Antioxidant levels in peripheral blood, disease activity and fibrotic stage in chronic hepatitis C
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Published on: August 5, 2012
Priyanka Bandara1, Jacob George, Geoffrey McCaughan
1Storr Liver Unit, Westmead Millennium Institute, Sydney, Australia.
Insights
Higher levels of glutathione (GSH) and vitamin C in chronic hepatitis C patients are linked to less liver inflammation and fibrosis. Antioxidant intake boosts vitamin C and E, but not GSH.
Area of Science:
- Hepatology
- Biochemistry
- Nutritional Science
Background:
- Investigated the link between peripheral blood antioxidants (glutathione, vitamin C, vitamin E) and liver disease severity in chronic hepatitis C (CHC).
- Assessed the impact of antioxidant supplementation on these levels and disease progression.
Purpose of the Study:
- To determine the association between antioxidant levels and histological activity/fibrosis in CHC patients.
- To evaluate if antioxidant supplementation affects disease severity and antioxidant status.
Main Methods:
- Collected clinical, biochemical, histological, and demographic data from 247 CHC patients.
- Measured whole blood glutathione (GSH), plasma vitamin C, and vitamin E using high-performance liquid chromatography.
- Performed statistical analyses to identify predictors of hepatic necroinflammation and fibrosis.
Main Results:
- GSH and vitamin C, but not vitamin E, correlated negatively with portal/periportal inflammation and fibrosis stage.
- GSH and vitamin C were independent negative predictors of inflammation and fibrosis.
- Antioxidant intake was associated with higher vitamin C and E levels, but not GSH.
Conclusions:
- Peripheral blood GSH and plasma vitamin C are negatively associated with liver inflammation and fibrosis in CHC.
- Further controlled studies on vitamin C and GSH-boosting agents are recommended for CHC treatment.
Background:
This study addressed the suggested association between levels of the antioxidants glutathione (GSH), vitamin C and vitamin E in peripheral blood and the histological activity and fibrosis stage in chronic hepatitis C (CHC). We then determined whether regular antioxidant supplementation influenced these antioxidant levels or disease severity.
Methods:
Clinical, biochemical, histological and demographic data were collected from 247 CHC patients at the time of liver biopsy. Whole blood total GSH, plasma vitamin C and E were assessed by high-performance liquid chromatography. Statistical analyses were performed to test for associations between the variables and to identify independent predictors for hepatic necroinflammatory and fibrosis scores.
Results:
GSH and vitamin C, but not vitamin E correlated with both portal/periportal activity (r = -0.19, P = 0.004; r = -0.19, P = 0.009 respectively) and fibrosis stage (r = -0.18, P = 0.007; r = -0.18, P = 0.009 respectively). GSH was an independent negative predictor of portal/periportal inflammation (P = 0.02) and fibrosis (P = 0.01). Vitamin C was an independent negative predictor of fibrosis stage (P = 0.02). Antioxidant intake was associated with higher vitamin C (P < 0.0001) and vitamin E (P = 0.005) levels, but not GSH.
Conclusions:
Whole blood GSH and plasma vitamin C are negatively associated with hepatic portal/periportal inflammation and fibrosis stage in CHC. Controlled intervention studies with vitamin C and agents that boost endogenous GSH levels are warranted.
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