Vein Thrombosis In Liver Cirrhosis Research Articles

Anticoagulation Treatment with Low Molecular-Weight Heparin for Portal Vein Thrombosis in Liver Cirrhosis: Efficacy and Risk of Hemorrhagic Complications

▪Introduction: Portal vein thrombosis (PVT) is a well-known complication caused by disturbed portal flows and hemostatic imbalances in liver cirrhosis (LC). Low molecular-weight heparin (LMWH) can be used as a treatment of PVT, but knowledge the about efficacy and safety of LMWH for LC patients remains limited. The aim of this study is therefore to investigate the clinical outcomes of cirrhotic patients with PVT treated with LMWH.Method: From September of 2013 to December of 2015, LC patients who had PVT were treated with therapeutic doses of LMWH, dalteparin or enoxaparin for six months. Patients with severely decompensated LC, a history of major bleeding in the last six months, and/or impaired renal function were excluded.Results: Ninety patients were enrolled. The median age was 63.5 years (range 38-65), and male patients numbered 66 (73.3%). The most common cause of LC was hepatitis B virus infection (55 patients, 61.1%), followed by alcohol abuse (12 patients, 13.3%). Fifty-eight patients (64.4%) had hepatocellular carcinoma. Half of the patients had Child-Pugh class A cirrhosis, and 41 patients (45.6%) had class B cirrhosis. Thirty patients had thrombocytopenia with platelet counts less than 50,000/mm3. All patients had thrombus in the main trunk or in branches of the portal vein. Splenic vein involvement was confirmed in four patients, and 25 patients had superior mesenteric vein thrombus. PVT was newly discovered in 30 patients (33.3%), previously established but recently progressed was found in 43 (47.8%), and chronic but stable thrombus was noted in 17 (18.9%). The median time from the initial diagnosis of PVT to the start of anticoagulation therapy was 8.7 months (range: 0-125.9 months). Dalteparin was prescribed to 81 patients (90.0%) and enoxaparin to 9 (10.0%). The median duration of treatment was 5.8 months (range: 1-34.6 months). The overall rate of recanalization was 58.9%. Complete recanalization was reported in 16 patients (17.8%) and partial recanalization in 37 (41.1%). Patients with a favorable Child-Pugh class and recently diagnosed thrombus showed significantly better responses (Table 1). Concomitant hepatocellular carcinoma had no effect on the recanalization rate. In the patients who responded to anticoagulation therapy, the post-treatment laboratory findings including serum bilirubin and albumin were slightly improved compared to the pre-treatment state. At the time of the analysis, 48 patients (53.3%) had finished six months of the initial LMWH treatment as scheduled, while treatments for five patients were ongoing. The relapse rate of PVT was 56.6%, and the median time from the cessation of anticoagulation to relapse was 4.2 months (range: 1.4-7.0 months). Eight patients (8.9%) suspended their use of LMWH due to adverse events. The most common adverse event was bleeding, which was reported in 13 patients (14.4%). A history of variceal bleeding was a significant risk factor for hemorrhagic complications. Patients denoted as Child-Pugh Classes B or C showed a higher incidence rate compared to those designated as Class A. Two patients died due to fatal bleeding events, which were in these cases intractable duodenal variceal bleeding and intracranial hemorrhage.Conclusion: Anticoagulation therapy using LMWH for PVT in LC is effective, with a recanalization rate of 59.6%. Advanced LC and a delayed start of anticoagulation since the initial diagnosis of PVT disrupted the recanalization effect of LMWH. Long-term maintenance of anticoagulation should be considered owing to the high recurrence rates, but much care is necessary with regard to hemorrhagic complications in patients with a past history of variceal bleeding. [Display omitted] DisclosuresNo relevant conflicts of interest to declare.

Portal vein thrombosis in liver cirrhosis - the added value of contrast enhanced ultrasonography.

Portal vein thrombosis (PVT) is a frequent complication of liver cirrhosis and its prevalence increases with the severity of liver disease. Patients with liver cirrhosis and hepatocellular carcinoma may have either malignant or blunt (benign) PVT. In these patients, the diagnosis and characterization of PVT is important for the prognosis and further treatment. Ultrasound (US) is the modality of choice for the diagnosis of PVT. The features of PVT on B-mode (gray-scale) US include: dilatation of the portal vein, visualization of the thrombus and, in chronic PVT- cavernous transformation. Sensitivity of US in the diagnosis of PVT is improved by the use of Doppler US and of ultrasound contrast agents. In the latter years, contrast enhanced ultrasound (CEUS) showed high sensitivity in the differential diagnosis between benign and malignant PVT and could be the diagnostic method of choice for the characterization of PVT. Blunt thrombi are avascular and will not enhance during CEUS examination, while a hyperenhancement pattern of the portal thrombus in the arterial phase, with "wash out" in the portal or late phase is typical for malignant PVT.

Presence of portal vein thrombosis in liver cirrhosis is strongly associated with low levels of ADAMTS-13: a pilot study.

Portal vein thrombosis (PVT) dramatically changes the prognosis of cirrhotic patients, especially those waiting for liver transplantation. However, the possible contribution to PVT of von Willebrand factor (VWF) and ADAMTS-13 is poorly documented. The aim of our study was to assess the presence of alterations of VWF and ADAMTS-13 serum levels in cirrhotic patients with PVT. Twenty-four patients with PVT (group PVT) and 60 without PVT (group without PVT) were enrolled. A comprehensive analysis of biochemical and hemostatic parameters was performed. ADAMTS-13 activity was significantly lower in group A (median 16.8 vs. 69.1%, p=0.0047). Group PVT, compared to group without PVT, showed a significantly higher VWF:act, (median 308.4 vs 203.3%, p=0.032), whereas no difference was observed for VWF:Ag, FVIII level and the presence of risk factors for venous thromboembolism. No correlation was found between the Child-Pugh score and ADAMTS-13 activity. In multivariable logistic regression analysis performed on data concerning both group PVT and without PVT, only the ADAMTS-13 activity (p=0.007) was independently and inversely associated with PVT. In conclusion, ADAMTS-13 activity is independently associated with PVT in cirrhotic patients.

Role of D-dimer in the Development of Portal Vein Thrombosis in Liver Cirrhosis: A Meta-analysis.

Background and Aims:A meta-analysis was performed to explore the role of the D-dimer in the development of portal vein thrombosis (PVT) in liver cirrhosis.Methods:All papers were searched via PubMed, EMBASE, China National Knowledge Infrastructure, Wan Fang, and VIP databases. A standardized mean difference (SMD) with 95% confidence interval (CI) was pooled.Results:Overall, 284 studies were initially identified, of which 21 were included. Cirrhotic patients with PVT had a significantly higher D-dimer concentration than those without PVT (pooled SMD = 1.249, 95%CI = 0.740–1.758). After the portal hypertension-related surgery, cirrhotic patients with PVT had a similar preoperative D-dimer concentration to those without PVT (pooled SMD = 0.820, 95%CI = −0.122–0.286), but a higher postoperative value of D-dimer concentration than those without PVT (pooled SMD = 2.505, 95%CI = 0.975–4.036). Notably, the D-dimer concentration at the 1st postoperative day was similar between cirrhotic patients with and without PVT (pooled SMD = 0.137, 95%CI = −0.827–1.101), but that at the 7th post-operative day was higher in cirrhotic patients with PVT than in those without PVT (pooled SMD = 1.224, 95%CI = 0.277–2.171).Conclusion:D-dimer might be regarded as a diagnostic marker for PVT in liver cirrhosis. In addition, postoperative D-dimer testing is worthwhile for the diagnosis of PVT after portal hypertension-related surgery.

Anticoagulation for the treatment of portal vein thrombosis in liver cirrhosis: A systematic review and meta-analysis of observational studies

Background & aimsSystematic review and meta-analysis were performed to evaluate the safety and efficacy of anticoagulation for the treatment of portal vein thrombosis (PVT) in cirrhotic patients. MethodsThe PubMed, EMBASE, Cochrane Library, and ScienceDirect databases were searched. The rates of bleeding complications and portal vein recanalization in patients who received anticoagulant therapy were pooled. The odds ratio (OR) with 95% confidence interval (CI) was calculated to express the difference in the rate of portal vein recanalization between anticoagulation and non-anticoagulation groups. All meta-analyses were conducted by using a random-effects model. ResultsSixteen of 960 initially identified papers were included. Two studies reported a low incidence of major anticoagulation-related complications (4% [2/55] and 3% [1/33]), but no lethal complications occurred. The rate of anticoagulation-related bleeding ranged from 0% to 18% with a pooled rate of 3.3% (95% CI=1.1%–6.7%). The heterogeneity was not significant in the meta-analysis. The total rate of portal vein recanalization ranged from 37% to 93% with a pooled rate of 66.6% (95% CI=54.7%–77.6%). The rate of complete portal vein recanalization ranged from 0% to 75% with a pooled rate of 41.5% (95% CI=29.2%–54.5%). However, the heterogeneity was significant in the 2 meta-analyses. The rate of complete portal vein recanalization was significantly higher in anticoagulation group than in non-anticoagulation group (OR=4.16, 95% CI=1.88–9.20, P=0.0004). The heterogeneity was not significant in the meta-analysis. ConclusionAnticoagulation could achieve a relatively high rate of portal vein recanalization in cirrhotic patients with PVT. Given that only a small number of non-randomized comparative studies are reported, randomized controlled trials are warranted to confirm the risk-to-benefit of anticoagulation in such patients, especially anticoagulation-related bleeding.

Progress in treatment of nontumoral portal vein thrombosis in liver cirrhosis

Progress in treatment of nontumoral portal vein thrombosis in liver cirrhosis

Management of portal vein thrombosis in liver cirrhosis

Portal vein thrombosis (PVT) is a fairly common complication of liver cirrhosis. Importantly, occlusive PVT might influence the prognosis of patients with cirrhosis. Evidence from a randomized controlled trial has shown that anticoagulation can prevent the occurrence of PVT in patients with cirrhosis without prior PVT. Evidence from several case series has also demonstrated that anticoagulation can achieve portal vein recanalization in patients with cirrhosis and PVT. Early initiation of anticoagulation therapy and absence of previous portal hypertensive bleeding might be positively associated with a high rate of portal vein recanalization after anticoagulation. However, the possibility of spontaneous resolution of partial PVT questions the necessity of anticoagulation for the treatment of partial PVT. In addition, a relatively low recanalization rate of complete PVT after anticoagulation therapy suggests its limited usefulness in patients with complete PVT. Successful insertion of a transjugular intrahepatic portosystemic shunt (TIPS) not only recanalizes the thrombosed portal vein, but also relieves the symptomatic portal hypertension. However, the technical difficulty of TIPS potentially limits its widespread application, and the risk and benefits should be fully balanced. Notably, current recommendations regarding the management of PVT in liver cirrhosis are insufficient owing to low-quality evidence.

Analysis of risk factors of portal vein thrombosis in liver cirrhosis

Objective To investigate the risk factors of portal vein thrombosis (PVT) in patients with liver cirrhosis.Methods From January 2009 to December 2011,the data of 294 hospitalized patients diagnosed as liver cirrhosis were retrospectively analyzed.PVT was diagnosed according to multislices spiral computed tomography or color doppler ultrasonography.Fifty-five patients with liver cirrhosis and PVT were in PVT group,239 patients with liver cirrhosis however no PVT were in non-PVT group.Age,gender,etiology of cirrhosis,Child-Pugh grading and score,blood routine examination,blood chemistries,blood coagulation function,D-dimer,main portal vein (MPV) internal diameter,portal vein velocity (PVV) and thickness of spleen were recorded and analyzed.The measurement data were analyzed by t test.Unconditional Logistic regression model was performed to screen corresponding risk factors.Area under curve (AUC) was calculated according to receiver operator characteristic (ROC) curve to evaluate the diagnostic value of each index.Results The results of white blood cell,hemoglobin,total bilirubin,creatinine,serum natrium,prothrombin time,activated partial prothrombin time,fibrinogen and international normalized ratio of PVT group were similar with those of non-PVT group and there were no statistically significant differences (all P＞ 0.05).Compared with those of non-PVT group,the differences in platelet count,albumin level,the level of D-dimer,MPV internal diameter,PVV,spleen thickness,and Child Pugh score of PVT group were statistically significant ((82.55 ± 23.04) × 109/L vs (99.66±20.23)×109/L(t=-0.308,P=0.022),(30.53±2.32) g/L vs (33.36±3.62) g/L(t=-2.117,P=0.036),(1.00±0.22) mg/L vs (0.77±0.15) mg/L(t=7.557,P=0.003),(15.11± 1.32) mmvs (13.40±1.43) mm(t=8.013,P=0.014),(13.51±1.51) cm/s vs (15.16±1.60) cm/s (t=-6.979,P=0.036),(59.35±5.45) mm vs (54.64±5.92) mm(t=1.9555,P=0.043),(11.73± 2.01) scores vs (8.18 ± 3.05) scores (t =6.225,P =0.006)).The results of unconditional Logistic regression model analysis indicated that D-dimer,Child-Pugh score,MPV and PVV were independent risk factors of PVT in patients with liver cirrhosis (OR=13.420,10.237,8.534,0.151; P=0.001,0.014,0.019,0.025).ROC curve analysis indicated that the AUC of D-dimer,Child-Pugh score,MPV and PVV was 0.868,0.823,0.810 and 0.756,respectively.The predicate value was D-dimer＞ Child-Pugh score＞ MPV＞ PVV.Conclusion D-dimmer,Child-Pugh score,MPV and PVV are independent risk factors of PVT in paitients with liver cirrhosis. Key words: Liver cirrhosis; Venous thrombosis; Fibrin fibrinogen degradation products; ROC curve; Portal vein; Risk factors

Portal vein thrombosis in liver cirrhosis

Portal vein thrombosis (PVT) is considered to be a frequent complication of liver cirrhosis. However, unlike PVT in patients without cirrhosis, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions, such as gastroesophageal bleeding and acute intestinal ischemia. Moreover, no consensus regarding PVT in cirrhosis exists. Suggested causes of PVT in cirrhosis include reduced portal blood flow velocity, multiple congenital or acquired thrombophilic factors, inherited or acquired conditions, and derangement of liver architecture. However, the understanding of PVT in cirrhosis is incomplete. In addition, information on the management of PVT in cirrhosis is inadequate. The aims of this review are to: (1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis; (2) describe the principal factors most frequently involved in PVT development; and (3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.

Effect of Antithrombin, Protein C and Protein S on Portal Vein Thrombosis in Liver Cirrhosis: A Meta-analysis

BackgroundThe effects of antithrombin (AT), protein C (PC) and protein S (PS) on the pathogenesis of portal vein thrombosis (PVT) in liver cirrhosis remain controversial in different studies. In this study, a systematic review and meta-analysis to examine this issue were performed. MethodsPubMed database was employed to identify all studies in which AT, PC and PS concentrations were measured in both cirrhotic patients with and without PVT. A standardized mean difference (SMD) with 95% confidence interval (CI) was calculated to evaluate the effect of AT, PC and PS on PVT. Data were pooled using both fixed-effect and random-effect models. Only the pooled data using random-effect model were considered appropriate, when significant heterogeneity was observed. ResultsNine studies involving 160 cirrhotic patients with PVT and 428 cirrhotic patients without PVT were eligible. AT and PC concentrations were similar between PVT and non-PVT groups (AT: SMD=−0.21, 95% CI=−0.56 to 0.14, P=0.24; PC: SMD=−0.23, 95% CI=−0.55 to 0.09, P=0.16). But PS concentration was significantly lower in the PVT group than in the non-PVT group (SMD=−0.29, 95% CI=−0.49 to −0.08, P=0.006). Subgroup analyses were further conducted in 4 studies in which baseline liver function was similar between cirrhotic patients with and without PVT, showing similar AT, PC and PS concentrations between the 2 groups (AT: SMD=−0.10, 95% CI=−0.36 to 0.16, P=0.57; PC: SMD=−0.18, 95% CI=−0.62 to 0.25, P=0.41; PS: SMD=−0.10, 95% CI=−0.59 to 0.39, P=0.69). ConclusionsAT, PC and PS concentrations might not be associated with the pathogenesis of PVT in liver cirrhosis, especially when the impact of liver function was excluded.

Portal vein thrombosis in liver cirrhosis

Portal vein thrombosis (PVT) is observed in 10-20% of patients with liver cirrhosis, which is responsible for 20% of all PVT cases. The main pathogenic factor of PVT in cirrhosis is the obstacle to portal flow, but acquired and inherited clotting abnormalities may play a role. The formation of collateral veins allows many patients to remain asymptomatic and prevents the onset of clinical complications also in patients with totally occlusive PVT. Gastrointestinal bleeding, thrombosis of superior mesenteric vein and refractory ascites are typical manifestations of PVT. Instrumental diagnosis can be obtained by colour-doppler ultrasonography. Future studies should verify whether asymptomatic PVT worsens liver failure, or if its life-threatening complications reduce survival in patients with cirrhosis. Moreover, randomized controlled trials should clarify the potential effectiveness of anticoagulant therapy in the treatment of PVT.

Ultrasound-guided fine needle aspiration biopsy of portal vein thrombosis in liver cirrhosis: results in 15 patients.

Between 1988 and 1992 ultrasound-guided fine needle aspiration biopsies of thromboses in the main branches of the portal vein were carried out in 15 patients with liver cirrhosis. The aims of the study were to evaluate the usefulness, feasibility and diagnostic accuracy of this procedure in cirrhotics with known or suspected hepatocellular carcinoma. The procedure was carried out only in patients with a platelet count > or = 40,000/microL and prothrombin activity > or = 40%. A single pass, with a 22 gauge spinal needle, was performed in the portal vein lumen. Diagnosis of the aetiology of the portal vein thrombosis was obtained in all 15 cases. In 12 cases, a cytological diagnosis of hepatocellular carcinoma was made. In one case, the neoplastic cells aspirated were compatible with adenocarcinoma, and a subsequent colonoscopy confirmed the presence of colonic cancer. The material aspirated was compatible with chemically-induced thrombosis in one patient who had undergone several percutaneous ethanol injection sessions for treatment of hepatocellular carcinoma, and in the last case only blood was aspirated, thus ruling out the coexistence of hepatic cancer. We conclude that fine needle aspiration biopsy of portal vein thrombosis is a feasible, low risk procedure that facilitates the diagnosis of hepatocellular carcinoma when fine needle biopsy of focal liver lesions fails. Fine needle aspiration biopsy of portal vein thrombosis is also useful in excluding neoplastic aetiology of portal vein thrombosis.

Incidence of portal vein thrombosis in liver cirrhosis: An angiographic study in 708 patients

Portal vein thrombosis was thought to be a common complication of liver cirrhosis in the past. The incidence of angiographically demonstrable portal vein thrombosis was studied in 708 consecutive patients with unequivocal cirrhosis seen in the past 10 yr in whom either transhepatic portography or superior mesenteric arterial portography clearly delineated the major portal vein system. Excluding 2 cases that were thought to be associated with past splenectomy, there were 4 cases of portal vein thrombosis related to cirrhosis, all in a decompensated stage. The calculated incidence of portal vein thrombosis was 0.573% of all cirrhotic patients without splenectomy in the past. They constituted 23.5% of the 17 cases of extrahepatic portal vein obstruction encountered during the same period. There were 78 cases of idiopathic portal hypertension similarly studied angiographically, and the incidence of portal vein thrombosis unrelated to splenectomy was 2.86%. A statistical survey based on 247,728 necropsies recorded in the Japan Autopsy Registries of 1975–1982 showed a 0.05489% incidence of portal vein thrombosis and a 6.58857% incidence of cirrhosis of all types among them, suggesting that portal vein thrombosis is not a common complication of cirrhosis in Japan in recent years.