Predicting de‐novo portal vein thrombosis after HCV eradication: A long‐term competing risk analysis in the ongoing PITER cohort

Abstract

Background & AimsSustained virological response (SVR) by direct‐acting antivirals (DAAs) may reverse the hypercoagulable state of HCV cirrhosis and the portal vein thrombosis (PVT) risk. We evaluated the incidence and predictive factors of de novo, non‐tumoral PVT in patients with cirrhosis after HCV eradication.MethodsPatients with HCV‐related cirrhosis, consecutively enrolled in the multi‐center ongoing PITER cohort, who achieved the SVR using DAAs, were prospectively evaluated. Kaplan‐Meier and competing risk regression analyses were performed.ResultsDuring a median time of 38.3 months (IQR: 25.1–48.7 months) after the end of treatment (EOT), among 1609 SVR patients, 32 (2.0%) developed de novo PVT. A platelet count ≤120,000/μL, albumin levels ≤3.5 mg/dL, bilirubin >1.1 mg/dL, a previous liver decompensation, ALBI, Baveno, FIB‐4, and RESIST scores were significantly different (p < 0.001), among patients who developed PVT versus those who did not. Considering death and liver transplantation as competing risk events, esophageal varices (subHR: 10.40; CI 95% 4.33–24.99) and pre‐treatment ALBI grade ≥2 (subHR: 4.32; CI 95% 1.36–13.74) were independent predictors of PVT. After HCV eradication, a significant variation in PLT count, albumin, and bilirubin (p < 0.001) versus pre‐treatment values was observed in patients who did not develop PVT, whereas no significant differences were observed in those who developed PVT (p > 0.05). After the EOT, esophageal varices and ALBI grade ≥2, remained associated with de novo PVT (subHR: 9.32; CI 95% 3.16–27.53 and subHR: 5.50; CI 95% 1.67–18.13, respectively).ConclusionsIn patients with HCV‐related cirrhosis, a more advanced liver disease and significant portal hypertension are independently associated with the de novo PVT risk after SVR.

Portal Vein Thrombosis: State-of-the-Art Review

“…In patients with a hepatitis C virus (HCV) infection, sustained virological response (SVR) by direct-acting antivirals (DAAs) could reverse the hypercoagulable state and the PVT risk [ 32 , 33 ]. Esophageal varices [hazard ratio (HR): 10.40; CI 95% 4.33–24.99] and pre-treatment albumin–bilirubin (ALBI) grade ≥ 2 (HR: 4.32; CI 95% 1.36–13.74) were independent predictors of PVT [ 32 ]. After the end of treatment, esophageal varices and ALBI grade ≥ 2 remained associated with de novo PVT (HR: 9.32; CI 95% 3.16–27.53 and HR: 5.50; CI 95% 1.67–18.13, respectively) [ 32 ].…”

“…Esophageal varices [hazard ratio (HR): 10.40; CI 95% 4.33–24.99] and pre-treatment albumin–bilirubin (ALBI) grade ≥ 2 (HR: 4.32; CI 95% 1.36–13.74) were independent predictors of PVT [ 32 ]. After the end of treatment, esophageal varices and ALBI grade ≥ 2 remained associated with de novo PVT (HR: 9.32; CI 95% 3.16–27.53 and HR: 5.50; CI 95% 1.67–18.13, respectively) [ 32 ].…”

“…In patients with a hepatitis C virus (HCV) infection, sustained virological response (SVR) by direct-acting antivirals (DAAs) could reverse the hypercoagulable state and the PVT risk [32,33]. Esophageal varices [hazard ratio (HR): 10.40; CI 95% 4.33-24.99] and pre-treatment albumin-bilirubin (ALBI) grade ≥ 2 (HR: 4.32; CI 95% 1.36-13.74) were independent predictors of PVT [32].…”