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Prevalence of Helicobacter pylori infection in patients with chronic hepatitis C
Abdelfattah M Attallah1, Mohamed S Albannan2, Mohamed F Ghaly3
1Biotechnology Research Center, 23 July St., Industrial Zone, New Damietta, 34517, Egypt.
Insights
Helicobacter pylori (H. pylori) infection is linked to worsening liver fibrosis in chronic hepatitis C (CHC) patients. Co-infection with H. pylori significantly increases the risk of developing cirrhosis in individuals with chronic hepatitis C virus (HCV).
Area of Science:
- Hepatology
- Gastroenterology
- Infectious Diseases
Background:
- The relationship between Helicobacter pylori (H. pylori) and chronic hepatitis C (CHC) is debated.
- This study investigates the potential impact of H. pylori on the progression of liver disease caused by the hepatitis C virus (HCV).
Purpose of the Study:
- To assess the role of H. pylori infection in the progression of liver fibrosis in patients with chronic hepatitis C.
- To determine if H. pylori co-infection increases the risk of cirrhosis in HCV patients.
Main Methods:
- Quantified H. pylori antigen in serum samples from 249 patients using ELISA.
- Correlated H. pylori positivity and antigen levels with liver fibrosis stages (F0-F4).
- Compared cirrhosis risk in HCV/H. pylori co-infected patients versus HCV mono-infected patients.
Main Results:
- H. pylori positivity significantly increased with liver fibrosis progression (44.45% in fibrotic, 71.88% in cirrhotic patients).
- Patients with advanced fibrosis (F4) showed significantly higher H. pylori antigen concentrations.
- H. pylori/HCV co-infected patients were 3.19 times more likely to develop cirrhosis compared to HCV mono-infected patients.
Conclusions:
- Elevated H. pylori antigen levels in HCV/H. pylori co-infection indicate heightened susceptibility to hepatic fibrosis progression.
- H. pylori co-infection is associated with an increased risk of developing cirrhosis in chronic hepatitis C patients.
Background:
Association between Helicobacter pylori (H. pylori) and chronic hepatitis C (CHC) still remains controversial. This work is concerned with assessing the potential role of H. pylori in the progression of hepatitis C virus (HCV)-related chronic liver disease.
Results:
A total of 449 individuals constituted this study (200 individuals were used to validate the assay while 249 individuals were used to assess the correlation between H. pylori infection and CHC). H. pylori antigen was quantified in serum samples using ELISA. As a consequence, our findings showed that H. pylori positivity was increased significantly (P = 0.021) with liver fibrosis progression as it was found in 44.45% of fibrotic patients and 71.88% of cirrhotic patients. We demonstrated that patients with F4 were accompanied by a significant (P < 0.05) increase in the concentration of H. pylori antigen displaying 16.52-fold and 1.34-fold increase in its level over F0 and F1-F3, respectively. Patients co-infected with H. pylori and HCV are 3.19 times (219%) more likely to experience cirrhosis than those who are mono-infected with HCV. This suggests that the risk for developing F4 was found to increase upon H. pylori co-infection when compared to CHC mono-infected patients.
Conclusion:
The elevated levels of H. pylori-antigen in HCV/H. pylori co-infection suggest increased susceptibility of co-infected patients for promoting hepatic fibrosis progression.
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