The aim of this study was to evaluate the efficacy and safety of the anticoagulants for the prevention of portal vein system thrombosis (PVST) in patients with cirrhosis after splenectomy and explore the optimal time of anticoagulant administration.

A systematic literature search was performed using PubMed, Embase and China Biology Medicine disc (CBM)databases, so as to screen out studies comparing the prognoses between cirrhotic post-splenectomy patients treated with and without anticoagulants. The parameters that were analyzed included the incidence of PVST and postoperative bleeding.

With a total of 592 subjects, we included 8 studies (6 observational and 2 randomized trials) that fulfilled the inclusion criteria. We found that the incidence of PVST was significantly lower in the anticoagulation group during the first 6 months of anticoagulant administration. And the largest difference in the incidence of PVST between the anticoagulation and control groups was observed at 3 months (odds ratio 0.17(0.11~0.27); P = 0.767; I2 = 0.0%) and 6 months (OR = 0.21(0.11~0.40); P = 0.714; I2 = 0.0%) postoperatively. The incidence of bleeding was not significantly higher in the anticoagulation group (odds ratio 0.71 (0.30~1.71); P = 0.580; I2 = 0.0%).

Low-molecular weight heparin (LMWH) and warfarin can decrease the incidence of PVST in post-splenectomy cirrhotic patients without an increased risk of bleeding. And the optimal use time of warfarin is 6 months after splenectomy.

Acute and chronic liver disease are associated with substantial alterations in the hemostatic system. Evidence from both experimental and clinical studies suggests that anticoagulants slow the progression of liver disease. Efficacy of those anticoagulant drugs is, in part, attributed to a reduction of microthrombi formation within the liver. Although anticoagulant drugs show promising results, bleeding risk associated with these drugs is an obvious drawback, particularly in patients with a complex coagulopathy driven by decreased liver function. Identifying therapies that reduce intrahepatic thrombosis with minimal bleeding risk would significantly advance the field. Among the hemostatic alterations observed in patients are substantially increased levels of the platelet-adhesive protein von Willebrand factor (VWF). In contrast, levels of A Disintegrin and Metalloproteinase with Thrombospondin motifs, the enzyme that regulates VWF activity, are significantly reduced in patients with liver disease. Highly elevated VWF levels are proposed to accelerate intrahepatic thrombus formation and thus be a driver of disease progression. Strong clinical evidence suggesting a link between liver disease and changes in VWF is now being matched by emerging mechanistic data showing a detrimental role for VWF in the progression of liver disease. This review focuses on clinical and experimental evidence supporting a connection between VWF function and the progression of acute and chronic liver diseases. Furthermore, with the recent anticipated approval of several novel therapies targeting VWF, we discuss potential strategies and benefits of targeting VWF as an innovative therapy for patients with liver disease.

A systematic review and meta-analysis were conducted to evaluate the efficacy and safety of early prophylactic anticoagulation for the prevention of portal vein system thrombosis (PVST) after splenectomy. A systematic search of the PubMed, EMBASE, Springer and Cochrane Library databases was performed to identify studies comparing the outcomes in patients receiving or not receiving regular prophylactic anticoagulation after splenectomy. The quality of the included studies was assessed using the Jadad Score and the Newcastle-Ottawa Scale. Heterogeneity was evaluated using the χ² and I² tests. The parameters that were analyzed included the incidence of PVST and anticoagulation-associated complications. A total of seven studies qualified for the review, involving 383 and 283 patients receiving or not receiving regular prophylactic anticoagulation, respectively. The incidence of PVST was significantly reduced with an odds ratio (OR) of 0.31 [95% confidence interval (CI), 0.21-0.46; P<0.00001] in the regular prophylactic anticoagulation group compared with the control group. No difference in the incidence of anticoagulation-associated complications was identified between the two groups (OR=0.60, 95% CI, 0.23-1.56; P=0.30). Early prophylactic anticoagulation was associated with a reduced incidence of PVST, although it was not associated with the incidence of anticoagulation-associated complications. These results indicate that prophylactic anticoagulation could be safely administered after splenectomy, even to cirrhotic patients.

To review current literature for anticoagulation in patients with cirrhosis and provide a summary of the effects of cirrhosis on the coagulation cascade, therapeutic monitoring through interpretation of antifactor Xa (anti-Xa), activated partial thromboplastin time (aPTT), and international normalized ratio (INR) as well as current prophylaxis and treatment recommendations in cirrhotic patients.

A systematic electronic literature search was conducted in PubMed using the key termsanticoagulation, warfarin, low-molecular-weight heparin(LMWH),unfractionated heparin(UFH),target-specific oral anticoagulants, deep-vein thrombosis(DVT),pulmonary embolism(PE),portal vein thrombosis(PVT),venous thromboembolism, anti-Xa, activated partial thromboplastin time, anticoagulation therapeutic monitoring, coagulopathy, coagulation cascade, chronic liver disease, cirrhosis, anddecompensated liver disease

Studies written in the English language from January 2000 to December 2015 were considered for this review article. All search results were reviewed, and the relevance of each article was determined by authors independently.

Patients with cirrhosis are at higher risk for both bleeding and thrombosis-related complications. Cirrhosis affects production of both procoagulant and anticoagulant factors, thus resulting in increased INR and aPTT levels and decreased anti-Xa levels. LMWH is the treatment of choice for the prevention and treatment of DVT/PE/PVT in patients with cirrhosis, and monitoring with anti-Xa levels for dose adjustment is not recommended. UFH is an alternative in cirrhotic patients for shorter-term use and in cases of severe renal dysfunction and/or hemodynamic instability. Cirrhotic patients on anticoagulation therapy should be monitored closely for signs and symptoms of bleeding and thrombosis.

Among the common complication of cirrhosis portal hypertension witnessed a major improvement of prognosis during the past decades. Principally due to the introduction of rational treatments based on new pathophysiological paradigms (concepts of thought) developed in the 1980s. The best example being the use of non-selective beta-blockers and of vasopressin analogs, somatostatin, and its analogs. Further refinement in the knowledge of the molecular mechanisms involved in the regulation of both the splanchnic and hepatic circulation has led to the emergence of new treatments, which are based on evidence that show not only structural but also vasoactive components increase the hepatic vascular resistance, as well as of angiogenesis. This knowledge and future improvements will most likely result in more effective treatment of portal hypertension and effective prevention of its complications in early stages.

Portal vein thrombosis (PVT) has a high incidence in patients with liver cirrhosis and determines a poor prognosis of hepatic disease. The aim of our study was to define the natural course of partial PVT in cirrhotic patients, including survival and decompensation rates.

We performed a prospective, cohort study, in a tertiary referral center. There were 22 cirrhotic patients with partial nonmalignant PVT, without anticoagulant treatment, who were followed-up between January 2011 and October 2013. All patients were evaluated by Doppler abdominal ultrasound and computed tomography. Kaplan-Meier method was used to determine the difference in clinical events between the study subgroups.

After a mean follow-up period of 20.22 months, partial PVT improved in 5 (22.73%), was stable in 11 (50%), and worsened in 6 (27.27%) patients. Hepatic decompensation rate at 6 and 18 months was higher in patients with worsened PVT than in those with stable/improved PVT (50% vs. 25%, P < 0.0001 and 100% vs. 56.25%, P < 0.0001, respectively). The survival rate at 6 months was 66.66% in worsened PVT group vs. 81.25% (P = 0.005) in stable/improved group, and 16.66% vs. 81.25% (P < 0.0001) at 18 months, respectively. Multivariate analysis showed that Model of End-Life Disease was the independent predictor of hepatic decompensation [hazard ratio (HR) 1.42; 95% confidence interval (CI): 1.08-1.87, P = 0.012] and survival (HR 1.76; 95% CI: 1.06-2.92, P = 0.028).

Nonmalignant partial PVT remained stable/improved in over half of cirrhotic patients and aggravated in more than one fourth in whom it negatively influenced the survival and decompensation rates.

To review the current literature on the risk of venous thromboembolism (VTE) in patients with chronic liver disease (CLD).

Literature was accessed through MEDLINE/PubMed (1996-December 2011) using the search terms liver disease, cirrhosis, venous thromboembolism, deep vein thrombosis, and pulmonary embolism.

Relevant observational and population-based studies were included to present background information. Bibliographies of all relevant articles were reviewed for additional citations.

Liver disease affects the synthesis of procoagulants and anticoagulants, resulting in hemostatic alterations and abnormal laboratory values. Retrospective studies characterized the VTE incidence to be 0.5-6.3%. Population-based studies reported VTE relative risks of 1.74-2.10 in patients with CLD compared with population controls and VTE odds ratios of 0.9-1.39 for hospitalized patients with CLD compared with controls without liver disease. There is a paucity of data on the use of pharmacologic prophylaxis in patients with CLD.

Patients with CLD should be assessed for VTE risk and given VTE prophylaxis when the benefits outweigh the risks. Diagnoses of CLD or elevated international normalized ratio do not confer protection against development of VTE and do not justify withholding pharmacologic prophylaxis based on this diagnosis.

Non-neoplastic portal vein thrombosis (PVT) is an increasingly recognized complication of liver cirrhosis. It is often diagnosed fortuitously and can be either partial or complete. The clinical significance of PVT is not obvious except in some situations such as when patients are on the waiting list for liver transplantation. The only known therapy is anticoagulation which has been shown to permit the disappearance of thrombosis and to prevent further extension. Anticoagulation is a challenging therapy in individuals with liver cirrhosis because of the well-recognized coagulation abnormalities observed in that setting and because of the increased risk of bleeding, especially from gastrointestinal tract caused by portal hypertension. We herein review the current knowledge on that topic in order to highlight the advantages and disadvantages of the currently proposed therapeutic attitudes in face of the diagnosis of PVT in individuals with cirrhosis.