Blood Antioxidant Status in Chronic Hepatitis C Patients Before and After Antioxidant Supplementation: a Randomized Clinical Trial

The WHO estimated that around 170 million people are infected by HCV, about 3% of the world population. HCV is the leading cause of acute hepatitis and chronic liver disease, which may lead to cirrhosis and hepatocellular carcinoma.

The combined therapy with interferon with or without pegylation associated with ribavirin has shown greater sustained virological response than monotherapy with interferon-alpha, however this response still represents around 60% of cases. The mechanisms by which HCV causes cellular damage are not yet well understood, however immune liver damage, direct cytotoxic damage mediated by different viral products and also oxidative stress have been implicated in the pathogenesis of chronic hepatitis C. Several studies support that reactive oxygen species (ROS) and oxidative stress are involved in the pathogenesis of hepatitis C, despite that increased ROS levels in HCV patients might be beneficial by suppressing HCV replication. ROS are involved in several diseases and cause oxidative damage to lipids, DNA, proteins and carbohydrates.

Inclusion criteria

• without the presence of illnesses associated with systemic diseases, no chronic alcoholism, without HIV coinfection, and were not participating in other studies.
• Patients with hepatitis C were selected according to the Clinical Protocol and Guidelines for Therapeutic Hepatitis C Viral.
• Group I - All subjects were negative for HCV, HBV, HIV, HBsAg, anti-HBc total, anti-HCV and normal serum transaminases.

Exclusion criteria

• Patients with one of the following laboratory abnormalities were also excluded: leukocytes, neutrophils, platelets, serum creatinine 1.5 times upper limit of normal, elevated thyroid stimulating hormone, alpha-fetoprotein above normal limits, and/or focal lesion on ultrasound performed within 1 month of study entry.