SUSTAINED VIROLOGICAL RESPONSE REDUCES RISK OF PORTAL VEIN THROMBOSIS IN HEPATITIS C PATIENTS WITH CIRRHOSIS

Document Type

Conference Proceeding

Publication Date

10-1-2023

Publication Title

Hepatology

Abstract

Background: Portal vein thrombosis (PVT) is a relatively common complication of liver cirrhosis. Prevalence estimates ranging from 10-25% of cirrhotic patients, but there are few studies investigating whether treatment of underlying liver disease affects risk of PVT. We used data on patients with cirrhosis and a history of chronic hepatitis C (HCV) infection to evaluate the impact of antiviral treatment status (treated or untreated) and treatment response (sustained virological response [SVR] or treatment failure) as well as patient demographic and clinical characteristics on risk of PVT. Methods: Patients were drawn from the multisite, US-based Chronic Hepatitis Cohort Study. PVT events were identified using ICD-CM codes. Events were excluded if they occurred< 1 month before or< 5 months after other thrombotic events (eg, deep vein thrombosis), malignant neoplasm, gastrointestinal inflammatory conditions (eg pancreatitis), pregnancy/ hormone therapy, or major abdominal surgery. Risk for PVT was assessed using a discrete survival model that include both fixed covariates (age, race, sex, history of thrombotic events, malignant neoplasm, gastrointestinal inflammatory conditions, pregnancy/hormone therapy, and major abdominal surgery) and time-dependent variables (BMI, compensated/decompensated cirrhosis, and treatment status/response). Time-dependent propensity score weighting was used to address treatment selection bias. Patients were followed until liver transplant (if applicable) or last encounter; death was considered a competing risk. Results: A total of 6098 HCV patients with cirrhosis were included, among whom 39% (1798) received antiviral therapy and 55% (2956) achieved SVR; 116 patients developed PVT across 10 years of follow-up. SVR significantly reduced risk of PVT compared to no treatment (aHR=0.29) and treatment failure (aHR=0.12). Compared to no treatment, treatment failure was associated with more than twice the risk of PVT (aHR=2.35). Sex and race were significantly associated with PVT: female patients had lower risk than male patients (aHR=0.83]; Black patients were at 50% higher risk than whites (aHR=1.5). Other significant risk factors included BMI (aHR=0.70 [< 25 vs 25-30] and aHR=0.85 [25-30 vs >=30), and history of malignancy (aHR=1.75); Decompensated cirrhosis increased risk more than 8-fold (aHR=8.06). Conclusion: In adjusted analyses, SVR from either interferon-based or direct-acting antiviral therapy is significantly and strongly associated with lower risk of PVT among HCV patients with cirrhosis. Male sex, Black race, and increasing BMI were associated with increased risk. Future studies to elucidate possible mechanisms for these observations are warranted.

Volume

78

First Page

S710-S711

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