Factor V Leiden polymorphism and the rate of fibrosis development in chronic hepatitis C virus infection
| Autor: | Branwen J. Hennig, Mark Wright, Susanne Knapp, Angela J. Frodsham, A V S Hill, Howard Thomas, S Cheng, Robert D. Goldin, Simon Hellier, R Apple, Mark Thursz |
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| Jazyk: | angličtina |
| Rok vydání: | 2003 |
| Předmět: |
Adult
Liver Cirrhosis Male Cirrhosis Genotype Hepatitis C virus medicine.disease_cause Sensitivity and Specificity Liver disease Fibrosis medicine Factor V Leiden Humans Polymorphism Genetic biology Gastroenterology Factor V Hepatitis C Hepatitis C Chronic medicine.disease Liver Immunology Multivariate Analysis biology.protein Disease Progression Female Hepatic fibrosis |
| Popis: | Background: The rate of progression to cirrhosis varies among individuals chronically infected with the hepatitis C virus (HCV). Coagulation pathway activation in models of hepatic fibrosis suggests variation in coagulation pathway components may influence the rate of fibrosis. We hypothesised that polymorphisms of the coagulation factors II and V affect the rate of progression to cirrhosis in HCV infected subjects. Methods: We studied the relationship between rate of fibrosis (calculated by dividing the fibrosis stage by duration of infection) and genotypes of specific coagulation pathway genes in 352 White European patients infected with HCV. Genotyping was performed using reverse line blot hybridisation. Results: The rate of fibrosis was significantly higher in patients with the factor V Leiden genotype (Arg560Gln) (ANOVA, p=0.004). In disease association studies, a significant association was seen (Fisher’s exact test, p=0.029; odds ratio 3.28 for fast progression to cirrhosis (expected to reach cirrhosis in less than 30 years) if heterozygous for factor V Leiden). No associations were seen between factor II genotype and fibrosis rate. Conclusions: Possession of the factor V Leiden polymorphism significantly increases the risk of rapid disease progression in HCV, suggesting a role for the coagulation system in the pathogenesis of fibrotic liver disease. |
| Databáze: | OpenAIRE |
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