Helicobacter pylori infection and liver diseases: Epidemiology and insights into pathogenesis

Both Helicobacter pylori(H. pylori) infection and liver diseases, including nonalcoholic fatty liver disease(NAFLD), viral hepatitis, and hepatocellular carcinoma(HCC), have high prevalences worldwide, and the relationship between H. pylori infection and liver disease has been discussed for many years. Although positive correlations between H. pylori and NAFLD have been identified in some clinical and experimental studies, nega-tive correlations have also been obtained in high-quality clinical studies. Associations between H. pylori and the pathogenesis of chronic viral hepatitis, mainly disease progression with fibrosis, have also been suggested in some clinical studies. Concerning HCC, a possible role for H. pylori in hepatocarcinogenesis has been identified since H. pylori genes have frequently been detected in resected HCC specimens. However, no study hasrevealed the direct involvement of H. pylori in promoting the development of HCC. Although findings regarding the correlations between H. pylori and liver disease pathogenesis have been accumulating, the existing data do not completely lead to an unequivocal conclusion. Further high-quality clinical and experimental analyses are necessary to evaluate the efficacy of H. pylori eradication in ameliorating the histopathological changes observed in each liver disease.

Assessment of disease progression in patients with transfusion-associated chronic hepatitis C using transient elastography

METHODS： Between December 2006 and June 2008, a total of 524 transfusion-associated HCV-RNA positive patients with or without HCC were enrolled, Liver stiffness was obtained noninvasively by using Fibroscan （Echosens, Paris, France）, The date of blood transfusion was obtained by interview, Duration of infection was derived from the interval between the date of bloodtransfusion and the date of liver stiffness measurement （LSM）. Patients were stratified into four groups based on the duration of infection （17-29 years; 30-39 years; 40-49 years; and 50-70 years）. The difference in liver stiffness between patients with and without HCC was assessed in each group. Multiple linear regression analysis was used to determine the factors associated with liver stiffness.RESULTS： A total of 524 patients underwent LSM. Eight patients were excluded because of unsuccessful measurements. Thus 516 patients were included in the current analysis （225 with HCC and 291 without）. The patients were 244 men and 272 women, with a mean age of 67.8 ±9.5 years. The median liver stiffness was 14.3 kPa （25.8 in HCC group and 7.6 in non HCC group）. The patients who developed HCC in short duration of infection were male dominant, having lower platelet count, with a history of heavier alcohol consumption, showing higher liver stiffness, and receiving blood transfusion at an old age. Liver stiffness was positively correlated with duration of infection in patients without HCC （r = 0.132, P = 0.024） but not in patients with HCC （r = -0.103, P = 0.123）. Liver stiffness was significantly higher in patients with HCC than in those without in each duration group （P 〈 0.0001）. The factors significantly associated with high liver stiffness in multiple regression were age at blood transfusion （P 〈 0.0001）, duration of infection （P = 0.0015）, and heavy alcohol consumption （P = 0.043）CONCLUSION： Although liver stiffness gradually increases over time, HCC develops in patients with high stiffness value regardless of the duration of infection.