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Aim of the studyWe aimed to assess oxidative stress factors, glutathione peroxidase (GPX) and malondialdehyde (MDA) in children with chronic hepatitis C (CHC) and their relation to treatment response.Material and methodsThe study included 50 children with chronic hepatitis C virus (HCV) before treatment (naïve HCV), 25 children responders to HCV treatment, 25 children non-responders to HCV treatment and 25 healthy controls. All patients and controls were subjected to GPX and MDA measurement by enzyme-linked immunosorbent assay.ResultsThe average GPX activity in erythrocytes of naïve CHC patients was 29.2 ±10.3 mU/ml. It was statistically significantly lower than the average activity of GPX in erythrocytes of the healthy control group (47.3 ±5.2 mU/ml) (p < 0.05). The average GPX activity in erythrocytes of the responder group was 34.93 ±3.17 mU/ml. It was statistically significantly higher than the average activity of GPX in erythrocytes of the non-responder group (11.7 ±4.2 mU/ml) (p < 0.05). Plasma MDA was significantly higher in naïve CHC patients than in healthy controls (9.7 ±3.7 nmol/ml vs. 3 ±1.1 nmol/ml, p < 0.0001). Furthermore, plasma MDA concentration was significantly decreased in the responder group (5.36 ±0.7 nmol/ml) and elevated in the non-responder group (16.05 ±2.9 nmol/ml).ConclusionsLower pretreatment levels of GPX and higher MDA level might be markers of oxidative stress occurring in HCV patients. Reversal of changes of these levels with completion of the treatment may indicate a correlation between oxidative stress and the viral pathogenesis.

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Fulminant hepatic failure is a life-threatening disease. Hepatitis A virus (HAV) can cause fulminant hepatic failure and death in about 0.2% of cases. Extensive destruction of infected hepatocytes by immune-mediated lysis is thought to be the cause. We aimed to evaluate the use of steroid therapy in children with fulminant HAV. This study included 33 children with fulminant HAV in two groups. Steroid group: comprised of 18 children who received prednisolone (1 mg/kg/d) or its equivalent dose of methylprednisolone, and the nonsteroid group: comprised another 15 children who did not receive steroid therapy. Age and sex were matched for both groups (P > .05), and they were comparable regarding baseline clinical and laboratory characteristics. Of the steroid group, 15 patients survived and 3 died, while in the nonsteroid group, 4 patients survived and 11 died (P = .001). Of the living patients, 15 of 19 (78.9%) received steroids while only 3 of 14 (21.4%) of the dead patients received steroids (P = .001). Stepwise regression analysis showed that steroid therapy was the only independent variable associated with recovery (P = .001). Steroid therapy in children with fulminant HAV associated significantly with improved outcome and survival. Future studies on a larger population size are strongly recommended.