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Genetic and acquired thrombotic factors in chronic hepatitis C

Armelle Poujol-Robert1, Olivier Rosmorduc, Lawrence Serfaty

  • 1Service d'Immunologie et Hématologie Biologiques, Hôpital Saint-Antoine Assistance Publique-Hôpitaux de Paris, Paris, France.

The American Journal of Gastroenterology
|April 2, 2004
PubMed

Insights

Patients with advanced liver fibrosis and cirrhosis show increased thrombotic risk factors. Protein C deficiency, elevated factor VIII, and hyperhomocysteinemia were more common, suggesting a role in liver disease progression.

Area of Science:

  • Hepatology
  • Thrombosis
  • Internal Medicine

Background:

  • Chronic liver disease progression to cirrhosis involves parenchymal remodeling and vascular lesions.
  • Intrahepatic thrombotic events are implicated in the pathogenesis of hepatic fibrosis.
  • Understanding thrombotic risk factors is crucial for managing chronic hepatitis C patients.

Purpose of the Study:

  • To investigate the prevalence of thrombotic risk factors in chronic hepatitis C patients.
  • To compare thrombotic risk factors between patients with and without extensive liver fibrosis or cirrhosis.

Main Methods:

  • Evaluated 68 hepatitis C patients with prothrombin activity >/= 80%.
  • Compared 34 patients with extensive fibrosis/cirrhosis against 34 without.
  • Assessed factor V Leiden, prothrombin mutation, antithrombin, protein C/S deficiencies, hyperhomocysteinemia, factor VIII, and lupus anticoagulant.

Main Results:

  • Protein C deficiency was significantly higher in patients with extensive fibrosis/cirrhosis (41% vs 9%, p=0.004).
  • Elevated factor VIII levels were more frequent in advanced fibrosis/cirrhosis patients (56% vs 18%, p=0.002).
  • Hyperhomocysteinemia was also more prevalent in patients with extensive fibrosis/cirrhosis (29% vs 6%, p=0.023).
  • The co-occurrence of two or more thrombotic factors was significantly higher in patients with extensive fibrosis/cirrhosis (56% vs 3%, p < 0.001).

Conclusions:

  • Multiple thrombotic risk factors frequently coexist in patients with advanced liver fibrosis and early cirrhosis.
  • These factors, potentially linked to local inflammation, may promote thrombotic events in the liver's microcirculation.
  • Identifying and managing these risks could be vital for patients with chronic hepatitis C and liver fibrosis.
Abstract

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