A long-term glycyrrhizin injection therapy reduces hepatocellular carcinogenesis rate in patients with interferon-resistant active chronic hepatitis C

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A long-term glycyrrhizin injection therapy reduces hepatocellular carcinogenesis rate in patients with interferon-resistant active chronic hepatitis C: a cohort study of 1249 patients.Ikeda K, Arase Y, Kobayashi M, Saitoh S, Someya T, Hosaka T, Sezaki H, Akuta N, Suzuki Y, Suzuki F, Kumada H.Department of Gastroenterology, Toranomon Hospital, Tokyo, Japan. ikedakenji@...To elucidate the influence of a glycyrrhizin therapy on hepatocarcinogenesis rate in interferon (IFN)-resistant hepatitis C, we retrospectively analyzed 1249 patients with chronic hepatitis with or without cirrhosis. Among 346 patients with high alanine transaminase value (twice or more of upper limit of normal), 244 patients received intravenous glycyrrhizin injection and 102 patients did not, after judgment of IFN resistance. Crude carcinogenesis rates in the treated and untreated group were 13.3%, 26.0% at the 5th year, and 21.5% and 35.5% at the 10th year, respectively (P = .0210). Proportional hazard analysis using time-dependent covariates disclosed that glycyrrhizin treatment significantly decreased the hepatocarcinogenesis rate (hazard ratio 0.49, 95% confidence interval 0.27-0.86, P = .014) after adjusting the background features with significant covariates. Glycyrrhizin injection therapy significantly decreased the incidence of hepatocellular carcinoma in patients with IFN-resistant active chronic hepatitis C, whose average aminotransferase value was twice or more of upper limit of normal after interferon.PMID: 16614974 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=16614974 & dopt=Abstract

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Glycyrrhizin

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Glycyrrhizin, glycyrrhizinic acid or glycyrrhizic acid, is the active principle of liquorice root. It is a powerful sweetener, 30–50 times as potent as sucrose (table sugar).

Chemically speaking, glycyrrhizin is a triterpene glycoside with the systematic name (3-beta,20-beta)-20-carboxy-11-oxo-30-norolean-12-en-3-yl 2-O-beta-D-glucopyranuronosyl-alpha-D-glucopyranosiduronic acid. The acid form is not particularly water-soluble, but its ammonium salt is soluble in water at pH greater than 4.5.

Although sweet, the taste of glycyrrhizin is different from that of sugar. Glycyrrhizin's sweetness has a slower onset than sugar's, and lingers in the mouth for some time. Additionally, its characteristic licorice flavor makes it unsuitable as a direct flavor substitute for sugar. Unlike the artificial sweetener aspartame, glycyrrhizin maintains its sweetness under heating.

In the United States, glycyrrhizin is Generally Recognized as Safe as a flavoring agent, although not as a sweetener. Glycyrrhizin is used as a flavoring in some candies, pharmaceuticals, and tobacco products.

In Japan, where concern over the safety of artificial sweeteners during the 1970s led to a shift towards plant-derived sugar substitutes, glycyrrhizin is a commonly used sweetener, often used in combination with another plant-based sweetener, stevia. However, glycyrrhizin appears to have some pharmacological side effects, and the Japanese government has asked its citizens to limit their consumption to 200 milligrams per day.

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Health effects

Glycyrrhizin and other licorice root products have been used for numerous medical purposes, particularly treatment of peptic ulcers and as an expectorant. The triterpene derivative of glycyrrhizin, glycyrrhetinic acid, is itself effective in treatment of peptic ulcer. A synthetic analog, carbenoxolone, was developed in Britain. Both glycyrrhetinic acid and carbenoxolone have a modulatory effect on neural signaling through gap junction channels.

The most widely reported side effects of glycyrrhizin use are hypertension and edema (water retention).

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Why Hypertension?

Glycyrrhizin inhibits the conversion of cortisol to cortisone by inhibiting the enzyme 11-Betahydroxysteroid Dehydrogenase. As a result, cortisol builds up at the collecting duct. Cortisol has intrinsic mineralocorticoid properties (that is, it acts like aldosterone and increases sodium reabsorption) that work on ENaC channels in the collecting duct. Hypertension develops due to this mechanism of sodium retention. Patients often have high blood pressure with a low renin and low aldosterone blood level.

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