6 research outputs found

    Synergic effect of chronic hepatitis C infection and beta thalassemia major with marked hepatic iron overload on liver fibrosis: a retrospective cross-sectional study

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    BACKGROUND: Increased hepatic iron is assumed to potentiate progression towards liver fibrosis in chronic hepatitis C virus (HCV) infection. In this study we have evaluated the potentiating effect of marked hepatic iron overload and chronic HCV infection on hepatic fibrosis in thalassemic patients. METHODS: Liver biopsies of one group of patients with beta thalassemia major and chronic HCV infection (group 1) was compared with two groups of patients (groups 2&3) with either chronic HCV infection or thalassemia major, respectively (20 patients in each group). Necroinflammation, fibrosis, and iron overload were graded and compared. RESULTS: Stage of fibrosis in group 1 patients was significantly higher than the other two groups (p < 0.05). Necroinflammatory grade was significantly lower, but iron score was significantly higher in thalassemic patients (group 3) in comparison to groups 1 and 2 (p < 0.05). CONCLUSION: Our results indicate that marked liver iron overload and HCV infection in thalassemic patients have potentiating effect on hepatic fibrogenesis

    Frequency of YMDD Mutations in Patients with Chronic Hepatitis B Untreated with Antiviral Medicines

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    Background: Investigators were suspicious of tyrosine-methionine-aspartate-aspartate (YMDD) mutations occurred only in patients who were treated by lamivudine. However, YMDD mutations of hepatitis B virus gene (HBV DNA) in patients with chronic hepatitis B (CHB) untreated with antiviral medicines was reported in some studies. The aim of this study was to evaluate YMDD mutations in Iranian Patients with chronic hepatitis B (CHB) untreated with antiviral medicines. Methods: In a cross sectional study, 151 adult patients with positive Hepatitis B surface antigen (HBsAg) (78 asymptomatic hepatitis B virus carriers, 73 active chronic hepatitis B patients or cirrhosis patients) were evaluated for YMDD mutants. The patients who were treated with interferon and Lamivudine or Adfovier in one year prior to the study were excluded. YMDD mutations of HBV DNA were detected by PCR-RFLP (PCR Restriction Fragment Length Polymorphism) in a single laboratory. Results: The mean (±SD) age of patients was 37±4 years. Eighty one (54%) cases were male and 70 (46%) were female. Eight cases (5.3%) out of 151 had YMDD mutations. The type of mutation in all of these patients was YSDD. There was no significant relationship between YMDD mutation and viral load and HDV Ab (p>0.05). Conclusions: The mutant strains of the YMDD motif of HBV polymerase can be found in some patients without lamivudine treatment. However, in view of rather clinically insignificant YMDD mutation frequency, routine testing for YMDD mutations prior to antiviral therapy is not recommended in these patients
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