 2016
Department of Medicine (DIMED), Endocrinology, University of Padua, Via Ospedale 105, 35128, Padua, Italy.
Pseudohyperaldosteronism is characterized by a clinical picture of hyperaldosteronism with suppression of renin and aldosterone. It can be due to endogenous or exogenous substances that mimic the effector mechanisms of aldosterone, leading not only to alterations of electrolytes and hypertension, but also to an increased inflammatory reaction in several tissues. Enzymatic defects of adrenal steroidogenesis (deficiency of 17α-hydroxylase and 11β-hydroxylase), mutations of mineralocorticoid receptor (MR) and alterations of expression or saturation of 11-hydroxysteroid dehydrogenase type 2 (apparent mineralocorticoid excess syndrome, Cushing's syndrome, excessive intake of licorice, grapefruits or carbenoxolone) are the main causes of pseudohyperaldosteronism.
View Article and Find Full Text PDFVSL#3 ® probiotic therapy does not reduce portal pressures in patients with decompensated cirrhosis.
Liver Int
November 2013
Department of Medicine, University of Calgary, Calgary, Alberta, Canada; Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.
Background & Aims: In patients with decompensated cirrhosis, bacterial translocation can contribute to splanchnic vasodilatation, decreased effective circulating volume, and portal hypertension. The primary objective of this randomized, double blind placebo controlled trial was to evaluate the effect of the probiotic VSL#3(®) on the hepatic venous pressure gradient (HVPG).
Methods: Seventeen patients with decompensated cirrhosis and an HVPG of ≥ 10 mmHg were randomized to receive 2 months of VSL#3(®) or an identical placebo.
Effect of hydrochlorothiazide on urinary calcium excretion in dent disease: an uncontrolled trial.
Am J Kidney Dis
December 2008
Université Paris 5, Faculté de Médecine Paris Descartes, Paris, France.
Background: Thiazide doses equivalent to 1 to 2 mg/kg/d of hydrochlorothiazide (HCTZ) have been proposed to correct hypercalciuria and prevent kidney failure in patients with Dent disease. However, they can cause adverse metabolic effects in the long term. In treating hypertension in children, lower thiazide doses have been shown to be as effective and well tolerated.
View Article and Find Full Text PDFNovel mutation in cytochrome P450c17 causes complete combined 17alpha-hydroxylase/17,20-lyase deficiency.
J Pediatr Endocrinol Metab
February 2008
Division of Pediatric Endocrinology, Infants and Children's Hospital of Brooklyn at Maimonides, Brooklyn, NY, USA.
Background: Cytochrome P450c17 (CYP17) has two principal enzyme activities, 17alpha-hydroxylase and 17,20-lyase, which are required for cortisol and androgen biosynthesis, respectively. Mutations in the gene encoding for CYP17 result in 17alpha-hydroxylase deficiency (17OHD), a rare form of congenital adrenal hyperplasia, a disorder characterized by adrenal insufficiency, hypertension, primary amenorrhea and sexual infantilism. We describe a case of complete combined 17OHD caused by mutations in the CYP17 gene.
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