Nonalcoholic Liver Disease Cases Research Articles

Changes of hepatic microtubules and secretory proteins in human alcoholic liver disease

It has been shown that alcohol consumption disrupts liver microtubules, impairs protein secretion and leads to ballooning of the hepatocytes in rats. Ethanol-induced hepatomegaly was accounted for by an increase of the hepatocytes volume. To study whether these changes occur in human alcoholic liver disease, hepatic tubular protein and export protein content were measured in 29 cases of alcoholic liver disease and were compared with those of 37 cases of non-alcoholic liver disease and 5 cases of non-hepatobiliary disease. Hepatic polymerized tubulin was significantly decreased in alcoholic liver disease compared to non-alcoholic liver disease ( p<0.01), while free tubulin was increased in alcoholic liver disease. Hepatic transferrin (one of the export proteins) content was significantly higher ( p<0.01) and serum transferrin level was significantly lower ( p<0.05) in alcoholic liver disease than in non-alcoholic liver disease. These findings indicated that even in humans, chronic alcohol consumption decreased hepatic microtubules by impairing polymelization of tubular protein and increased hepatic export protein content. This decrease in hepatic microtubules by chronic alcohol consumption may play an important role in the development of human alcoholic liver disease.

Biochemical and Hematologic Correlates of Alcoholism and Liver Disease

Quadratic multiple discriminant analysis of 25 commonly ordered laboratory tests resulted in correct classification of 100% of nonalcoholics without overt liver disease, 98% of alcoholism treatment program patients with presumed mild liver involvement, 96% of alcoholics with liver disease, and 89% of nonalcoholics with liver disease. Direct comparison of the biopsy-verified alcoholic and nonalcoholic liver disease groups resulted in 100% discrimination, and removal of traditionally evaluated liver tests from the battery of 25 tests did not substantially alter the original classification accuracy. Alcoholic and nonalcoholic liver disease was still 100% differentiable when equated for number of patients with cirrhosis, hepatitis, and hepatitis combined with cirrhosis or fibrosis. Additional utility of the quadratic discriminant approach was demonstrated when 83% alcoholic and 83% nonalcoholic liver disease cases were diagnosed correctly in a prospective manner. In contrast, use of aspartate aminotransferase to alanine aminotransferase ratios (ie, SGOT to SGPT) identified correctly 75% and 33% of patients, respectively.

The SGOT/SGPT ratio in alcoholic liver disease.

The SGOT/SGPT ratio has been estimated in 207 patients with alcoholic liver disease and in 3 control groups (43 viral hepatitis, 30 non-alcoholic chronic liver disease and 42 obstructive jaundice). The SGOT/SGTP ratio in alcoholic liver disease group was significantly higher (2.63 ± 1.82) than in any of the 3 control groups. If we consider the different alcoholic liver diseases the ratio is 1.82 ± 1.27 in Steatosis, lowest value of all; 3.00 ± 2.33 in Acute alcoholic hepatitis; 2.45 ± 1.62 in Cirrhosis; 2.19 ± 1.94 in Cirrhosis with Steatosis; 3.48 ± 1.63 in Cirrhosis with AAH. Values higher than 1.5 are suggestive of alcoholic liver disease and higher than 2.0 are almost diagnostic and found in 56% of the patients with alcoholic liver disease and only in 1 case of non-alcoholic liver disease.