In this study we investigated the relationship between vitamin D and markers of oxidative stress and apoptosis in patients with liver cirrhosis stratified according serum GGT activity. Forty-eight patients with liver cirrhosis of various aetiology were selected, among which 58% cases (n=28) diagnosed with alcoholic liver cirrhosis and 42% (n=20) with cirrhosis after hepatitis virus infection. Each group was divided into three quartiles according GGT activity. 25-hydroxyvitamin D [25-(HO) vit D], markers of oxidative stress (catalase, superoxide dismutase) and apoptosis (M30) were compared. Higher levels of GGT were correlated with elevated AST, ALT and ALP values in both groups. A statistically significant difference was observed when comparing 25-(OH) vit D levels of patients suffering from ethanol-induced liver cirrhosis versus control group for all the quartiles as well as for those from the first quartile of viral-induced liver cirrhosis. For SOD, statistically significant differences were noticed between all cirrhosis subgroups and the control group. CAT values in all cirrhosis subgroups were lower than in control, but significant differences were only between Q2.2 and Q1.3 quartiles and Q2.2 and control. Correlation of 25-(OH) vit D versus SOD yields statistically significant results in ethanol-induced cirrhosis patients. M30 activity was increased in patients with alcoholic cirrhosis compared to controls and those with virus-induced cirrhosis, being correlated with the degree of GGT activity. Our results emphasized that vitamin D deficiency is associated with enhanced liver dysfunction regardless of the trigger responsible for disease onset. Furthermore, vitamin D deficiency augments liver injury by promoting oxidative stress which influence the survival mechanisms of parenchymal liver cells.
Keywords: 25-(OH) vitamin D; Alcohol-induced liver cirrhosis; HBV/HCV-induced liver cirrhosis; apoptosis; oxidative stress.
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