Portal Vein Thrombosis In Cirrhosis Research Articles

Comparison of the efficacy and safety between rivaroxaban and dabigatran in the treatment of acute portal vein thrombosis in cirrhosis

BackgroundNew oral anticoagulants (NOACs) have been becoming prevalent in recent years and are increasingly used in the treatment of port vein thrombosis. The difference of the efficacy and safety between rivaroxaban and dabigatran remains unclear in the treatment of cirrhotic patients with acute portal vein thrombosis (PVT).MethodsThis retrospective study included all consecutive cirrhotic patients with acute portal vein thrombosis in our institute from January 2020 to December 2021. The patients received oral anticoagulation with rivaroxaban or dabigatran. The demographic, clinical, and imaging data of patients were collected. The diagnosis of acute PVT was confirmed by imaging examinations. The severity of liver cirrhosis was assessed using Child–Pugh score and Model for End-Stage Liver Disease (MELD) score. Outcomes included recanalization (complete, partial, and persistent occlusion), liver function, bleedings, and survival. The log-rank test was used to compare Kaplan–Meier distributions of time-to-event outcomes. The Cox proportional hazards model was used to calculate hazard ratios (HRs) with 95% confidence intervals (CIs).ResultsA total of 94 patients were included, 52 patients (55%) received rivaroxaban and 42 (45%) with dabigatran. The complete and partial recanalization of PVT was observed in 41 patients. There was no significant difference in complete recanalization, partial recanalization, and persistent occlusion between the two groups. With multivariate analysis, D-dimer (HR 1.165, 95% CI 1.036–1.311, p = 0.011) was independent predictors of complete recanalization. The Child–Pugh score (p = 0.001) was significantly improved in both two groups after anticoagulation, respectively. However, there was no difference between the two groups. The probability of survival was 94%, 95% in the rivaroxaban and dabigatran groups (log-rank p = 0.830). Major bleedings were reported in 3 patients (6%) in rivaroxaban group and 1 patient (2%) in dabigatran group (p = 0.646). Six patients (12%) in rivaroxaban group experienced minor bleeding, and five (12%) from dabigatran group (p = 0.691).ConclusionsThe efficacy and safety were comparable between rivaroxaban and dabigatran in the treatment of cirrhotic patients with acute portal vein thrombosis. And D-dimer can contribute to the prediction of PVT recanalization in cirrhotic patients.

Natural history of portal vein thrombosis in cirrhosis: A systematic review with meta-analysis.

Progression of liver disease in cirrhosis is associated with an increased incidence of portal vein thrombosis (PVT) in cirrhosis. However, evidence suggests that spontaneous recanalization of PVT may occur even without anti-thrombotic therapy. Thus, the present meta-analysis was conducted to study the natural history of PVT in cirrhosis, facilitating decisions regarding anticoagulation. Three electronic databases were searched from 2000 to August 2022 for studies reporting the outcome of PVT in cirrhotics without anticoagulation. The pooled proportions with their 95% confidence intervals (CIs) were calculated using a random-effect model. A total of 26 studies (n=1441) were included in the final analysis. Progression of PVT on follow-up was seen in 22.2% (95% CI 16.1-28.4), while 77.7% (95% CI 71.6-83.9) remained non-progressive (improved or stable). The most common outcome was a stable PVT with a pooled event rate of 44.6% (95% CI 34.4-54.7). The pooled rates of regression and complete recanalization of PVT in cirrhotics were 29.3% (95% CI 20.9-37.7) and 10.4% (95% CI 5.0-15.8), respectively. On follow-up after improvement, pooled recurrence rate of PVT was 24.0% (95% CI 14.7-33.4). MELD score, and presence of ascites had a negative association, while a longer follow-up duration had positive association with PVT regression. Approximately 25% of the cases of PVT in cirrhosis are progressive, 30% cases improve, and 45% remain stable. Future studies are needed to analyze the predictors of spontaneous regression.

Portal vein thrombosis in cirrhosis: A literature review.

Portal Vein Thrombosis (PVT), a common complication of advanced liver disease, is defined as an obstruction of the portal vein due to thrombus formation that can extend to the superior mesenteric and splenic veins. It was believed that PVT occurred predominantly due to prothrombotic potential. However, recent studies have shown that decreased blood flow related to portal hypertension appears to increase PVT risk as per Virchow's triad. It is well known that there is a higher incidence of PVTs in cirrhosis with a higher MELD and Child Pugh score. The controversy for management of PVTs in cirrhotics lies in the individualized assessment of risks versus benefits of anticoagulation, since these patients have a complex hemostatic profile with both bleeding and procoagulant propensities. In this review, we will systematically compile the etiology, pathophysiology, clinical features, and management of portal vein thrombosis in cirrhosis.

Increased Factor VIII Activity Is Predictive of the Occurrence of Portal Vein Thrombosis in Cirrhosis.

The aim of this study was to identify the role of factor VIII (FVIII) in portal vein thrombosis (PVT) occurrence in cirrhotic patients with gastroesophageal variceal bleeding. A total of 453 cirrhotic patients with gastroesophageal varices were enrolled. Computed tomography was performed at baseline and patients were divided into PVT and non-PVT groups (n = 131 vs. 322). Individuals without PVT at baseline were followed up for the development of PVT. Time-dependent receiver operating characteristic analysis of FVIII for PVT development was performed. The Kaplan-Meier methodology was used to analyze the predictive ability of FVIII for PVT incidence at 1 year. FVIII activity (177.00 vs. 153.70, p = 0.001) was significantly increased in the PVT group compared with the non-PVT group in cirrhotic patients with gastroesophageal varices. FVIII activity was positively correlated with the severity of PVT (161.50 vs. 171.07 vs. 187.05%, p = 0.001). Furthermore, FVIII activity (hazard ratio [HR]: 3.48, 95% confidence interval [CI]: 1.14-10.68, p = 0.029 in model 1; HR: 3.29, 95% CI: 1.03-10.51, p = 0.045 in model 2) was an independent risk factor of 1-year PVT development in patients without PVT at baseline, which was confirmed by two separate Cox regression analysis and competing risk models. Patients with elevated FVIII activity exhibit a higher incidence of PVT in the non-PVT group at 1 year (15.17 vs. 3.16%, p < 0.001). The predictive value of FVIII remains significant in individuals who have never received splenectomy (14.76 vs. 3.04%, p = 0.002). Elevated FVIII activity was potentially associated with the occurrence and the severity of PVT. It might be helpful to identify cirrhotic patients at risk of PVT.

Presence of Hepatocellular Carcinoma Does Not Affect Course and Response to Anticoagulation of Bland Portal Vein Thrombosis in Cirrhotic Patients.

Malignancies are generally considered a risk factor for deep vein thrombosis and may hamper the recanalisation of thrombosed veins. We investigate whether the natural course and response to anticoagulant treatment of bland portal vein thrombosis (PVT) in patients with cirrhosis complicated by hepatocellular carcinoma (HCC) differ from those without HCC. Retrospective study in two hepatology referral centres, in Italy and Romania where patients with a diagnosis of PVT on cirrhosis and follow-up of at least 3 months with repeated imaging were included. A total of 162 patients with PVT and matching inclusion and exclusion criteria were identified: 30 with HCC were compared to 132 without HCC. Etiologies, Child-Pugh Score (7 vs 7) and MELD scores (11 vs 12, p=0.3679) did not differ. Anticoagulation was administered to 43% HCC vs 42% nonHCC. The extension of PVT in the main portal trunk was similar: partial/total involvement was 73.3/6.7% in HCC vs 67.4/6.1% in nonHCC, p=0.760. The remainder had intrahepatic PVT. The recanalization rate was 61.5% and 60.7% in HCC/nonHCC in anticoagulated patients (p=1). Overall PVT recanalisation, including treated and untreated patients, was observed in 30% of HCC vs 37.9% of nonHCC, p=0.530. Major bleeding incidence was almost identical (3.3% vs 3.8%, p=1). Progression of PVT after stopping anticoagulation did not differ (10% vs 15.9%, respectively, HCC/nHCC, p=0.109). The course of bland non-malignant PVT in cirrhosis is not affected by the presence of active HCC. Treatment with anticoagulation in patients with active HCC is safe and as effective as in nonHCC patients, this can potentially allow us to use otherwise contraindicated therapies (ie TACE) if a complete recanalization is achieved with anticoagulation.

Treatment of portal vein thrombosis in cirrhosis: a multicenter real life cοhort study.

Portal vein thrombosis (PVT) is a common complication of cirrhosis and can be a cause or consequence of liver disease progression. It is unclear whether PVT treatment is affecting clinical outcomes in cirrhotics. This is a multicenter study of cirrhotics with PVT, initially retrospectively and thereafter prospectively registered in a data base. We studied the impact of PVT treatment on this population for efficacy, safety and the impact on survival. In survival analysis Mantel-Cox and Wilcoxon-Breslow-Gehan tests were used. A P value of <0.05, was considered significant. For statistical computations the STATA 12.1 was used. Seventy-six patients were included (76% decompensated, median MELD score 12 and Child-Pugh score 7), 47% with concomitant HCC. Fifty-one patients with PVT were treated with Vitamin-K antagonists or Low-Molecular-Weight Heparin. Patients were followed up for at least 6 months after PVT diagnosis, or until death or transplantation. PV patency after 6 months was not statistically different between patients receiving or not anticoagulation (complete-partial recanalization 27.4% of treated vs. 20% of untreated, P=0.21). Median survival was statistically worse between patients treated with anticoagulation than those untreated (10 vs. 15 months, P=0.036). Less portal hypertensive bleeding and less decompensation rates were found in treated cirrhotics vs. untreated (45.8% vs. 54.2%, P=0.003 and 78% vs. 80.9%, P=0.78, respectively). Patients with HCC had worse survival when treated vs. untreated (P=0.047). In our cohort of cirrhotics with PVT, treatment was feasible with acceptable side effects, but without meaningful clinical benefits.

Portal Vein Recanalization-Transjugular Intrahepatic Portosystemic Shunt (PVR-TIPS) Facilitates Liver Transplantation in Cirrhotic Patients with Occlusive Portal Vein Thrombosis.

Portal vein thrombosis (PVT) is a heterogeneous condition with multiple possible etiologies and to varying degrees has historically limited candidacy for liver transplant (LT) in the cirrhotic patient population due to resultant difficulties in constructing a robust portal vein anastomosis. While intraoperative approaches to managing PVT are well-described, methods which approximate normal portal physiology are not always feasible depending on the extent of PVT, and other nonphysiologic techniques are linked with substantial morbidity and poor long-term outcomes. Portal vein recanalization-transjugular intrahepatic portosystemic shunt (PVR-TIPS) creation is an efficacious method of restoring physiologic portal flow in cirrhotic patients prior to LT allowing for end-to-end PV anastomosis, and is the product of decades-long institutional expertise in TIPS/LT and the support of a multidisciplinary liver tumor board. To follow is a review of the pertinent pathophysiology of PVT in cirrhosis, the rationale leading to the development and subsequent evolution of the PVR-TIPS procedure, technical lessons learned, and a summary of outcomes to date.

Safety, efficacy and prognosis of anticoagulant therapy for portal vein thrombosis in cirrhosis: a retrospective cohort study

BackgroundThe role of anticoagulants in the treatment of cirrhotic PVT remains controversial. This study aimed to analyze the safety and efficacy of anticoagulant therapy in patients with cirrhotic portal vein thrombosis (PVT) and its impact on prognosis.MethodsA retrospective cohort study was conducted for PVT patients with liver cirrhosis in our hospital. The primary outcome of the study was the PVT recanalization rate. Other outcomes included bleeding rate, liver function, and mortality. Cox and Logistic regression were used to explore the risk factors of outcomes.ResultsThis study included 77 patients that 27 patients in the anticoagulant group and 50 in the non-anticoagulant group. Anticoagulant therapy was associated with higher rate of PVT recanalization (44.4% vs 20.0%, log-rank P = 0.016) and lower rate of PVT progression (7.4% vs 30.0%, log-rank P = 0.026), and without increasing the rate of total bleeding (14.8% vs 24%, P = 0.343), major bleeding (3.7% vs 6%, P = 0.665) and variceal bleeding (3.7% vs 16%, P = 0.109). The safety and efficacy of different anticoagulants were similar. The Child-Pugh grade of the anticoagulant therapy group was better than that of the non-anticoagulant therapy group (P = 0.030). There was no significant difference in the 2-year survival rate of the two groups.ConclusionAnticoagulants could increase the PVT recanalization rate and reduce the PVT progression rate without increasing the rate of bleeding. Anticoagulants may be beneficial to improving the liver function of patients with cirrhotic PVT. There was no significant difference in the safety and efficacy of different anticoagulants in the treatment of cirrhotic PVT.

Anticoagulation for the Treatment of Portal Vein Thrombosis in Cirrhosis: A Systematic Review and Meta-Analysis of Comparative Studies

Portal vein thrombosis (PVT) leads to significant morbidity and mortality burden in patients with cirrhosis. An improved understanding of the utility of anticoagulation in patients with PVT will aid clinical decision making and inform future research. This meta-analysis aimed to evaluate the association between anticoagulation therapy and clinical outcomes in the context of treatment for PVT in cirrhosis. Pubmed, Embase, and Web of Science were searched from inception to February 13, 2022, for studies comparing the use of anticoagulation to other modalities as treatment for PVT in cirrhosis. Pooled odds ratios (OR) were calculated using a random-effects model for PVT improvement, recanalization, progression, bleeding events, and all-cause mortality in treatment studies. We identified 944 records, of which 16 studies (n= 1126) examining anticoagulation as PVT treatment were included for subsequent analysis. Anticoagulation as PVT treatment was associated with PVT improvement (OR 3.64; 95% CI 2.56-5.17), PVT recanalization (OR 3.73; 95% CI 2.45-5.68), decreased PVT progression (OR 0.38; 95% CI 0.23-0.63), and decreased all-cause mortality (OR 0.47; 95% CI 0.29-0.75). The use of anticoagulation was not associated with bleeding events (OR 0.80; 95% CI 0.39-1.66). All analyses demonstrated low heterogeneity. These results support the use of anticoagulation in cirrhosis as treatment for PVT. These findings may inform the clinical management of PVT and highlight the need for further studies such as large randomized controlled trials characterizing the safety and efficacy of anticoagulation for PVT in cirrhosis.

A novel potential mechanism for the development of portal vein thrombosis in cirrhosis based on portal hemodynamics

BackgroundMarked changes in hemodynamics have been suggested to be a potential contributing factor to portal vein thrombosis (PVT) development. This study investigated the effect of portal hemodynamics based on the anatomical structure of the portal venous system on PVT development.MethodsThe morphological features of portal venous system in patients with PVT and those without PVT subgroups were compared. In addition, idealized PV models were established to numerically evaluate the effect of the variation in the angulation of superior mesenteric vein (SMV) and splenic vein (SV) on the hemodynamics of portal venous system.ResultsThe angle α (angulation of SMV and SV) in patients with PVT was lower than that in patients without PVT (p < 0.0001), which was the only independent risk factor (odds ratio (OR), 0.90 (95% CI 0.84–0.95); p < 0.0001) for the presence of PVT. With the change in angle α, the flow pattern of blood flow changed greatly, especially the helical flow. When α = 80°, helical flow only appeared at the local PV near the intersection of SMV and SV. When α = 120°, most regions were occupied by the helical flow. In addition, the h2 gradually increased with increasing α, when α = 80°, h2 = 12.6 m/s2; when α = 120°, h2 = 29.3 m/s2.ConclusionsThe angulation of SV and SMV was closely associated with PVT development. Helical flow changed following the varying angulation of SV and SMV. Therefore, angulation of SV and SMV may help to identify high-risk cohorts for future PVT development earlier.

Endoscopic Variceal Therapy (EVT) may Increase the Risk of Portal Vein Thrombosis in Cirrhosis: A Clinical Case Report and Literature Review

Oesophagogastric varices (EGV) are a common complication occurring secondary to cirrhotic portal hypertension. Endoscopic methods are often used for primary prevention and treatment in such patients. However, it has been found in clinical practice that patients undergoing repeated endoscopic variceal therapy (EVT) may develop portal vein thrombosis (PVT). Herein, we reported the case of a patient with cirrhosis who developed PVT after repeated EVT and further progressed to cavernous transformation of the portal vein (CTPV) after anticoagulant therapy to learn from the clinical treatment of this patient. Written informed consent was obtained from the patient to publish this case report, including the attached imaging data.

S3216 When to Start Anticoagulation? A Case of Portal Vein Thrombosis in a Post-Partum Cirrhosis Patient With Variceal Bleeding

Introduction: While portal vein thrombosis (PVT) is a relatively rare disease in the general population, the prevalence of PVT in cirrhosis increases in parallel with the severity of cirrhosis. The pathogenesis of PVT in cirrhosis is thought to be multifactorial resulting mainly from alterations in the different components of Virchow’s triad. Case Description/Methods: Here we report a case of a 36-year-old woman with history of alcoholic cirrhosis who presented 2 weeks status post c-section complaining of acute onset abdominal pain, bloating, and nausea with two episodes of hematemesis. Her initial vital signs were unremarkable and hemoglobin was 7.4 gm/dL. Her model for end-stage liver disease (MELD) score was 16. She underwent upper endoscopy (EGD) with successful banding of 3 columns of large varices which showed stigmata of recent bleeding. Patient also underwent diagnostic and therapeutic paracentesis which did not show signs of spontaneous bacterial peritonitis (SBP). However, she did have history of wound dehiscence of her cesarean incision with persistent leakage of serous fluid despite prior negative pressure wound therapy. Therefore, CT abdomen/pelvis was obtained which demonstrated nonocclusive thrombus in the main portal vein extending into both the right and left branches. Due to finding of PVT, MRI was also obtained which showed no evidence of malignancy. As her hemoglobin remained stable ( >7 gm/dL) during hospitalization, she was started on therapeutic low molecular weight heparin (LMWH). Unfortunately, patient was re-admitted five days later for hematemesis and drop in her hemoglobin to 5.6 gm/dL. She received blood products, and repeat EGD showed cratered and superficial esophageal ulcers at the site of prior variceal treatment. Ultimately LMWH was held and resumed after hemoglobin stabilized. Discussion: This case demonstrates the conundrum of if/when to treat PVT in patients with cirrhosis. Current guidelines recommend anticoagulation as the mainstay of PVT treatment. However, this is can be complicated by other sequelae of decompensated cirrhosis such as variceal bleeding. Consequences of non-treatment include further increase in resistance to portal blood thus worsening portal hypertension. In this case, patient’s post-partum status also favors anticoagulation as other society guidelines have recommended anticoagulation with LMWH for postpartum patients with vascular disease of the liver. Therefore, individualized treatment algorithms should be developed and used to guide management.

Platelet-derived TGF-β1 is related to portal vein thrombosis in cirrhosis by promoting hypercoagulability and endothelial dysfunction.

BackgroundPortal vein thrombosis (PVT) is a serious complication of cirrhosis accompanied by unclear pathogenesis. Transforming growth factor-beta (TGF-β) has been implicated in atherosclerosis and venous thrombosis whereas study regarding its part in PVT is lacking. The aim of this study was to explore the role of cytokine TGF-β1 in PVT and the potential mechanism.Materials and methodsWe included patients with cirrhotic gastroesophageal varices and divided them into two groups according to the presence of PVT. Serum levels of TGF-β1 were detected using Cytometric Bead Array kit and compared between two groups. Coagulation status was assessed using thromboelastography (TEG). Primary liver sinusoidal endothelial cells were treated with TGF-β1 and evaluated for endothelial dysfunction by RT-PCR.ResultsOur results uncovered that TGF-β1 (6,866.55 vs. 3,840.60 pg/ml, P = 0.015) significantly increased in the PVT group. Splenectomy might promote PVT by increasing platelet-derived TGF-β1 levels. Other cytokines showed no difference between PVT and non-PVT groups. Besides, TGF-β1 was correlated with platelet, fibrinogen, TEG-CI, TEG-MA, and TEG-α (coef = 0.733, 0.494, 0.604, 0.608, and 0.511; P < 0.001, 0.027, 0.004, 0.004, and 0.021, respectively), which indicated a hypercoagulable state in PVT patients. RT-PCR of liver sinusoidal endothelial cells showed a markable increment of von Willebrand Factor (vWF), thrombomodulin(TM), intercellular adhesion moleclar-1(ICAM-1), and vascular endothelial growth factor(VEGF) after TGF-β1 treatment, suggesting the involvement of endothelial dysfunction.ConclusionElevated platelet-derived TGF-β1 exhibited association with hypercoagulability and promoting effect on endothelial dysfunction, closely related with PVT in cirrhotic patients.

The portal vein in patients with cirrhosis is not an excessively inflammatory or hypercoagulable vascular bed, a prospective cohort study

BackgroundA hypercoagulable state is not associated with development of portal vein thrombosis in cirrhosis, as we previously demonstrated. However, some groups demonstrated elevated levels of inflammatory markers and activation of hemostasis in the portal vein (PV) compared to posthepatic veins, but because the liver is involved in clearance of these markers, we hypothesize that interpretation of these data is not straightforward. AimTo determine whether the PV has particular proinflammatory/hypercoagulable characteristics by comparing plasma sampled in the PV, hepatic vein (HV), and the systemic circulation. MethodsPlasma samples from 51 cirrhotic patients with portal hypertension undergoing transjugular intrahepatic portosystemic shunt placement, were taken from the PV, HV, and jugular vein (JV). Markers of inflammation (lipopolysaccharide, tumor necrosis factor‐α, interleukin‐6, thiobarbituric acid‐reactive substances), neutrophil‐extracellular‐traps (cfDNA, MPO‐DNA), endothelial damage (von Willebrand factor [VWF]), and hemostasis were determined and compared among the three vascular beds. ResultsMarkers of inflammation were slightly, but significantly higher in the PV than in the HV and systemic circulation. VWF and markers of hemostasis were modestly elevated in the PV. Levels of multiple markers were lower in the HV compared with the PV and systemic circulation. Higher model for end‐stage liver disease score was associated with a more prothrombotic state in all three sample sites. ConclusionIn contrast to published studies, we did not detect a clear proinflammatory or prothrombotic environment in the PV of cirrhotic patients. Many markers are lowest in the HV, indicating that the low levels of these markers in the HV, at least in part, reflect clearance of those markers in the liver.

Anticoagulation in Cirrhosis: Evidence for the Treatment of Portal Vein Thrombosis and Applications for Prophylactic Therapy.

The clinical utility of anticoagulation for patients with cirrhosis and asymptomatic portal vein thrombosis (PVT) is widely debated. Complex hemostatic derangements in cirrhosis that increase risk of both bleeding and thrombosis, as well as a lack of randomized controlled data, limit conclusive assessments regarding optimal management of anticoagulation in this setting. In this review, we summarize the relevant literature pertaining to PVT in cirrhosis, including the effect of untreated PVT on the natural progression of liver disease and the overall impact of anticoagulation on clot burden and other relevant clinical outcomes. Apart from patients who are symptomatic or listed for liver transplantation, data supporting anticoagulation for the treatment of PVT is limited and without clear consensus guidelines. In patients with cirrhosis without PVT, emerging evidence for the role of prophylactic anticoagulation to mitigate the progression of fibrosis suggests an optimal risk-benefit tradeoff with decreased rates of liver decompensation and mortality, without a heightened risk of bleeding. In summation, as our understanding of the role of both prophylactic and therapeutic anticoagulation in cirrhosis continues to evolve, ongoing risk stratification of patients with asymptomatic PVT demands further attention.

The Pathophysiology of Portal Vein Thrombosis in Cirrhosis: Getting Deeper into Virchow's Triad.

Portal vein thrombosis (PVT) is a common complication among patients with cirrhosis. However, its pathophysiology is not well established and there are currently very few predictive factors, none of which are actually useful, from a clinical perspective. The contribution of each of the vertices of Virchow’s triad, e.g., blood hypercoagulability, blood flow, and portal vein endothelial damage in the development of PVT is not clear. In this review, we aim to recapitulate the latest studies on the field of PVT development in order to understand its mechanisms and discuss some of the future directions in the study of this important complication of cirrhosis.

Narrative review of portal vein thrombosis in cirrhosis: pathophysiology, diagnosis, and management from an interventional radiology perspective.

This paper examines the incidence, clinical presentation, and pathophysiology of portal vein thrombosis (PVT) in cirrhosis. Additionally, we have reviewed the literature regarding the current status of medical and interventional radiology management of PVT and have proposed a novel algorithm for the management given different clinical scenarios. Lastly two representative cases displaying endovascular treatment options are provided. Portal vein thrombus in the setting of cirrhosis is an increasingly recognized clinical issue with debate on its pathophysiology, natural course, and optimal treatment. Approximately one-third of patients are asymptomatic, and detection of the thrombus is an incidental finding on imaging performed for other reasons. In 30% to 50% of patients, PVT resolves spontaneously. However, there is increased post-transplant mortality in patients with completely occlusive PVT, therefore effective early revascularization strategies are needed for patients with complete PVT who are expected to undergo liver transplant. Additionally, no consensus has been reached regarding PVT treatment in terms of timing and type of interventions as well as type and duration of anticoagulation. Computerized literature search as well as discussion with experts in the field. Management of PVT is complex, as many variables affect which treatments can be used. Anticoagulation appears to be the optimal first-line treatment in patients with acute PVT but without bleeding varices or mesenteric ischemia. Minimally invasive treatments include various methods of mechanical thrombectomy, chemical thrombolysis, and transjugular intrahepatic portosystemic shunt (TIPS) placement with or without variceal embolization. Definitive recommendations are difficult due to lack of high quality data and continued research is needed to evaluate the efficacy of different anticoagulants as well as the timing and use of various minimally invasive therapies in specific circumstances.

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

Portal vein thrombosis (PVT) is a well-known consequence of cirrhosis. Its pathophysiology is complex, with possible downstream hepatic decompensation. This study was conducted to describe the changes of protein C (PC), protein S (PS) and D-dimer blood levels associated with PVT formation in cirrhosis and the relation to the degree of liver dysfunction. This was a case-control study that included 50 cirrhotic patients who presented with acute de novo non-malignant PVT and 50 cirrhotic patients without PVT as a control group. The severity of liver disease was classified as per the Child-Turcotte-Pugh (CTP) score. Doppler ultrasonography identified acute portal vein occlusion, and dynamic contrast-enhanced computed tomography confirmed the extent and nature of PVT. Blood PC, PS and D-dimer levels were measured using enzyme-linked immunosorbent assay. PC and PS levels were significantly lower, and the D-dimer level was significantly higher, in cirrhotic patients with PVT compared to the control group. PC and PS levels were significantly decreased in patients with higher CTP score of both groups. The D-dimer level did not vary significantly with the degree of liver dysfunction in patients of either group. PC, PS and D-dimer at the cut-off points of ≤ 77 IU/dl, ≤ 63 IU/dl, and > 300 ng/ml, respectively, significantly suggested PVT occurrence. Alteration of the anticoagulant proteins and D-dimer contributed to PVT formation in cirrhotic patients and could help stratify the degree of liver dysfunction. Blood level of these hemostatic proteins could be incorporated into a probability score for early diagnosis and treatment of PVT in cirrhosis.

Correction to: Anticoagulation and Transjugular Intrahepatic Portosystemic Shunt for the Management of Portal Vein Thrombosis in Cirrhosis: A Prospective Observational Study.

Correction to: Anticoagulation and Transjugular Intrahepatic Portosystemic Shunt for the Management of Portal Vein Thrombosis in Cirrhosis: A Prospective Observational Study.

Direct oral anticoagulants for portal vein thrombosis in cirrhosis: Good news from meta-analysis?

In the current issue of Digestive and Liver Disease, the meta-analysis by Koh and colleagues [1] addresses the efficacy and safety of direct oral anticoagulants (DOAC) versus vitamin K antagonist (VKA) for (non-malignant) portal vein thrombosis (PVT) in cirrhosis. It shows that DOAC attain higher rates of PVT recanalization and lower risk of PVT progression as compared to VKA, with similar risks of major bleeding, variceal bleeding, and death. This is a good news since DOAC overcome several disadvantages of VKA in patients with cirrhosis, mainly the confounding effect of an already prolonged INR and the inaccuracy of the INR scale, which do not qualify VKA as optimal anticoagulants in such patients.