Risk factors associated with portal vein thrombosis in liver cirrhosis: A case-control study

Abstract

Portal vein thrombosis (PVT) in patients with liver cirrhosis is a common complication associated with adverse outcomes. Aim. To build a predictive model for PVT in cirrhotic patients. Materials and methods. A single centre case-control study was carried out. From the database of 1512 cirrhotic patients 94 with newly diagnosed PVT based on contrast-enhanced computed tomography were referred to the Case group. Malignant PVT was an exclusion criterion. Patients without PVT were stratified and matched according to sex, age and etiology of cirrhosis; case-control ratio was 1 : 3-4. The prevalence of PVT in the database, clinical, laboratory, instrumental parameters of the groups were evaluated. Logistic regression model was used to estimate association between variables and PVT. Results and discussion. The overall prevalence of PVT was 6.2% with the highest rates among the patients with HBV infection - 16.7%, nonalcoholic steatohepatitis - 15.6%, alcohol abuse in combination with HCV infection - 11.7%. The best predictive model included variables: Child-Pugh classes B-C (coefficient of regression β=1.853, р=0.001), ascites (β=0.460, р=0.003), hepatocellular carcinoma without vascular invasion (β=2.126, р=0.0001), endoscopic band ligation (β=0.774, р=0.003), azygoportal disconnection (β=2.734, р=0.001), portal hypertensive gastropathy (β=0.793, р=0.017), portal vein diameter (β=0.203, р=0.004), and local factors - ulcerative colitis flare, Clostridium difficile enterocolitis, spontaneous bacterial peritonitis, colorectal cancer, splenectomy, cholecystectomy (β=2.075, р=0.017). The model had accuracy 85.8% (95% CI 81.7-89.4%), sensitivity - 55.1% (95% CI 43.4-66.4%), specificity - 95% (95% CI 91.6-97.3%), and AUC - 0.871 (95% CI 0.826-0.916). Conclusion. Child-Pugh classes B-C, severe portal hypertension, hepatocellular carcinoma without vascular invasion, and local factors were estimated as risk factors of PVT in cirrhotic patients.

Portal vein thrombosis and renal dysfunction: a national comparative study of liver transplant recipients for NAFLD versus alcoholic cirrhosis

“…To the best of our knowledge, no other studies have reported a similar observation in LT recipients. The only publication that signaled that spontaneous bacterial peritonitis might be a risk factor for PVT in cirrhotic patients was by Nadinskaia et al [56] who reported that Child-Pugh class B and C, the presence of hepatocellular carcinoma, the history of surgical azygoportal disconnection, and the presence of any intra-abdominal acute conditions that included spontaneous bacterial peritonitis were predictors for PVT. Therefore, it is conceivable that intra-peritoneal infections or other noninfectious inflammatory processes can induce a locoregional pro-thrombotic condition that predisposes to the formation of PVT.…”

The Predictive Role of Variceal Band Ligation in the Development of Portal Vein Thrombosis in Cirrhotic Patients

“…(12,13) Furthermore, as the present study shows, it seems like VBL for primary prevention could Some studies have already demonstrated that VBL leads to an increase in PV pressure at least temporary and the impact on hemodynamics is influenced by the remaining collaterals . (16,17) Thus, in a study conducted by Piecha et al (18) rapid increase in liver stiffness was associated with VBL and MC Hou et al had Only some case reports highlighted the (20,21) occurrence of portal vein thrombosis immediately after variceal band ligation but to our knowledge this is the first retrospective study that focuses on the possibility of promoting portal vein thrombosis through primary VBL.…”

Significance of altered anticoagulant proteins and D-dimer in cirrhotic portal vein thrombosis: relation to the degree of liver dysfunction

“…The present study showed that most cirrhotic patients of the PVT group were classified in CTP classes B and C and had higher CTP scores than the control group. This finding could be explained by the more profound liver dysfunction in cirrhotic patients with PVT as evidenced by a lower albumin level, and prolonged PT [28]. Cirrhotic patients of the PVT group showed higher incidence and grades of esophageal varices, ascites and HE.…”