Portal vein thrombosis in cirrhosis: A literature review.
Ontology highlight
ABSTRACT:
SUBMITTER: Prakash S
PROVIDER: S-EPMC10169608 | biostudies-literature | 2023
REPOSITORIES: biostudies-literature
Publications
Portal vein thrombosis in cirrhosis: A literature review.
Prakash Swathi S Bies Jared J Hassan Mariam M Mares Adriana A Didia S Claudia SC
Frontiers in medicine 20230426
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 ...[more]
Similar Datasets
Project description:Portal vein thrombosis constitutes the most common thrombotic event in patients with cirrhosis, with increased rates in the setting of advanced liver disease. Despite being a well-known complication of cirrhosis, the contribution of portal vein thrombosis to hepatic decompensation and overall mortality is still a matter of debate. The incorporation of direct oral anticoagulants and new radiological techniques for portal vein recanalization have expanded our therapeutic arsenal. However, the lack of large prospective observational studies and randomized trials explain the heterogenous diagnostic and therapeutic recommendations of current guidelines. This article seeks to make a comprehensive review of the pathophysiology, clinical features, diagnosis, and treatment of portal vein thrombosis in patients with cirrhosis.
| S-EPMC9655000 | biostudies-literature
Project description:Background and aimsHypoalbuminemia, as defined by serum albumin (SA) levels ≤35 g/L, is associated to venous and arterial thrombosis in general population and in patients at risk of cardiovascular disease. It is unknown if SA ≤35 g/L is also associated to portal vein thrombosis (PVT) in cirrhosis.MethodsCirrhotic patients enrolled in the Portal vein thrombosis Relevance On Liver cirrhosis: Italian Venous thrombotic Events Registry (PRO-LIVER) study (n = 753), were followed-up for 2 years to assess the risk of PVT, that was diagnosed by Doppler ultrasonography. Child-Pugh classes, Model for End-Stage Liver Disease score, presence of hepatocellular carcinoma and laboratory variables including SA, D-dimer, and high-sensitivity C-reactive protein (hs-CRP) were measured at baseline.ResultsSA ≤35 g/L was detected in 52% of patients. A logistic multivariate regression analysis showed that higher Child-Pugh class, hepatocellular carcinoma and thrombocytopenia were significantly associated to SA ≤35 g/L. In a subgroup of patients where data regarding hs-CRP and D-dimer were available, SA ≤35 g/L was inversely associated with hs-CRP and D-dimer. During the follow-up, a total of 61 patients experienced PVT. A Kaplan Meier survival analysis showed SA ≤35 g/L was associated to increased risk of PVT compared to SA >35 g/L (P = .005). A multivariate Cox proportional hazards regression analysis showed that male sex, lower platelet count, and SA ≤35 g/L remained associated to PVT after adjusting for confounding factors.ConclusionCirrhotic patients with SA ≤35 g/L are at higher risk of experiencing PVT compared to those with SA >35 g/L and could be considered as potential candidates to anticoagulant prophylaxis for PVT prevention.
| S-EPMC11330931 | biostudies-literature
Project description:Portal vein thrombosis (PVT) is encountered in liver cirrhosis, particularly in advanced disease. It has been a feared complication of cirrhosis, attributed to significant worsening of liver disease, poorer clinical outcomes and potential inoperability at liver transplantation; also catastrophic events such as acute intestinal ischaemia. Optimal management of PVT has not yet been addressed in any consensus publication. We review current literature on PVT in cirrhosis; its prevalence, pathophysiology, diagnosis, impact on the natural history of cirrhosis and liver transplantation, and management. Studies were identified by a search strategy using MEDLINE and Google Scholar. The incidence of PVT increases with increasing severity of liver disease: less than 1% in well-compensated cirrhosis, 7.4%-16% in advanced cirrhosis. Prevalence in patients undergoing liver transplantation is 5%-16%. PVT frequently regresses instead of uniform thrombus progression. PVT is not associated with increased risk of mortality. Optimal management has not been addressed in any consensus publication. We propose areas for future research to address unresolved clinical questions.
| S-EPMC4462717 | biostudies-literature
Project description:BackgroundCirrhotic patients with portal vein thrombosis (PVT) may have a high risk of hepatic decompensation and increased mortality. This study aimed to investigate if increased portal vein diameter is associated with PVT development.MethodsA total of 174 cirrhotic patients were enrolled between February 1 and August 31, 2017. All participants were divided into PVT (n=62) and non-PVT (n=112) groups based on the thrombus that was detected by ultrasonography and confirmed by computed tomography angiography (CTA).ResultsThe study participants, aged 54.7±10.5 years (PVT) and 55.8±11.6 years (non-PVT), were included in this analysis. The Child-Pugh score of PVT or non-PVT was 6.6±1.3 and 5.8±0.9, respectively. Hepatitis B virus (HBV) is the primary etiological agent of cirrhosis. Logistic regression, receiver operating characteristic (ROC), and nomograph analysis designated portal diameter as the strongest independent risk factor for predicting PVT development [odds ratio (OR): 3.96, area under the ROC curve (AUC): 0.88; P<0.01], and the cutoff with predictive value for PVT development was >12.5 mm. No differences were observed in the overall survival (OS) in cirrhosis with or without PVT or stratifying on portal diameter based on the cutoff value.ConclusionsIncreased portal diameter is associated with an increased risk of PVT development. Patients with cirrhosis and increased portal diameter are a high-risk subgroup that may need thromboprophylaxis.
| S-EPMC7944309 | biostudies-literature
Project description:Nontumoral portal vein thrombosis (PVT) is an increasingly recognized complication in patients with cirrhosis. Substantial evidence shows that portal flow stasis, complex thrombophilic disorders, and exogenous factors leading to endothelial dysfunction have emerged as key factors in the pathogenesis of PVT. The contribution of PVT to hepatic decompensation and mortality in cirrhosis is debatable; however, the presence of an advanced PVT increases operative complexity and decreases survival after transplantation. The therapeutic decision for PVT is often determined by the duration and extent of thrombosis, the presence of symptoms, and liver transplant eligibility. Evidence from several cohorts has demonstrated that anticoagulation treatment with vitamin K antagonist or low molecular weight heparin can achieve recanalization of the portal vein, which is associated with a reduction in portal hypertension-related events and improved survival in cirrhotic patients with PVT. Consequently, interest in direct oral anticoagulants for PVT is increasing, but clinical data in cirrhosis are limited. Although the most feared consequence of anticoagulation is bleeding, most studies indicate that anticoagulation therapy for PVT in cirrhosis appears relatively safe. Interestingly, the data showed that transjugular intrahepatic portosystemic shunt represents an effective adjunctive therapy for PVT in cirrhotic patients with symptomatic portal hypertension if anticoagulation is ineffective. Insufficient evidence regarding the optimal timing, modality, and duration of therapy makes nontumoral PVT a challenging consequence of cirrhosis. In this review, we summarize the current literature and provide a potential algorithm for the management of PVT in patients with cirrhosis.
| S-EPMC7782107 | biostudies-literature
Project description:We analyzed whether serum albumin is independently associated with portal vein thrombosis (PVT) in liver cirrhosis (LC) and if a biologic plausibility exists. This study was divided into three parts. In part 1 (retrospective analysis), 753 consecutive patients with LC with ultrasound-detected PVT were retrospectively analyzed. In part 2, 112 patients with LC and 56 matched controls were entered in the cross-sectional study. In part 3, 5 patients with cirrhosis were entered in the in vivo study and 4 healthy subjects (HSs) were entered in the in vitro study to explore if albumin may affect platelet activation by modulating oxidative stress. In the 753 patients with LC, the prevalence of PVT was 16.7%; logistic analysis showed that only age (odds ratio [OR], 1.024; P = 0.012) and serum albumin (OR, -0.422; P = 0.0001) significantly predicted patients with PVT. Analyzing the 112 patients with LC and controls, soluble clusters of differentiation (CD)40-ligand (P = 0.0238), soluble Nox2-derived peptide (sNox2-dp; P < 0.0001), and urinary excretion of isoprostanes (P = 0.0078) were higher in patients with LC. In LC, albumin was correlated with sCD40L (Spearman's rank correlation coefficient [rs ], -0.33; P < 0.001), sNox2-dp (rs , -0.57; P < 0.0001), and urinary excretion of isoprostanes (rs, -0.48; P < 0.0001) levels. The in vivo study showed a progressive decrease in platelet aggregation, sNox2-dp, and urinary 8-iso prostaglandin F2α-III formation 2 hours and 3 days after albumin infusion. Finally, platelet aggregation, sNox2-dp, and isoprostane formation significantly decreased in platelets from HSs incubated with scalar concentrations of albumin. Conclusion: Low serum albumin in LC is associated with PVT, suggesting that albumin could be a modulator of the hemostatic system through interference with mechanisms regulating platelet activation.
| S-EPMC6442692 | biostudies-literature
Project description:This retrospective study investigated factors influencing the portal vein thrombosis (PVT) volume and recurrence in 52 cirrhosis patients with PVT from November 2008 to September 2018. All patients were treated with danaparoid sodium with or without additional antithrombin III. Blood platelet counts significantly correlated with the PVT volume (r2 = 0.17; P < 0.01). Computed tomography confirmed recurrence as PVT aggravation was reported in 43 patients, with ≥50% PVT volume reduction following anticoagulation therapy. In 43 patients, recurrence significantly correlated with the pretreatment PVT volume (P = 0.019). Factors influencing recurrence included a Child-Pugh score >8 (P = 0.049) and fibrosis index ≤7.0 based on four factors (FIB-4) (P = 0.048). Moreover, the relationship between recurrence and correlating factors showed that 15 patients who received warfarin experienced recurrence more often when Child-Pugh scores were >8 (P = 0.023), regardless of maintenance treatment. For patients who did not receive warfarin, a PVT volume ≥3.0 mL significantly influenced recurrence (P = 0.039). Therefore, the platelet count influences the PVT volume. The pretreatment PVT volume correlated with recurrence after anticoagulation therapy. According to the Kaplan-Meier curve, risk factors for PVT recurrence after anticoagulation therapy included Child-Pugh scores >8 and FIB-4 ≤7.0. Therefore, the FIB-4 is a unique factor that shows trends opposing other liver function markers.
| S-EPMC7555202 | biostudies-literature
Project description:Portal vein thrombosis is an important cause of portal hypertension. PVT occurs in association with cirrhosis or as a result of malignant invasion by hepatocellular carcinoma or even in the absence of associated liver disease. With the current research into its genesis, majority now have an underlying prothrombotic state detectable. Endothelial activation and stagnant portal blood flow also contribute to formation of the thrombus. Acute non-cirrhotic PVT, chronic PVT (EHPVO), and portal vein thrombosis in cirrhosis are the three main variants of portal vein thrombosis with varying etiological factors and variability in presentation and management. Procoagulant state should be actively investigated. Anticoagulation is the mainstay of therapy for acute non-cirrhotic PVT, with supporting evidence for its use in cirrhotic population as well. Chronic PVT (EHPVO) on the other hand requires the management of portal hypertension as such and with role for anticoagulation in the setting of underlying prothrombotic state, however data is awaited in those with no underlying prothrombotic states. TIPS and liver transplant may be feasible even in the setting of PVT however proper selection of candidates and type of surgery is warranted. Thrombolysis and thrombectomy have some role. TARE is a new modality for management of HCC with portal vein invasion.
| S-EPMC4415192 | biostudies-other
Project description:ObjectivesEvidences for anticoagulation strategies in cirrhotic with portal vein thrombosis (PVT) are still insufficient. This study aims to comprehensively compare the therapeutic effects of different therapeutic therapeutic measures in individuals suffering from cirrhosis with PVT, with the ultimate goal of providing evidence-based recommendations for thrombolytic therapy in this population.MethodsStarting from 20 October 2023, a comprehensive search about therapeutic strategies for portal vein thrombosis in cirrhosis was conducted on PubMed, EMBASE, and Cochrane Library.Results19 studies were eventually incorporated into this study. Comparison with control in network meta-analysis, direct oral anticoagulants (DOACs) (RR = 2.15, 95%CI: 1.33, 3.48), LMWH (RR = 1.41, 95%CI: 1.01, 1.99), TIPS (RR = 5.68, 95%CI: 2.63, 12.24), warfarin (RR = 2.16, 95%CI: 1.46, 3.21), EBL plus propranolol (RR = 2.80, 95%CI: 1.18, 6.60), LMWH-DOACs sequential (RR = 7.92, 95%CI: 2.85, 21.99) and LMWH-warfarin sequential (RR = 2.26, 95%CI: 1.16, 4.42) significantly improved the incidence of complete recanalization. The anticoagulation drugs were ranked based on their SUCRA values, with the LMWH-DOACs sequential (92.7%), TIPS plus warfarin (91.3%), and TIPS (80.3%) emerging as the top three effective treatments.ConclusionIn this study, active anticoagulants were recommended for cirrhosis with PVT. The TIPS plus warfarin, LMWH-DOACs sequential, and TIPS improved the complete recanalization rate most effectively, and the EBL plus propranolol, heparin plus DOACs plus warfarin, and DOACs were highly recommended for increasing the incidence of partial recanalization. Warfarin and TIPS were recommended for reducing the frequency of bleeding events, while LMWH plus warfarin and DOACs proved to be most effective in decreasing the rate of major bleeding events. Warfarin, heparin plus DOACs plus warfarin, and DOACs demonstrated the most significant reduction in mortality rates, highlighting its potential as an effective intervention. TIPS plus warfarin, LMWH-DOACs sequential, and TIPS were recommended for reducing the occurrence of PVT expansion. Heparin plus DOACs plus warfarin was recommended for reducing the occurrence of hepatic encephalopathy, and protocols that involve TIPS were generally associated with a higher risk of hepatic encephalopathy. However, a longer follow-up period is necessary to comprehensively evaluate the efficacy of active anticoagulants therapy in patients with PVT in cirrhosis.
| S-EPMC11743941 | biostudies-literature
Project description: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.
| S-EPMC9748017 | biostudies-literature