Abstract

Objectives: To investigate the impact of portal vein thrombosis (PVT) on cirrhosis decompensation and survival of cirrhosis.Methods: In this retrospective observational study between January 2012 and August 2020, 117 patients with cirrhotic PVT and 125 patients with cirrhosis were included. Propensity score matching (PSM) was applied to reduce the bias. The clinical characteristics of non-tumoral PVT in cirrhosis and its influence on cirrhosis decompensation and survival were analyzed.Results: The median follow-up for the PVT group was 15 (8.0–23.0) months and for the non-thrombosis group 14 (8.0–23.5) months. The presence of PVT was related with esophageal varices, higher Child-Pugh score and MELD score (P < 0.05). Most PVTs were partial (106/117). Non-occlusive PVT disappeared on later examinations in 32/106 patients (30.19%), of which six patients reappeared. All the 11 patients with occlusive PVT remained occlusive, among which five patients (45.45%) developed portal cavernoma. There was no significant correlation between PVT and decompensation or survival before or after PSM. Multivariate analysis identified only Child-Pugh score (HR = 2.210, 95% CI: 1.332–3.667) and serum sodium level (HR = 0.818, 95% CI: 0.717–0.933) as independent factors for death.Conclusion: Though PVT is associated with greater Child-Pugh score and MELD score, it has no significant impact on the progression of cirrhosis.

Highlights

  • Portal vein thrombosis (PVT) is a common complication of patients with cirrhosis

  • We retrospectively explored the impact of PVT on the hepatic decompensation and survival rate in 117 patients with cirrhotic PVT and 125 patients without PVT

  • Propensity scores were estimated using based on serum albumin level, hemoglobin level, Child-Pugh score, MELD score, the history of splenectomy, varices grade III/IV according to Paquet, portal vein diameter and D-dimer

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Summary

Introduction

Portal vein thrombosis (PVT) is a common complication of patients with cirrhosis. It is associated with relative venous stasis caused by portal hypertension, endothelial injury, hypercoagulability, splenectomy and other factors. Acute PVT can have severe abdominal pain, while chronic PVT can be asymptomatic. Many asymptomatic PVT have been accidentally discovered by the widespread application of medical imaging technology. It was reported that the 5-year cumulative incidence of PVT was 10.7% after regular follow-up of 1,243 Child A and B cirrhosis [1]. Non-tumoral PVT is present at liver transplantation in 5–26% of cirrhotic patients [2]. The annual incidence of PVT in patients with advanced cirrhosis may be 10–15% [3].

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