BACKGROUND: Venous thrombosis may complicate the clinical course of liver cirrhosis (LC), but the pathogenesis is still uncertain. We have previously demonstrated that antiphospholipid (aPL) antibodies were a risk factor for thrombosis. In the same study it was also evident that there was a higher prevalence of hepatitis C virus (HCV) infection in patients with thrombosis, and an association between anti-HCV positivity and aPL. METHODS: In a case-control study, 18 consecutive patients with LC, who had suffered from splanchnic venous thrombosis (n = 12), or thrombophlebitis (n = 6), were matched for age, sex, and degree of liver failure with 36 LC patients without thrombosis. RESULTS: In comparison to patients without thrombosis, patients with thrombosis had higher prevalence of HCV infection (p = 0.0027), positivity for aPL antibodies (p = 0.0003), and higher values of fragment F1+2, a marker of thrombin generation (p = 0.0083). While F1+2 values were similar in aPL (+) and aPL (-) patients, HCV patients had significantly higher values of F1+2 than patients with hepatitis B virus (HBV) infection and/or alcoholism (2.6 +/- 0.94 vs 1.5 +/- 0.66, p = 0.0001). CONCLUSIONS: These data suggest that in LC, HCV infection may contribute to clotting system activation, thus predisposing patients to venous thrombosis.
BACKGROUND:Venous thrombosis may complicate the clinical course of liver cirrhosis (LC), but the pathogenesis is still uncertain. We have previously demonstrated that antiphospholipid (aPL) antibodies were a risk factor for thrombosis. In the same study it was also evident that there was a higher prevalence of hepatitis C virus (HCV) infection in patients with thrombosis, and an association between anti-HCV positivity and aPL. METHODS: In a case-control study, 18 consecutive patients with LC, who had suffered from splanchnic venous thrombosis (n = 12), or thrombophlebitis (n = 6), were matched for age, sex, and degree of liver failure with 36 LC patients without thrombosis. RESULTS: In comparison to patients without thrombosis, patients with thrombosis had higher prevalence of HCV infection (p = 0.0027), positivity for aPL antibodies (p = 0.0003), and higher values of fragment F1+2, a marker of thrombin generation (p = 0.0083). While F1+2 values were similar in aPL (+) and aPL (-) patients, HCVpatients had significantly higher values of F1+2 than patients with hepatitis B virus (HBV) infection and/or alcoholism (2.6 +/- 0.94 vs 1.5 +/- 0.66, p = 0.0001). CONCLUSIONS: These data suggest that in LC, HCV infection may contribute to clotting system activation, thus predisposing patients to venous thrombosis.
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