Glutathione S-transferases in alcoholic liver disease

Article Abstract:

Prolonged, excessive consumption of alcohol can lead to a variety of deleterious effects, some of which involve the liver. Notably, the level of liver enzymes responsible for removing alcohol (among other substances) from the blood is reported to be altered. This phenomenon is typified by the increased levels of the enzyme gamma glutamyltranspeptidase found in patients with alcoholic liver disease. Animal studies have demonstrated increases in liver glutathione S-transferases (GST; a class of enzyme which removes drugs, herbicides, and carcinogens from the blood) in alcohol-fed mice. Additionally, it has been reported that alcoholism in humans can result in structural changes in liver cells which may be reflected in enzymatic changes. In order to investigate the effects of chronic alcohol consumption in humans on GST levels, a study was performed in which liver biopsy specimens were removed from 40 patients with a history of alcohol abuse and from six normal controls. Levels of the three predominant forms of GST were measured. The liver cells of alcoholic patients were found to co-express two subtypes of GST (the alpha and pi subtypes). The pi subtype is not normally found in liver cells except for those in the bile duct, but in alcoholic liver disease, non-bile duct cells come to resemble bile duct cells structurally, and the presence of this characteristic enzyme type is consistent with such a change. Co-expression of the two enzyme subtypes has only been seen as a developmental stage in human fetal liver cells, and in precancerous sites in chemically induced liver cancer in rats. (Consumer Summary produced by Reliance Medical Information, Inc.)

Methods, Measurement, Physiological aspects, Alcohol metabolism, Liver cirrhosis, Enzymatic analysis, Glutathione metabolism

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Anorectal varices - their frequency in cirrhotic and non-cirrhotic portal hypertension

Article Abstract:

When the blood flowing to the liver in the hepatic portal vein encounters excessive resistance to flow, the pressure in the portal vein rises; this condition is known as portal hypertension. This can happen in a variety of circumstances, including cirrhosis of the liver (hardening, non-functioning). In many cases, the increased pressure in the portal vein leads to the development of varices, the abnormal swelling, or bulging, of blood vessels. These varices can occur at the junction of the esophagus and stomach, in the anal region, near the ligaments connected to the liver, and on other abdominal organs where they contact the rear surface of the abdominal cavity. Varices are prone to bleeding, which can be quite serious. It has been reported that a high number of patients with cirrhotic portal hypertension develop varices in the region of the anus and rectum; the incidence of anorectal varices in patients with noncirrhotic portal hypertension is not as well known. To further characterize this phenomenon, 72 consecutive patients with portal hypertension were assessed; 25 had cirrhosis as determined by liver biopsy, and 47 had noncirrhotic portal hypertension. Overall, 72 percent of the patients had anorectal varices. Patients with cirrhosis had anorectal varices much less frequently than similar patients with noncirrhotic portal hypertension (56 percent versus 89 percent). Anorectal varices are frequently large, but they are less likely to bleed than esophageal or other forms of varices. (Consumer Summary produced by Reliance Medical Information, Inc.)

Portal hypertension

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