[Long-term prognostic implications of portal vein thrombosis in patients with hepatitis B-related cirrhosis].

Abstract

Objective: To analyze the features of portal vein thrombosis (PVT) in patients with hepatitis B-related cirrhosis and its impact on long-term prognosis. Methods: Clinical data from a cohort of patients with hepatitis B-related cirrhosis from May 2009 to August 2020 were analyzed, enhanced CT examination was employed for the diagnosis and classification of PVT. Patients with hepatitis B-related cirrhosis without PVT at baseline were enrolled. The endpoint events of follow-up were death related to liver disease, liver transplantation, liver cancer, or followed up until December 31, 2023. During the follow-up, patients were divided into PVT group and control group based on the presence or absence of PVT. Changes in clinical data were compared between the groups at baseline and endpoint time; besides, Kaplan-Meier survival curve, Log-rank test, and Cox regression analysis were employed to assess the influence of PVT on prognosis. Results: A total of 267 patients with hepatitis B-related cirrhosis were included, with a median follow-up time of 52.0 (46.7, 57.3) months. The PVT group had 99 patients, and the control group had 168 patients. In the PVT group, 28.28% (28/99) had spleen resection, and 74.7% (74/99) did not receive anticoagulant treatment. Main portal vein thrombosis, portal vein branch thrombosis, and both were found in 34.3% (34/99), 23.2% (23/99), and 15.2% (15/99) of patients, respectively, with 27.3% (27/99) involving the splenic vein or superior mesenteric vein. During follow-up, 63.6% (63/99) of PVT cases remained stable, 31.3% (31/99) progressed, and 5.1% (5/99) showed resolution. In the PVT group, white blood cells, hemoglobin, and platelet counts decreased significantly (P<0.05), international normalized ratio (INR) increased from baseline [1.28 (1.14, 1.39) vs. 1.33 (1.19, 1.46), P=0.041], and spleen length increased [163.84±30.68 mm vs. 177.26±32.61 mm, P<0.001]. The incidence of esophageal variceal bleeding was significantly higher in the PVT group compared to the control group (57.0% vs. 28.7%, P<0.001), while the incidence of hepatic encephalopathy showed no significant difference (P>0.05). The proportion of ascites patients was reduced in the control group (63.1% vs. 41.7%, P<0.001), but there was no significant difference in ascites between the PVT group and the control group (P>0.05). The incidence of composite clinical endpoint events was 21.2% (21/99) in the PVT group and 4.2% (7/168) in the control group (P<0.05). Among PVT patients, those who did not receive anticoagulant treatment had a higher incidence of composite clinical endpoint events compared to those treated with anticoagulation (25.7% vs. 8%, P=0.062). Cox regression analysis showed that PVT formation was an independent risk factor for liver-related adverse events in hepatitis B cirrhosis patients (HR=9.36, 95%CI: 3.65-24.02, P=0.001). Conclusions: The formation of PVT in hepatitis B-related cirrhosis is closely associated with an increased risk of liver-related adverse outcomes. Screening and early prevention of PVT in hepatitis B cirrhosis patients should be emphasized.