OXIDATIVE DAMAGE MARKERS IN ALCOHOLIC HEPATITIS

Introduction and objective

Alcohol hepatitis (AH) is a clinical syndrome in patients with excessive and chronic alcohol consumption. Ethanol metabolism produces free radicals: reactive oxygen species (ROS) and reactive nitrogen species (RNS). This contributes to cellular damage in AH. The malondialdehyde (MDA) and carbonylated proteins are markers of oxidative damage in lipids and proteins. Our objective is to evaluate the levels of serum MDA and carbonylated proteins in AH patients with.

Materials and methods

This transversal study included 147 individuals divided into two groups: the control group (n=100), which consists of individuals with alcohol consumption ≤ 10 g/day and AUDIT score ≤ 7, and the group with AH patients (n=47). We measured the serum levels of MDA (thiobarbituric acid method) and carbonylated proteins (DNPH reaction). The statistical analysis was performed by the Windows SPSS v22 software. Data were expressed as mean values ± SEM. Comparisons were carried out by analysis of variance (ANOVA). A p-value <0.05 was considered statistically significant.

Results

The control group (CT), with a mean of 30.47±0.52 years old, had a consumption of 2.32±0.21g of alcohol daily (gOH/day) and an AUDIT score of 2.24±0.10. The AH patients, with a mean of 41.68±1.3 years old, had a consumption of 354.25±39.54 gOH/day and an AUDIT score of 30±1.45. The AST, ALT, GGT, total and indirect bilirubin serum levels were higher in AH compared to CT (p<0.0001), with a ratio of AST/ALT ≥2. The albumin serum levels were lower (p<0.0001) in AH vs. CT. The carbonylated proteins serum levels were higher in patients with AH compared to CT (p<0.0001). No differences in MDA serum levels were found between both groups.

Discussion

We reported greater MDA serum levels (p=0.001) in alcoholic liver cirrhosis patients when compared to the control group; and an insignificant difference in carbonylated proteins serum level between both participant groups. The alcoholic hepatitis patients have an increase in carbonylated proteins oxidative damage while there is no lipidic damage.

Conclusions

Our results suggest that carbonylated proteins may a damage oxidative marker in the AH Mexican population. This damage may increase the risk of malnutrition, susceptibility to infections and sepsis, deficient coagulation factors production, gastrointestinal bleeding, among other complications that increase mortality. It is necessary to counteract oxidative damage to improve and complement the actual treatment in alcoholic hepatitis.

Competing interests. The authors declare they have no competing interests.

This work was partially financed by CONACyTSALUD-2016-272579 and PAPIIT- UNAMTA200515