Correlational study on portal vein thrombosis of liver cirrhosis

Abstract

Objective: To study the relevant factors influencing the portal vein thrombosis (PVT) in patients with liver cirrhosis, and the effect of PVT formation on the complications and clinical manifestations of liver cirrhosis. And further investigate the treatment of PVT. Methods: 199 cirrhotic cases with portal vein thrombosis who were hospitalized from January 1, 2014 to October 31, 2018 were selected as PVT group. 199 cirrhotic cases without portal vein thrombosis during the same period were randomly selected as control group to collect the relevant clinical data. Univariate analysis and logistic regression model analysis were carried out on the factors that may affect the formation of PVT, and the complications of cirrhotic patients with PVT were statistically analyzed. According to different data, statistical analysis was performed by t-test, Z- test, χ2 test or Fisher's exact probability method. Results: Univariate analysis results showed that there were statistical differences (P < 0.05) between the two groups on the parts of etiologies of cirrhosis, portal vein width, white blood cells, red blood cells, hemoglobin, platelets, alanine transaminase, aspartate transaminase, alkaline phosphatase, γ - glutamyltransferase, cholinesterase (CHE), blood sugar, total cholesterol, triglyceride, prothrombin time, fibrinogen and thrombin time. Logistic regression model analysis results showed that alcoholic cirrhosis [OR = 3.125 (95% confidence interval, 1.414-6.906), P = 0.005], and portal vein widening [OR = 5.814 (95% confidence interval, 2.746-12.307), P < 0.001] were independent influencing factors of PVT formation in cirrhosis. PVT formation in cirrhosis made patients more susceptible to leukopenia [OR = 1.594 (95% confidence interval, 1.015-2.502), P = 0.043] and CHE reduction [OR = 4.267 (95% confidence interval, 2.313-7.869) P < 0.001]. Gastroesophageal variceal bleeding, ascites, pleural effusion, esophageal varices, severe gastroesophageal varices, and hospitalization length were significantly elevated in PVT group than the control group, and the difference was statistically significant (P < 0.05). Conclusion: Alcoholic cirrhosis and portal vein widening are the factors influencing the formation of PVT in liver cirrhosis. Patients with PVT in liver cirrhosis are more susceptible to leukopenia and CHE reduction. The formation of PVT makes patients with liver cirrhosis more susceptible to rupture and bleeding of gastroesophageal varices, severe gastroesophageal varices, ascites, and pleural effusion and other clinical manifestations, thereby prolonging the length of hospital stay.