Abstract
Aim & Background: The mechanism of steatosis in Hepatitis C virus infection is multifactorial; therefore, it is complex and unclear. The aim of this study was to investigate the effects of methylentetrahydrofolate reductase (MTHFR) gene polymorphisms on the course of chronic hepatitis C virus infection and the development of steatosis due to hepatitis C virus. Methods: This study included 109 patients with chronic hepatitis C virus infection. Necroinflammatory activity, degrees of fibrosis and steatosis and MTHFR gene polymorphisms were investigated. Polymerase chain reaction-restriction fragment length polymorphism was used to determine MTHFR C677T and A1298C polymorphisms. Results: Fibrosis was correlated with age (r = 0.336, p = 0.002), platelet (r = ?0.448, p was a relation between MTHFR C677T and the degree of fibrosis but not A1298C (p = 0.014, p = 0.187 respectively). Conclusion: We found that MTHFR C677T polymorphism contributed to the development of fibrosis in patients with chronic hepatitis C virus infection.
Highlights
Hepatitis C virus (HCV) is a major cause of chronic liver disease worldwide
We found that methylentetrahydrofolate reductase (MTHFR) C677T polymorphism contributed to the development of fibrosis in patients with chronic hepatitis C virus infection
The logistics regression analysis was done that to examine the real relationship between gene polymorphisms and the liver steatosis and fibrosis
Summary
Hepatitis C virus (HCV) is a major cause of chronic liver disease worldwide. Hepatic steatosis is the most common cause of elevated aminotransferases and probably the most common cause of chronic liver disease worldwide [2]. An increased prevalence of steatosis in patients with HCV is well established [3,4,5,6,7,8,9]. Most studies have reported approximately 50% prevalence of steatosis among patients undergoing a liver biopsy because of HCV [10,11,12,13,14,15,16,17,18,19,20,21]
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