Abstract
Background: The MTHFR (methylenetetrahydrofolate reductase) rs1801133 polymorphism leads to higher circulating levels of homocysteine, which is related to several liver diseases. We aimed to evaluate the relationship between MTHFR rs1801133 polymorphism and liver fibrosis progression in HCV-infected patients.Methods: We conducted a preliminary retrospective cohort study in 208 non-cirrhotic HCV-infected patients. These subjects had at least two liver stiffness measurements (LSM), which were assessed using transient elastography, and no patient had cirrhosis at baseline. We analyzed the association between MTHFR rs1801133 and outcome variables using Generalized Linear Models.Results: HCV-infected patients were 47 years old, around 54% were males, a low frequency of high alcohol intake (13.5%) or prior use of intravenous drugs (10.1%). A total of 26 patients developed cirrhosis (LSM1 ≥ 12.5) during a median follow-up of 46.6 months. The presence of the rs1801133 C allele showed an inverse association with the LSM2/LSM1 ratio (adjusted AMR = 0.90; 95%CI = 0.83–0.98; p = 0.020) and the cirrhosis progression (adjusted OR = 0.43; 95%CI = 0.19–0.95; p = 0.038). Besides, rs1801133 CT/CC genotype had an inverse association with the LSM2/LSM1 ratio (adjusted AMR = 0.80; 95%CI = 0.68–0.95; p = 0.009) and the cirrhosis progression (adjusted OR= 0.21; 95%CI = 0.06–0.74; p = 0.015).Conclusions: MTHFR rs1801133 C allele carriers presented a diminished risk of liver fibrosis progression and development of cirrhosis than rs1801133 T allele carriers. This statement supports the hypothesis that MTHFR rs1801133 polymorphism appears to play a crucial role in chronic hepatitis C immunopathogenesis.
Highlights
According to the world health organization, viral hepatitis is a significant public health problem that causes 1.34 million deaths per year due to chronic liver disease (720,000 by cirrhosis) and primary liver cancer (47,000 by hepatocellular carcinoma) [1]
We found a decrease in the proportion of patients with a low stage of fibrosis (F0–F1; p < 0.001), whereas both liver stiffness measurement (LSM) values and the rate of patients who developed an F4 stage raised (p < 0.001) (Table 3)
The present study focused on the potential relationship of methylenetetrahydrofolate reductase (MTHFR) rs1801133 polymorphism and the development of liver fibrosis and cirrhosis on hepatitis C virus (HCV)-infected patients, using two LSM values with an interval of at least 12 months
Summary
According to the world health organization, viral hepatitis is a significant public health problem that causes 1.34 million deaths per year due to chronic liver disease (720,000 by cirrhosis) and primary liver cancer (47,000 by hepatocellular carcinoma) [1]. The staging of liver fibrosis provides essential clinical information that allows the adequate management and prognosis of CHC patients [8]. Noninvasive approaches, as the transient elastography or FibroScan, have been widely used to the liver fibrosis assessment, with excellent accuracy in advanced fibrosis and cirrhosis [10]. In this context, the evaluation of liver stiffness measurement (LSM), an intrinsic physical property of liver parenchyma, provides quantitative data that correlates with fibrosis stage in CHC [11]. We aimed to evaluate the relationship between MTHFR rs1801133 polymorphism and liver fibrosis progression in HCV-infected patients
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