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Vascular liver disorders (VLDs) comprise a wide spectrum of clinical-pathological entities that primarily affect the hepatic vascular system of both cirrhotic and non-cirrhotic patients. VLDs more frequently involve the portal and the hepatic veins, as well as liver sinusoids, resulting in an imbalance of liver homeostasis with serious consequences, such as the development of portal hypertension and liver fibrosis. Surprisingly, many VLDs are characterized by a prothrombotic phenotype. The molecular mechanisms that cause thrombosis in VLD are only partially explained by the alteration in the Virchow's triad (hypercoagulability, blood stasis, and endothelial damage) and nowadays their pathogenesis is incompletely described and understood. Studies about this topic have been hampered by the low incidence of VLDs in the general population and by the absence of suitable animal models. Recently, the role of coagulation imbalance in liver disease has been postulated as one of the main mechanisms linked to fibrogenesis, so a novel interest in vascular alterations of the liver has been renewed. This review provides a detailed analysis of the current knowledge of molecular mechanisms of VLD. We also focus on the promising role of anticoagulation as a strategy to prevent liver complications and to improve the outcome of these patients.

Background and Aims: In cirrhosis, decreased portal flow velocity, thrombophilia factors, and portal hypertension are considered risk factors for portal vein thrombosis (PVT). In cirrhosis, the transformation of the stellate cells causes a progressive decrease of ADAMTS-13, while VWF multimers secretion by endothelial cells is strongly enhanced. This imbalance leads to an accumulation of ultra-large VWF multimers that in sinusoidal circulation could favor PVT both in intra- and extra-hepatic branches, mostly in decompensated cirrhosis. This prospective study was aimed at identifying possible clinical, biochemical, and hemostatic factors predictive for non-tumoral PVT in a cohort of patients with compensated cirrhosis., Methods: Seventynine compensated cirrhosis patients were prospectively followed for 48 months, receiving a periodic Doppler-ultrasound liver examination associated with an extensive evaluation of clinical, biochemical, and hemostatic profile., Results: Five patients developed PVT (cumulative prevalence = 6.3%), occurring 4-36 months after enrollment. In logistic regression analysis, the ADAMTS-13/VWF:GpIbR ratio < 0.4 was the only independent variable significantly associated with PVT (OR 14.6, 95% C.I.:1.36-157.2, p = 0.027). A Cox-regression-analysis confirmed this finding (HR = 7.7, p = 0.027)., Conclusions: The ADAMTS-13/VWF ratio < 0.4 measured in compensated cirrhosis could be a reliable predictive biomarker for PVT development, paving the way to novel therapeutic strategies to prevent and treat PVT in this clinical setting., Competing Interests: Conflict of Interest Authors declare that they have no conflict of interest., (Copyright © 2022. Published by Elsevier Ltd.)

Background: Portal vein thrombosis (PVT) and venous thromboembolism (VTE) are fearsome complications of liver cirrhosis., Objectives: To assess the prevalence and the main risk factors for venous thrombotic complications in hospitalized cirrhotic patients., Patients/methods: We retrospectively reviewed electronic administrative discharge data of 19461 cirrhotic patients hospitalized over a 35-year period; univariate and multivariate logistic regression was used to asses risk factors for PVT or VTE and their impact on hospital stay and mortality., Results: 382 out of 7445 patients (5.1%) were diagnosed with PVT and 95 (1.3%) with VTE. Liver cirrhosis complications were observed in 45% of patients. Hepatic encephalopathy (HE) (OR 13.88 [10.76-17.98] p < 0.0001), endoscopic signs of portal hypertension (OR 1.33 [1.02-1.75] p = 0.02), hepatocellular carcinoma (HCC) (OR 4.59 [3.6-5.84] p < 0.0001), diabetes (OR 1.68 [1.27-2.22] p = 0.0001), abdominal surgery/invasive procedures (OR 2.03 [1.56-2.64] p < 0.0001) emerged as independent predictors of PVT. Higher risk of VTE was observed in patients with HE (OR 3.21 [1.78-5.79] p < 0.0001), HCC (OR 1.98 [1.23-3.19] p = 0.002) or other tumors (OR 2.48 [1.42-4.32] p = 0.001), acute illnesses (infections OR 3.01 [1.84-5.05] p = 0.0001; cardiac/respiratory insufficiency OR 2.4 [1.27-4.53] p = 0.003; acute myocardial infarction/stroke OR 7.86 [1.76-35.12] p = 0.003). VTE was the only independent predictor of in-hospital mortality (OR 4.45 [1.05-18.81] p = 0.042)., Conclusions: Liver disease complications related to portal hypertension, HCC or other tumors, diabetes, acute illnesses (i.e. infections, cardiac/pulmonary insufficiency, acute myocardial infarction/stroke) and abdominal interventions are associated with increased risk of PVT or VTE in hospitalized cirrhotic patients, and should be considered to define personalized preemptive approaches., (© 2022. The Author(s).)

Background and Aims: To date, no study has explored the potential role of ElastPQ, a novel point-SWE technique, in the assessment of clinically significant portal hypertension. The aim of our study was to determine a liver stiffness (LS) cut-off value measured by ElastPQ and laboratory parameters that could help to identify those patients who can safely avoid screening endoscopy., Methods: Data were collected on 1422 patients who underwent ElastPQ measurement from January 2013 to January 2016 in our Department. Inclusion criteria were a LS value of ≥7 kPa, an upper gastrointestinal endoscopy within 12 months and a diagnosis of compensated chronic liver disease. Exclusion criteria were history of decompensated liver disease, evidence of porto-spleno-mesenteric vein thrombosis and non-cirrhotic portal hypertension. Varices were graded as low-risk varices (grade <2) or varices needing treatment (VNT, grade ≥2)., Results: The study included 195 patients (120 [61%] HCV, 171 [88%] Child-Pugh A). Varices were present in 35% cases, with 10% prevalence of VNT. According to ROC curve analysis, LS measurement and platelet count were evaluated as predictors of VNT. Overall, 75/195 (38%) met the 'BAVElastPQ' criteria (that is, LS < 12 kPa and platelet count >150 000/μL). Within this group, 11/75 (15%) had any grade of varices and only 1/75 (1%) had VNT. The BAVElastPQ criteria gave sensitivity of 0.95, specificity of 0.42, positive predictive value of 0.15 and negative predictive value of 0.99., Conclusions: The BAVElastPQ criteria correctly identified 99% of patients without VNT. By applying such criteria, we could have potentially avoided 38% of surveillance endoscopies in our cohort., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: Upper endoscopy is the main tool for the accurate assessment of the risk of bleeding in cirrhotic patients., Aim: To evaluate the diagnostic accuracy of upper endoscopy, in cirrhotic subjects, during common clinical practice., Methods: 120 endoscopic reports produced in different hospitals in our region were retrospectively and randomly selected. After a general evaluation, aimed at assessing the description of various endoscopic features, reports were evaluated by four expert endoscopists and four expert hepatologists. Experts were asked to fill in a questionnaire for each single endoscopic procedure, regarding the diagnostic accuracy of the report., Results: Endoscopic reports lacked descriptions of the size of esophageal varices and red signs in 14% and 29% of cases respectively. Presence (or absence) of gastric varices or portal hypertensive gastropathy were not reported in 62% and 34% of cases respectively. According to expert endoscopists 41% of the reports were incomplete, while, according to hepatologists, reports were incomplete and inadequate for clinical purposes in 36% of cases., Conclusion: Our study clearly evidenced a significant lack of information in reports on upper endoscopy in cirrhotic patients, and supports the prompt adoption of corrective strategies., (Published by Elsevier Ltd.)