Abstract
Background/aim: Thiol-disulfide homeostasis is an important antioxidant defense mechanism. This study was conducted to investigate dynamic thiol-disulfide homeostasis in patients with hepatitis B virus-related chronic hepatitis and liver cirrhosis. Materials and methods: Seventy-one treatment-naive patients with chronic hepatitis B (CHB), 50 patients with hepatitis B virusassociated liver cirrhosis, and 45 healthy controls were included in the study. Serum total and native thiol concentrations and serum disulfide concentrations were measured using an automated method. Results: Mean serum total thiol concentrations in the control, CHB, and cirrhosis groups were 481.64 ± 37.87 µmol/L, 438.50 ± 71.35 µmol/L, and 358.07 ± 80.47 µmol/L, respectively (P < 0.001), and mean serum native thiol concentrations in the control, CHB, and cirrhosis groups were 452.92 ± 36.43 µmol/L, 400.16 ± 65.92 µmol/L, and 328.15 ± 74.91 µmol/L, respectively (P < 0.001). Mean serum disulfide concentrations in the control, CHB, and cirrhosis groups were 14.38 ± 3.38 µmol/L, 19.19 ± 6.16 µmol/L, and 14.98 ± 5.53 µmol/L, respectively (P < 0.001). There was a progressive decrease in both mean serum native and total thiol concentrations parallel to the liver fibrosis stage. Conclusion: : Thiol-disulfide homeostasis is disturbed in patients with hepatitis B virus-related chronic hepatitis and liver cirrhosis.
Highlights
Hepatitis B is an important healthcare problem
There was a progressive decrease in both mean serum native and total thiol concentrations parallel to the liver fibrosis stage
Conclusion: : Thiol-disulfide homeostasis is disturbed in patients with hepatitis B virus-related chronic hepatitis and liver cirrhosis
Summary
Hepatitis B is an important healthcare problem. Hepatitis B virus (HBV) causes a wide spectrum of liver diseases ranging from inactive chronic carrier state to end-stage liver disease and it is one of the most important causes of hepatocellular carcinoma (HCC) worldwide. The pathogenesis of chronic hepatitis B is complex. Rather than the cytopathic effect of HBV itself, hosts’ immune responses are shown to play key roles in viral persistence and hepatocellular necroinflammation. Several complex interactions involving viral factors, hepatocytes, nonparenchymal liver cells, and inflammatory cells have been described during the course of HBV-related liver diseases [2]. Several cytokines have been shown to be important in the pathogenesis of viral persistence, hepatocellular inflammation, and fibrosis [3,4,5].
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