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Thrombotic risk in hepatitis C: Interplay between hepatic dysfunction, viral-driven inflammation, and cardiovascular
Mohammed Zohery1, Sarah Jahangir2, Hamed Carter Jenna2
1George Washington School of Medicine and Health Sciences, The George Washington University, Washington, DC 20052, United States.
Insights
Hepatitis C virus (HCV) infection causes systemic inflammation and increases thrombosis risk. Direct-acting antivirals improve outcomes, but ongoing surveillance is vital for high-risk patients.
Area of Science:
- Hepatology
- Vascular Biology
- Infectious Diseases
Background:
- Hepatitis C virus (HCV) is increasingly recognized as a systemic disease, not just a liver-specific condition.
- Chronic HCV infection establishes a pro-inflammatory and pro-thrombotic state, elevating risks for venous and arterial thrombotic events.
- This systemic impact involves endothelial dysfunction, platelet activation, coagulation imbalance, and immune-mediated vascular injury.
Purpose of the Study:
- To review the complex interplay between chronic Hepatitis C virus infection, systemic inflammation, and thrombotic complications.
- To highlight the mechanisms driving virus-induced coagulopathy and its clinical manifestations.
- To emphasize the impact of direct-acting antiviral (DAA) therapy and the need for continued risk assessment.
Main Methods:
- Literature review of studies on Hepatitis C virus, thrombosis, inflammation, and endothelial function.
- Analysis of clinical manifestations and mechanistic pathways linking HCV to thrombotic events.
- Evaluation of the impact of direct-acting antiviral therapy on systemic complications.
Main Results:
- Chronic HCV infection promotes a pro-thrombotic state through endothelial dysfunction, platelet activation, and coagulation/fibrinolysis imbalance.
- Clinical manifestations include portal vein thrombosis, venous thromboembolism, coronary artery disease, and ischemic stroke.
- Direct-acting antiviral therapy effectively reduces inflammation and thrombotic risks, but high-risk patients require ongoing monitoring.
Conclusions:
- Hepatitis C virus infection is a systemic condition with significant thrombotic implications, challenging the traditional view of cirrhosis.
- Effective treatment with DAAs can reverse many systemic effects, but residual risk persists in advanced disease.
- Integrating thrombotic risk assessment into HCV patient care is crucial for comprehensive management.
Abstract:
Hepatitis C virus (HCV) infection, traditionally regarded as a hepatotropic disease, is increasingly recognized as a systemic condition with significant thrombotic implications. Chronic HCV induces a persistent proinflammatory and prothrombotic state that substantially elevates the risk of both venous and arterial events. Mechanistically, HCV drives endothelial dysfunction, enhances platelet activation, disrupts coagulation and fibrinolytic balance, and promotes immune-mediated vascular injury through cryoglobulinemia and chronic systemic inflammation. Clinical manifestations range from portal vein thrombosis and venous thromboembolism to coronary artery disease and ischemic stroke, highlighting the far-reaching consequences of virus-driven coagulopathy. Emerging evidence challenges the historical view of cirrhosis as a "naturally anticoagulated" state, instead describing a fragile hemostatic balance prone to both bleeding and thrombosis. Direct-acting antiviral therapy has transformed outcomes, not only achieving sustained virological response but also reversing systemic inflammation, improving endothelial function, and reducing thrombotic complications. However, patients with advanced fibrosis and comorbidities remain at elevated risk despite viral clearance, underscoring the need for ongoing surveillance. This minireview highlights the interplay between hepatic dysfunction, viral-induced inflammation, and cardiovascular sequelae in chronic HCV, emphasizing the importance of integrating thrombotic risk assessment into clinical care and research frameworks.
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