Vein Thrombosis In Liver Cirrhosis Research Articles

Portal Vein Thrombosis in Liver Cirrhosis. Part 2: Treatment, Primary and Secondary Prevention

Portal Vein Thrombosis in Liver Cirrhosis. Part 2: Treatment, Primary and Secondary Prevention

Analysis of factors related to recanalization of portal vein thrombosis in liver cirrhosis: a retrospective cohort study

BackgroundPortal vein thrombosis (PVT) is a common complication of liver cirrhosis, yet there are fewer studies about predictors of PVT recanalization. We aimed to further explore the predictors of recanalization in cirrhotic PVT to facilitate accurate prediction of patients’ clinical status and timely initiation of appropriate treatment and interventions. To further investigate the benefits and risks of anticoagulant therapy in cirrhotic PVT patients.MethodsA retrospective cohort study of patients with cirrhotic PVT in our hospital between January 2016 and December 2022, The primary endpoint was to analyze predictors of PVT recanalization by COX regression. Others included bleeding rate, liver function, and mortality.ResultsThis study included a total of 82 patients, with 30 in the recanalization group and 52 in the non-recanalization group. Anticoagulation therapy was the only independent protective factor for portal vein thrombosis recanalization and the independent risk factors included massive ascites, history of splenectomy, Child-Pugh B/C class, and main trunk width of the portal vein. Anticoagulation therapy was associated with a significantly higher rate of PVT recanalization (75.9% vs. 20%, log-rank P < 0.001) and a lower rate of PVT progression (6.9% vs. 54.7%, log-rank P = 0.002). There was no significant difference between different anticoagulation regimens for PVT recanalization. Anticoagulation therapy did not increase the incidence of bleeding complications(P = 0.407). At the end of the study follow-up, Child-Pugh classification, MELD score, and albumin level were better in the anticoagulation group than in the non-anticoagulation group. There was no significant difference in 2-year survival between the two groups.ConclusionAnticoagulation, massive ascites, history of splenectomy, Child-Pugh B/C class, and main portal vein width were associated with portal vein thrombosis recanalization. Anticoagulation may increase the rate of PVT recanalization and decrease the rate of PVT progression without increasing the rate of bleeding. Anticoagulation may be beneficial in improving liver function in patients with PVT in cirrhosis.

Timing of TIPS for the management of portal vein thrombosis in liver cirrhosis.

Timing of TIPS for the management of portal vein thrombosis in liver cirrhosis.

Potential contribution of the gut microbiota to the development of portal vein thrombosis in liver cirrhosis.

Portal vein thrombosis (PVT) is a serious complication of liver cirrhosis (LC) and is closely related to gut homeostasis. The study aimed to investigate the composition of gut microbiota and its putative role in PVT development in LC. 33 patients with LC admitted between January 2022 and December 2022 were enrolled in this study. Based on imaging findings, they were categorized into LC without PVT (n = 21) and LC with PVT (n = 12) groups. Fecal samples were collected from each participant and underwent 16S rDNA sequencing. D-Dimer and platelet elevations were the main clinical features of LC with PVT. The alpha and beta diversity of the gut microbiota in LC with PVT group was found to be significantly higher compared to the control group. The structure of the gut microbiota was significantly different between the two groups. Based on LEfSe data, the genera Akkermansia, Eubacterium hallii group, Fusicatenibacter, and Anaerostipes were enriched in the LC with PVT, while Enterococcus, Weissella, Bacteroides, and Subdoligranulum were enriched in those of the LC subjects. Changes in microbiota structure result in significant differences in gut microbiota metabolism between the two groups. Altered levels of the microbiota genera were shown to be correlated with coagulation factor parameters. In animal experiments, the addition of Bacteroides reversed the CCl4-induced PVT. Liver cirrhosis with PVT led to a disorder in the gut microbiota, which was characterized by an increase in pathogenic bacteria and a decrease in beneficial bacteria. Furthermore, modulating the gut microbiota, especially Bacteroides, may be a promising therapeutic approach to reduce the progression of PVT in LC.

Understanding the pathogenesis of portal vein thrombosis in liver cirrhosis: We are still on the way.

Portal vein thrombosis (PVT) is a common complication of liver cirrhosis. In this issue of the Journal of Clinical Ultrasound: Sonography and other Imaging Techniques, a systematic review and meta‐analysis by Giri et al assessed the role of portal system hemodynamics for predicting the presence and development of PVT in liver cirrhosis.

Timing of anticoagulation for the management of portal vein thrombosis in liver cirrhosis.

Timing of anticoagulation for the management of portal vein thrombosis in liver cirrhosis.

Analysis of related factors of portal vein thrombosis in liver cirrhosis

Background and aimsTo investigate the usefulness of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), protein C (PC), and thromboelastography (TEG) to serve as a predictor of portal vein thrombosis (PVT) in patients with liver cirrhosis. Additionally, we examined the clinical significance of the above indicators in terms of disease progression.MethodsA total of 123 patients with liver cirrhosis were recruited from May 2021 to December 2021, according to the imaging findings. They were divided into the PVT group (n = 52) and the non-PVT group (n = 71). Furthermore, patients with PVT were divided into plasma transfusion groups (n = 13) and non-plasma transfusion groups (n = 39). The basic general information, past medical history, laboratory, and imaging examination data were collected and analyzed.ResultsIn univariate analysis, there was no significant difference between the two groups in IL-6, PC, reaction time (R), alpha angle (Angle), maximum amplitude, or coagulation index (CI) (P > 0.05). TNF-α in the PVT group was significantly lower than that in the non-PVT group (P = 0.001). K-time (K) in the PVT group was significantly higher than that in the non-PVT group (P = 0.031). There was no significant difference in IL-6, TNF-α, PC, or TEG between different Child–Pugh classification groups (P > 0.05). There were no significant differences in TEG between the plasma transfusion group and the non-plasma transfusion group. In Binary logistic regression analysis, TNF-α (OR = 0.9881, 95%CI = 0.971, 0.990, P < 0.001), K(OR = 1.28, 95% = 1.053, 1.569, P = 0.014), activate partial thromboplastin time (APTT) (OR = 0.753, 95%CI = 0.656, 0.865, P < 0.001), portal vein diameter (OR = 1.310, 95%CI = 1.108, 1.549, P = 0.002)and the history of splenectomy or embolism (OR = 7.565, 95%CI = 1.514, 37.799, P = 0.014)were related to the formation of PVT.ConclusionsTNF-α, K, APTT, portal vein diameter, and splenectomy or embolism history were associated with PVT formation, but IL-6 was not.

Safety of anticoagulation use for treatment of portal vein thrombosis in liver cirrhosis and its effect on hospital-based outcomes: an insight from a US nationwide database

Background and aimAnticoagulation use for portal vein thrombosis (PVT) in patients with advanced liver disease is controversial. We investigated the effect of anticoagulation on outcomes in patients with PVT with...

Metabolic Disorders and Risk of Portal Vein Thrombosis in Liver Cirrhosis: A Systematic Review and Meta-Analysis.

Portal vein thrombosis is considered to be an indicator of worse outcomes in patients with hepatic cirrhosis. More and more evidence shows that metabolic disorders are noticeable pro-thrombotic factors. However, whether or not metabolic disorders increase the risk of cirrhotic portal vein thrombosis is controversial. We aim to quantify the magnitude of the association between metabolic disorders and the risk of cirrhotic portal vein thrombosis. Databases were searched for papers to identify studies in which metabolic disorders were compared in liver cirrhosis with or without portal vein thrombosis. Based on data from the eligible studies, metabolic disorders related to portal vein thrombosis included diabetes mellitus, nonalcoholic fatty liver disease, hypercholesterolemia, and body mass index. Pooled adjusted odds ratios with 95% CIs were calculated. Data for 22 studies with a total of 57 371 portal vein thrombosis cases and 3 979 015 participants were included. Statistically significant pooled odds ratios for portal vein thrombosis were obtained for diabetes mel- litus (odds ratio 1.80, 95% CI 1.42-2.28), nonalcoholic fatty liver disease (odds ratio 1.61, 95% CI 1.34-1.95), and hypercholesterolemia (odds ratio 3.59, 95% CI 1.83-7.03). Body mass index was likely irrelevant with cirrhotic portal vein thrombosis (odds ratio 1.01, 95% CI 0.87-1.17), both in overall and subgroup meta-analyses. Significant heterogeneities among studies were observed, except for the hypercholesterolemia group. Metabolic disorders, such as diabetes mellitus, nonalcoholic fatty liver disease, and hypercholesterolemia, increased the risk of portal vein thrombosis in cirrhotic patients by 1.80-fold, 1.61-fold, and 3.59-fold, respectively. Body mass index did not appear to be a risk predictor of cirrhotic portal vein thrombosis. Further, well-designed clinical and mechanistic studies are required to strengthen the arguments, especially in obese patients.

Comparison of transjugular intrahepatic portosystemic with endoscopic treatment plus anticoagulation for esophageal variceal bleeding and portal vein thrombosis in liver cirrhosis

Background and aim The optimal management of esophageal variceal bleeding (EVB) and portal vein thrombosis (PVT) in liver cirrhosis has not been well-established. The aim of the present study was to compare the efficacy and safety of transjugular intrahepatic portosystemic shunt (TIPS) and endoscopic treatment (ET) plus anticoagulation in cirrhotic patients with EVB and PVT. Patients and methods A total of 66 cirrhotic patients with PVT and EVB (31 in the TIPS group and 35 in the ET plus anticoagulation group) were evaluated retrospectively between January 2016 and January 2022. Results During the follow-up period, 85.5% of patients in the TIPS group achieved complete recanalization of the portal vein, as compared with 19.6% in the ET plus anticoagulation group (p < .001). The cumulative 5-year rate of variceal rebleeding in the TIPS group was significantly lower than that in the ET plus anticoagulation group (31.0 vs. 50.1%; p = .017). The TIPS group exhibited a significantly higher incidence of overt hepatic encephalopathy (HE) than the ET plus anticoagulation group (25.8 vs. 5.7%; p = .037). No difference in the 5-year survival rate (74.1 vs. 85.7%; p = .692) and probability of other complications was observed between the two groups. Conclusion TIPS was superior to ET plus anticoagulation in preventing variceal rebleeding and achieving recanalization of PVT but increased the incidence of overt HE without improving the survival rate.

Complexities and challenges in the management of portal vein thrombosis in cirrhosis

Portal vein thrombosis is a common complication of liver cirrhosis. Based on the recent "Expert Consensus on the Management of Portal Vein Thrombosis in Liver Cirrhosis (2020, Shanghai)", we analyzed a series of differences in the field of portal vein thrombosis in liver cirrhosis and point out the complexities and challenges faced by clinical anticoagulation treatment, so as to provide a reference for further clinical exploration of the standardized management of portal vein thrombosis in liver cirrhosis.

Consensus for management of portal vein thrombosis in liver cirrhosis (2020, Shanghai).

Portal vein thrombosis (PVT) is a common and severe complication of liver cirrhosis. So far, there have been few consensuses or practice guidelines on the management of PVT in liver cirrhosis. In this expert consensus, we systematically review the epidemiology, risk factors, imaging examinations, diagnosis, assessment of disease severity, and treatment strategy of PVT in liver cirrhosis, based on the most recent evidence and expert opinions, to further standardize the diagnosis and treatment of the disease in clinical practice.

Consensus for management of portal vein thrombosis in liver cirrhosis (2020, Shanghai)

门静脉血栓是肝硬化常见的严重并发症之一。当前，国内外尚无专门针对肝硬化门静脉血栓管理的指南或共识。本专家共识基于最新研究证据及国内专家共识意见，系统阐述了肝硬化门静脉血栓的流行病学、危险因素、影像学检查、诊断、病情评估以及治疗策略，以进一步规范临床诊疗实践。.

No Association between Ischemic Stroke and Portal Vein Thrombosis in Liver Cirrhosis.

Background and Aims There seems to be a higher risk of ischemic stroke and portal vein thrombosis in liver cirrhosis. Both of them may be associated with hypercoagulability. We aim to explore the association between ischemic stroke and portal vein thrombosis in liver cirrhosis. Study Design and Methods. We selected patients from our prospectively established database of liver cirrhosis from December 2014 to July 2019. The difference between patients with and without stroke was compared. A 1 : 1 propensity score matching (PSM) analysis was performed to adjust the effect of age, sex, Child-Pugh score, and MELD score on our statistical results. Results There were 349 cirrhotic patients in the cross-sectional study. The prevalence of stroke, ischemic stroke, hemorrhagic stroke, and portal vein thrombosis was 8.88% (31/349), 8.31% (29/349), 1.15% (4/349), and 28.65% (100/349) in liver cirrhosis, respectively. Patients with ischemic stroke were significantly older and had significantly higher proportions of alcohol abuse, smoking, and arterial hypertension and higher levels of white blood cell and low-density lipoprotein. However, statistical analyses with and without PSM did not find any significant association between ischemic stroke and portal vein thrombosis in patients with liver cirrhosis. Conclusion Ischemic stroke might not be associated with portal vein thrombosis in liver cirrhosis.

Advances in the study of gastroesophageal varices with portal vein thrombosis in liver cirrhosis

Portal vein thrombosis (PVT) is one of the serious complications in the decompensated stage of liver cirrhosis, which is often accompanied by the aggravation of liver cirrhosis and other complications and in severe cases; it may induce gastroesophageal variceal hemorrhage and endanger the lives of patients. Furthermore, the most common complication in decompensated stage of cirrhosis is history of gastroesophageal variceal hemorrhage and the formation of PVT that may be a risk factor to promote each other. Presently, there are guidelines for diagnosis and treatment of gastroesophageal variceal hemorrhage in liver cirrhosis, but there is still a lack of in-depth understanding of cirrhosis complicated with PVT. This paper summarizes advances in the study of gastroesophageal variceal hemorrhage complicated with PVT in liver cirrhosis in order to enhance the understanding of risk factors for diagnosis and treatment.

Nonselective beta-blockers and development of portal vein thrombosis in liver cirrhosis: a systematic review and meta-analysis.

Portal vein thrombosis (PVT), which is associated with reduced portalvein velocity, is considered to be an indicator for worse outcomes in liver cirrhosis. Nonselective beta-blockers (NSBBs), which are widely used for primary and secondary prophylaxis of esophageal variceal bleeding in liver cirrhosis, can significantly decrease the portal vein velocity. We proposed a hypothesis that the use of NSBBs might facilitate the development of PVT in cirrhotic patients. The PubMed, EMBASE, and Cochrane Library databases were searched. Major meeting abstracts and randomized-controlled trials regardingthe use of NSBBs in liver cirrhosis were also hand-searched. The number of patients who developed PVT in groups treated with or without NSBBs was pooled. Odds ratios (ORs) or risk ratios (RRs) with 95% confidence intervals (CIs) were calculated. Subgroup meta-analyses were performed according to the type of studies,region, and study quality. Meta-regression and sensitivity analyses were performed to explore the source of heterogeneity. Nine of the 6416 retrieved papers were finally included. Overall, meta-analysis demonstrated that NSBBs were significantly associated with the development of PVT (OR 4.62, 95% CI 2.50-8.53; p < 0.00001). The heterogeneity was statistically significant (I2 = 80%; p < 0.00001). Subgroup meta-analyses still demonstrated a significantly positive association of NSBBs with the development of PVT in cohort studies (RR 2.57, 95% CI 1.46-4.51; p = 0.001) and case-control studies (OR 8.17, 95% CI 2.46-27.06; p = 0.0006). Sensitivity analyses based on subgroups find the source of heterogeneity. Based on the systematic review and meta-analysis, we found that the use of NSBBs increased a 4.62-fold risk of PVT in cirrhotic patients.

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

To build a predictive model for PVT in cirrhotic patients. 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. 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). 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.

Timing of Anticoagulation for Portal Vein Thrombosis in Liver Cirrhosis: A US Hepatologist's Perspective.

Timing of Anticoagulation for Portal Vein Thrombosis in Liver Cirrhosis: A US Hepatologist's Perspective.

Timing of Anticoagulation for Portal Vein Thrombosis in Liver Cirrhosis: An Italian Internist's Perspective.

Conflict of Interest: Walter Ageno has received a research grant from Bayer to support a clinical study in patients with splanchnic vein thrombosis. Nicoletta Riva has no relevant conflicts to declare in relation to this paper.

Low-molecular-weight heparin treatment for portal vein thrombosis in liver cirrhosis: Efficacy and the risk of hemorrhagic complications

IntroductionPortal vein thrombosis (PVT) is a well-known complication in patients with liver cirrhosis (LC). The aim of this study is to investigate the outcomes of cirrhotic patients with PVT treated with low-molecular-weight heparin (LMWH). MethodNinety-one LC patients with PVT were treated with dalteparin or enoxaparin for six months. Patients with major bleeding during the last three months, severe thrombocytopenia, or impaired renal function were excluded. ResultsThe median age was 62.9 years, and 59 patients had hepatocellular carcinoma. The overall recanalization rate was 61.5%. Patients with a favorable Child-Pugh class and those recently diagnosed as having a thrombus showed significantly better responses. In those who responded to the anticoagulation therapy, the post-treatment bilirubin and platelet levels were improved compared to those in the pre-treatment state. The relapse rate for PVT was 56.6%, and the median time to relapse was 4.0 months. Bleeding was reported in 13 patients (14.4%), and two patients died due to fatal bleeding. A history of variceal bleeding and low serum albumin were risk factors for bleeding. ConclusionLMWH therapy for PVT in LC is effective. Advanced LC and a delayed start of anticoagulation treatment decrease the effect of LMWH. Despite its effectiveness, there is a risk of hemorrhage, hence anticoagulation should be carefully considered, especially in patients with advanced LC and a history of variceal bleeding.