Relationship Between Serum Levels of Anti-Low-Density Lipoprotein-Acetaldehyde-Adduct Antibody and Aldehyde Dehydrogenase 2 Heterozygotes in Patients With Alcoholic Liver Injury

We prepared low-density lipoprotein (LDL)-acetaldehyde-adduct (hereafter abbreviated as LDL-adduct) and anti-LDL-adduct antibody by using Watanabe hyperlipidemic rabbits, and determined values of serum anti-LDL-adduct antibody levels by the ELISA method in healthy adults and patients with alcoholic liver injury. In the nondrinking group in healthy adults, values of anti-LDL-adduct antibody levels were 25 ± 13 μ g/ml, and there was no significant difference between moderate drinkers without diseases and the nondrinking group in healthy adults. Values of anti-LDL-adduct antibody in alcoholic disease groups, 17 ± 9 μ g/ml for the patients with the fatty liver group, 21 ± 14 μ g/ml for the hepatic fibrosis group, 70 ± 21 μ g/ml for the alcoholic hepatitis group, 41 ± 50 μ g/ml for the alcoholic cirrhosis group, and 19 ± 18 μ g/ml for the alcoholic pancreatitis group. Examinations of aldehyde dehydrogenase 2 (ALDH2) genetic variations by the polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) method in the healthy group and the liver injury group revealed a tendency for patients with ALDH2¹/2² in the liver injury group to have relatively mild liver lesions. When comparing anti-LDL-adduct antibody levels between ALDH2 genetic variations, those for the patients with ALDH2¹/2¹ (36 ± 40 μ g/ml) were significantly higher than those for patients with ALDH¹/2² (11 ± 5 μ g/ml). Results of the present study suggest that genetic variation may influence the progression of liver injury.