FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2053646670> ?p ?o ?g. }

• W2053646670 endingPage "331" @default.
• W2053646670 startingPage "320" @default.
• W2053646670 abstract "Portal vein thrombosis (PVT) is being increasingly recognized in patients with advanced cirrhosis and in those undergoing liver transplantation. Reduced flow in the portal vein is probably responsible for clotting in the spleno-porto-mesenteric venous system. There is also increasing evidence that hypercoagulability occurs in advanced liver disease and contributes to the risk of PVT. Ultrasound based studies have reported a prevalence of PVT in 10–25% of cirrhotic patients without hepatocellular carcinoma. Partial thrombosis of the portal vein is more common and may not have pathophysiological consequences. However, there is high risk of progression of partial PVT to complete PVT that may cause exacerbation of portal hypertension and progression of liver insufficiency. It is thus, essential to accurately diagnose and stage PVT in patients waiting for transplantation and consider anticoagulation therapy. Therapy with low molecular weight heparin and vitamin K antagonists has been shown to achieve complete and partial recanalization in 33–45% and 15–35% of cases respectively. There are however, no guidelines to help determine the dose and therapeutic efficacy of anticoagulation in patients with cirrhosis. Anticoagulation therapy related bleeding is the most feared complication but it appears that the risk of variceal bleeding is more likely to be dependent on portal pressure rather than solely related to coagulation status. TIPS has also been reported to restore patency of the portal vein. Patients with complete PVT currently do not form an absolute contraindication for liver transplantation. Thrombectomy or thromboendovenectomy is possible in more than 75% of patients followed by anatomical end-to-end portal anastomosis. When patency of the portal vein and/or superior mesenteric vein is not achieved, only non-anatomical techniques (reno-portal anastomosis or cavo-portal hemitransposition) can be performed. These techniques, which do not fully reverse portal hypertension, are associated with higher morbidity and mortality risks in the short term. Portal vein thrombosis (PVT) is being increasingly recognized in patients with advanced cirrhosis and in those undergoing liver transplantation. Reduced flow in the portal vein is probably responsible for clotting in the spleno-porto-mesenteric venous system. There is also increasing evidence that hypercoagulability occurs in advanced liver disease and contributes to the risk of PVT. Ultrasound based studies have reported a prevalence of PVT in 10–25% of cirrhotic patients without hepatocellular carcinoma. Partial thrombosis of the portal vein is more common and may not have pathophysiological consequences. However, there is high risk of progression of partial PVT to complete PVT that may cause exacerbation of portal hypertension and progression of liver insufficiency. It is thus, essential to accurately diagnose and stage PVT in patients waiting for transplantation and consider anticoagulation therapy. Therapy with low molecular weight heparin and vitamin K antagonists has been shown to achieve complete and partial recanalization in 33–45% and 15–35% of cases respectively. There are however, no guidelines to help determine the dose and therapeutic efficacy of anticoagulation in patients with cirrhosis. Anticoagulation therapy related bleeding is the most feared complication but it appears that the risk of variceal bleeding is more likely to be dependent on portal pressure rather than solely related to coagulation status. TIPS has also been reported to restore patency of the portal vein. Patients with complete PVT currently do not form an absolute contraindication for liver transplantation. Thrombectomy or thromboendovenectomy is possible in more than 75% of patients followed by anatomical end-to-end portal anastomosis. When patency of the portal vein and/or superior mesenteric vein is not achieved, only non-anatomical techniques (reno-portal anastomosis or cavo-portal hemitransposition) can be performed. These techniques, which do not fully reverse portal hypertension, are associated with higher morbidity and mortality risks in the short term. Non-tumoral portal vein thrombosis (PVT) is not an uncommon complication occurring during the course of liver cirrhosis, frequently in its advanced stages. Alteration of blood flow within the portal vein probably plays an important role in the development of PVT with a possible contribution from the altered coagulation state in end stage liver disease. There has been an increased recognition of PVT due to frequent diagnostic imaging in patients with cirrhosis and especially in those awaiting transplantation. Development of PVT in a cirrhotic patient is expected to lead to an increase in portal pressure and decreased blood flow to the liver, thus increasing the risk of gastrointestinal bleeding, worsening of liver function, and worsening of ascites. However, the exact impact of PVT on the natural history of cirrhosis remains unclear. There are asymptomatic cirrhotic patients in whom PVT is detected incidentally on imaging and it is unclear whether it would be beneficial to treat such patients. At present there is no consensus regarding the anticoagulant drug, duration of treatment and monitoring to patients with cirrhosis and PVT. Presence of PVT has relevance during liver transplantation, since restoring both portal and arterial blood flow to the allograft is a necessary condition for liver transplantation to be successful. In this setting, PVT may be a source of technical difficulties with a negative impact on outcome. Occasionally, it may represent a definitive contraindication for transplantation. This review examines issues concerning the incidence, predisposing factors, pathogenesis and management of non-tumoral PVT in patients with cirrhosis and in candidates for liver transplantation. We also discuss surgical options in patients with extensive thrombosis undergoing liver transplantation. The prevalence of PVT in cirrhotic patients is quite variable and has been reported from 1% to 28% depending upon the modality used for diagnosis and whether PVT was detected radiologically or intra-operatively at the time of liver transplantation.1Englesbe M.J. Kubus J. Muhammad W. et al.Portal vein thrombosis and survival in patients with cirrhosis.Liver Transpl. 2010; 16: 83-90Crossref PubMed Scopus (179) Google Scholar, 2Okuda K. Ohnishi K. Kimura K. et al.Incidence of portal vein thrombosis in liver cirrhosis. An angiographic study in 708 patients.Gastroenterology. 1985; 89: 279-286Abstract PubMed Google Scholar, 3Francoz C. Belghiti J. Vilgrain V. et al.Splanchnic vein thrombosis in candidates for liver transplantation: usefulness of screening and anticoagulation.Gut. 2005; 54: 691-697Crossref PubMed Scopus (407) Google Scholar, 4Llado L. Fabregat J. Castellote J. et al.Management of portal vein thrombosis in liver transplantation: influence on morbidity and mortality.Clin Transplant. 2007; 21: 716-721PubMed Google Scholar, 5Manzanet G. Sanjuan F. Orbis P. et al.Liver transplantation in patients with portal vein thrombosis.Liver Transpl. 2001; 7: 125-131Crossref PubMed Scopus (153) Google Scholar, 6Yerdel M.A. Gunson B. Mirza D. et al.Portal vein thrombosis in adults undergoing liver transplantation: risk factors, screening, management, and outcome.Transplantation. 2000; 69: 1873-1881Crossref PubMed Scopus (501) Google Scholar, 7Gayowski T.J. Marino I.R. Doyle H.R. et al.A high incidence of native portal vein thrombosis in veterans undergoing liver transplantation.J Surg Res. 1996; 60: 333-338Abstract Full Text PDF PubMed Scopus (85) Google Scholar, 8Amitrano L. Brancaccio V. Guardascione M.A. et al.Inherited coagulation disorders in cirrhotic patients with portal vein thrombosis.Hepatology. 2000; 31: 345-348Crossref PubMed Scopus (214) Google Scholar, 9Maruyama H. Okugawa H. Takahashi M. Yokosuka O. De novo portal vein thrombosis in virus-related cirrhosis: predictive factors and long-term outcomes.Am J Gastroenterol. 2013; 108: 568-574Crossref PubMed Scopus (148) Google Scholar, 10Fimognari F.L. De Santis A. Piccheri C. et al.Evaluation of D-dimer and factor VIII in cirrhotic patients with asymptomatic portal venous thrombosis.J Lab Clin Med. 2005; 146: 238-243Abstract Full Text Full Text PDF PubMed Scopus (53) Google Scholar, 11Gaiani S. Bolondi L. Li Bassi S. Zironi G. Siringo S. Barbara L. Prevalence of spontaneous hepatofugal portal flow in liver cirrhosis. Clinical and endoscopic correlation in 228 patients.Gastroenterology. 1991; 100: 160-167PubMed Google Scholar Studies based on ultrasonography have reported a prevalence of 10%–28%, in unselected cirrhotic patients excluding those with hepatocellular carcinoma.8Amitrano L. Brancaccio V. Guardascione M.A. et al.Inherited coagulation disorders in cirrhotic patients with portal vein thrombosis.Hepatology. 2000; 31: 345-348Crossref PubMed Scopus (214) Google Scholar, 9Maruyama H. Okugawa H. Takahashi M. Yokosuka O. De novo portal vein thrombosis in virus-related cirrhosis: predictive factors and long-term outcomes.Am J Gastroenterol. 2013; 108: 568-574Crossref PubMed Scopus (148) Google Scholar, 10Fimognari F.L. De Santis A. Piccheri C. et al.Evaluation of D-dimer and factor VIII in cirrhotic patients with asymptomatic portal venous thrombosis.J Lab Clin Med. 2005; 146: 238-243Abstract Full Text Full Text PDF PubMed Scopus (53) Google Scholar, 11Gaiani S. Bolondi L. Li Bassi S. Zironi G. Siringo S. Barbara L. Prevalence of spontaneous hepatofugal portal flow in liver cirrhosis. Clinical and endoscopic correlation in 228 patients.Gastroenterology. 1991; 100: 160-167PubMed Google Scholar Maruyama et al did a retrospective analysis of 150 patients with hepatitis B or C related cirrhosis followed up for a median period of 66 months and reported a cumulative overall incidence of PVT of 12.8% at 1 year, 18.6% at 3 years, 20% at 5 years, and 38.7% at 8–10 years. Majority of these patients (73.8%) had partial PVT.9Maruyama H. Okugawa H. Takahashi M. Yokosuka O. De novo portal vein thrombosis in virus-related cirrhosis: predictive factors and long-term outcomes.Am J Gastroenterol. 2013; 108: 568-574Crossref PubMed Scopus (148) Google Scholar The prevalence of PVT most likely increases with the severity of cirrhosis. It has been reported to be quite low (1%) in patients with well compensated cirrhosis2Okuda K. Ohnishi K. Kimura K. et al.Incidence of portal vein thrombosis in liver cirrhosis. An angiographic study in 708 patients.Gastroenterology. 1985; 89: 279-286Abstract PubMed Google Scholar while it is reported to be 8%–26% in decompensated cirrhotics awaiting liver transplantation.3Francoz C. Belghiti J. Vilgrain V. et al.Splanchnic vein thrombosis in candidates for liver transplantation: usefulness of screening and anticoagulation.Gut. 2005; 54: 691-697Crossref PubMed Scopus (407) Google Scholar, 4Llado L. Fabregat J. Castellote J. et al.Management of portal vein thrombosis in liver transplantation: influence on morbidity and mortality.Clin Transplant. 2007; 21: 716-721PubMed Google Scholar, 5Manzanet G. Sanjuan F. Orbis P. et al.Liver transplantation in patients with portal vein thrombosis.Liver Transpl. 2001; 7: 125-131Crossref PubMed Scopus (153) Google Scholar, 6Yerdel M.A. Gunson B. Mirza D. et al.Portal vein thrombosis in adults undergoing liver transplantation: risk factors, screening, management, and outcome.Transplantation. 2000; 69: 1873-1881Crossref PubMed Scopus (501) Google Scholar, 7Gayowski T.J. Marino I.R. Doyle H.R. et al.A high incidence of native portal vein thrombosis in veterans undergoing liver transplantation.J Surg Res. 1996; 60: 333-338Abstract Full Text PDF PubMed Scopus (85) Google Scholar The prevalence of PVT in candidates for transplantation seems to be similar to that found in cirrhotic patients who were not necessarily evaluated for transplantation but had similar disease severity.1Englesbe M.J. Kubus J. Muhammad W. et al.Portal vein thrombosis and survival in patients with cirrhosis.Liver Transpl. 2010; 16: 83-90Crossref PubMed Scopus (179) Google Scholar, 8Amitrano L. Brancaccio V. Guardascione M.A. et al.Inherited coagulation disorders in cirrhotic patients with portal vein thrombosis.Hepatology. 2000; 31: 345-348Crossref PubMed Scopus (214) Google Scholar, 12Amitrano L. Guardascione M.A. Brancaccio V. et al.Risk factors and clinical presentation of portal vein thrombosis in patients with liver cirrhosis.J Hepatol. 2004; 40: 736-741Abstract Full Text Full Text PDF PubMed Scopus (418) Google Scholar It has been observed that at the time of evaluation for transplant, the model for end stage liver disease (MELD) and Child-Pugh scores seems to be higher in patients with PVT than in those without.1Englesbe M.J. Kubus J. Muhammad W. et al.Portal vein thrombosis and survival in patients with cirrhosis.Liver Transpl. 2010; 16: 83-90Crossref PubMed Scopus (179) Google Scholar, 6Yerdel M.A. Gunson B. Mirza D. et al.Portal vein thrombosis in adults undergoing liver transplantation: risk factors, screening, management, and outcome.Transplantation. 2000; 69: 1873-1881Crossref PubMed Scopus (501) Google Scholar A significant number of patients may have unrecognized PVT. In recent series, up to 50% of patients with PVT were detected for the first time at the time of transplant surgery.3Francoz C. Belghiti J. Vilgrain V. et al.Splanchnic vein thrombosis in candidates for liver transplantation: usefulness of screening and anticoagulation.Gut. 2005; 54: 691-697Crossref PubMed Scopus (407) Google Scholar, 13Dumortier J. Czyglik O. Poncet G. et al.Eversion thrombectomy for portal vein thrombosis during liver transplantation.Am J Transplant. 2002; 2: 934-938Crossref PubMed Scopus (102) Google Scholar This may be due to either false negatives on imaging or to PVT occurring while on the waiting list. Even in patients undergoing systematic ultrasound at close intervals of three months, the rate of previously unrecognized thrombosis remains relatively high.13Dumortier J. Czyglik O. Poncet G. et al.Eversion thrombectomy for portal vein thrombosis during liver transplantation.Am J Transplant. 2002; 2: 934-938Crossref PubMed Scopus (102) Google Scholar In patients waiting for transplant, the 12-month risk incidence of developing PVT has been reported in one study to be 7%.3Francoz C. Belghiti J. Vilgrain V. et al.Splanchnic vein thrombosis in candidates for liver transplantation: usefulness of screening and anticoagulation.Gut. 2005; 54: 691-697Crossref PubMed Scopus (407) Google Scholar The development of portal vein thrombosis in patients with end stage liver disease is a multifactorial process, resulting primarily from a reduction in portal blood flow and hypercoagulability. Traditionally, cirrhosis is considered as a hypocoagulable state and the degree of prolongation of prothrombin time (PT) and international normalized ratio (INR) has been taken as a marker of the severity of coagulopathy. The INR has been designed primarily to assess hypocoagulability in patients on vitamin K antagonists. In patients with liver disease it probably overestimates the bleeding risk.14Arjal R. Trotter J.F. International normalized ratio of prothrombin time in the model for end-stage liver disease score: an unreliable measure.Clin Liver Dis. 2009; 13: 67-71Abstract Full Text Full Text PDF PubMed Scopus (23) Google Scholar This might explain the paradox of the poor prediction of bleeding in cirrhotics even with marked prolonged of conventional coagulation tests. It appears that in the setting of hepatic synthetic impairment, both pro- and anticoagulant proteins are reduced to a similar degree and the net result in most cirrhotic patients is a compensated hemostatic balance with no tendency for bleeding or thrombosis.15Monroe D.M. Hoffman M. The coagulation cascade in cirrhosis.Clin Liver Dis. 2009; 13: 1-9Abstract Full Text Full Text PDF PubMed Scopus (53) Google Scholar (Table 1). Various clinical as well as in-vitro studies have actually shown that some patients with cirrhosis may have a thrombotic potential.16Tripodi A. Primignani M. Chantarangkul V. et al.An imbalance of pro- vs anti-coagulation factors in plasma from patients with cirrhosis.Gastroenterology. 2009; 137: 2105-2111Abstract Full Text Full Text PDF PubMed Scopus (404) Google ScholarTable 1Hemostatic abnormalities associated with liver disease.Factors promoting bleedingFactors promoting thrombosisDecreased levels of the followingDecreased levels of the following Coagulation factors II, V, VII, IX, X, XI Protein C α2-antiplasmin Protein S Thrombin-activatable fibrinolysis inhibitor Protein Z Histidine-rich glycoprotein Antithrombin α2-macroglobulinPlatelet abnormalities Heparin cofactor II Thrombocytopenia Plasminogen Impaired platelet functionIncreased levels of the following: Impaired platelet–wall interaction Factor VIII Enhanced platelet inhibition by nitric oxide and prostacyclin von Willebrand factorFibrinogen abnormalities Qualitative QuantitativeIncreased level of plasma tissue-type plasminogen activatorNutritional deficiency (vitamin K, folate) Open table in a new tab All procoagulant factors except factor VIII are reduced in hepatic insufficiency. By contrast, the levels of factor VIII/vWF are increased in cirrhosis.15Monroe D.M. Hoffman M. The coagulation cascade in cirrhosis.Clin Liver Dis. 2009; 13: 1-9Abstract Full Text Full Text PDF PubMed Scopus (53) Google Scholar, 17Jennings I. Calne R.Y. Baglin T.P. Predictive value of von Willebrand factor to ristocetin cofactor ratio and thrombin-antithrombin complex levels for hepatic vessel thrombosis and graft rejection after liver transplantation.Transplantation. 1994; 57: 1046-1051Crossref PubMed Google Scholar Since all of the components in the “extrinsic” pathway are produced by hepatocytes, the degree of prolongation of the PT has been used extensively as a measure liver synthetic function. However, even anticoagulants such as Proteins C and S as well as the levels of circulating protease inhibitors are reduced in hepatic insufficiency.18De Caterina M. Tarantino G. Farina C. et al.Haemostasis unbalance in Pugh scored liver cirrhosis: characteristic changes of plasma levels of protein C versus protein S.Haemostasis. 1993; 23: 229-235PubMed Google Scholar, 19Raya-Sanchez J.M. Gonzalez-Reimers E. Rodriguez-Martin J.M. et al.Coagulation inhibitors in alcoholic liver cirrhosis.Alcohol. 1998; 15: 19-23Abstract Full Text PDF PubMed Scopus (28) Google Scholar The physiologic effects of a deficiency of anticoagulants is not reflected in the PT or APTT, which measure only the procoagulant side of the hemostatic pathway. In vivo it is always the balance between the procoagulant and anticoagulant factors that ultimately determines whether bleeding, thrombosis, or appropriate hemostasis will occur in a particular setting. The hemostatic balance in liver disease can be thought of not as intrinsically pro- or anticoagulant, but rather as a state in which there is a reduced ability to maintain this balance. In cirrhosis, there is a relatively balanced reduction in both pro- and anticoagulant proteins, and therefore the net result is that there is very little change in the ability of the system to generate hemostatic levels of thrombin under ordinary circumstances.15Monroe D.M. Hoffman M. The coagulation cascade in cirrhosis.Clin Liver Dis. 2009; 13: 1-9Abstract Full Text Full Text PDF PubMed Scopus (53) Google Scholar, 20Tripodi A. Salerno F. Chantarangkul V. et al.Evidence of normal thrombin generation in cirrhosis despite abnormal conventional coagulation tests.Hepatology. 2005; 41: 553-558Crossref PubMed Scopus (523) Google Scholar In patients with stable cirrhosis, thrombin generation was found to be normal in in-vitro studies, when the natural anticoagulant pathway was activated by the addition of thrombomodulin.20Tripodi A. Salerno F. Chantarangkul V. et al.Evidence of normal thrombin generation in cirrhosis despite abnormal conventional coagulation tests.Hepatology. 2005; 41: 553-558Crossref PubMed Scopus (523) Google Scholar, 21Oliver J.A. Monroe D.M. Church F.C. et al.Activated protein C cleaves factor Va more efficiently on endothelium than on platelet surfaces.Blood. 2002; 100: 539-546Crossref PubMed Scopus (46) Google Scholar However, when the coagulation system in cirrhotic patients is stressed, for example by infection the system has limited buffer capacity and gets tipped out of balance into either a state of hemorrhage or thrombosis.22Violi F. Ferro D. Basili S. et al.Association between low-grade disseminated intravascular coagulation and endotoxemia in patients with liver cirrhosis.Gastroenterology. 1995; 109: 531-539Abstract Full Text PDF PubMed Scopus (118) Google Scholar Patients with cirrhosis also suffer from defects of platelet function and number that can contribute to a bleeding tendency.23Tripodi A. Primignani M. Chantarangkul V. et al.Thrombin generation in patients with cirrhosis: the role of platelets.Hepatology. 2006; 44: 440-445Crossref PubMed Scopus (286) Google Scholar However, the platelet defects get balanced by increased levels of factor VIIIa/vWF, which increases platelet adhesion.24Lisman T. Bongers T.N. Adelmeijer J. et al.Elevated levels of von Willebrand factor in cirrhosis support platelet adhesion despite reduced functional capacity.Hepatology. 2006; 44: 53-61Crossref PubMed Scopus (437) Google Scholar Three recent independent studies have been published specifically evaluating the prevalence of deep vein thrombosis (DVT) and pulmonary embolism (PE) in patients with cirrhosis.25Gulley D. Teal E. Suvannasankha A. Chalasani N. Liangpunsakul S. Deep vein thrombosis and pulmonary embolism in cirrhosis patients.Dig Dis Sci. 2008; 53: 3012-3017Crossref PubMed Scopus (146) Google Scholar, 26Northup P.G. McMahon M.M. Ruhl A.P. et al.Coagulopathy does not fully protect hospitalized cirrhosis patients from peripheral venous thromboembolism.Am J Gastroenterol. 2006; 101: 1524-1528Crossref PubMed Scopus (286) Google Scholar, 27Garcia-Fuster M.J. Abdilla N. Fabia M.J. Fernandez C. Oliver V. Forner M.J. Venous thromboembolism and liver cirrhosis.Rev Esp Enferm Dig. 2008; 100: 259-262Crossref PubMed Google Scholar The incidence of DVT/PE ranged from 0.5% to 1.87% in these studies. Interestingly one fifth of cirrhotic patients were receiving antithrombotic prophylaxis with drugs or compression devices at the time they experienced the thrombotic event.26Northup P.G. McMahon M.M. Ruhl A.P. et al.Coagulopathy does not fully protect hospitalized cirrhosis patients from peripheral venous thromboembolism.Am J Gastroenterol. 2006; 101: 1524-1528Crossref PubMed Scopus (286) Google Scholar Thus, even patients with cirrhosis and a prolonged PT receiving antithrombotic drugs can develop a venous thrombosis. Decreased hepatic synthetic function as reflected by albumin levels was associated with increased risk of DVT/PE, suggesting a greater tendency to thrombosis in advanced stages of cirrhosis.25Gulley D. Teal E. Suvannasankha A. Chalasani N. Liangpunsakul S. Deep vein thrombosis and pulmonary embolism in cirrhosis patients.Dig Dis Sci. 2008; 53: 3012-3017Crossref PubMed Scopus (146) Google Scholar, 26Northup P.G. McMahon M.M. Ruhl A.P. et al.Coagulopathy does not fully protect hospitalized cirrhosis patients from peripheral venous thromboembolism.Am J Gastroenterol. 2006; 101: 1524-1528Crossref PubMed Scopus (286) Google Scholar The incidence of PVT has also been reported to be higher in patients with more severe cirrhosis.12Amitrano L. Guardascione M.A. Brancaccio V. et al.Risk factors and clinical presentation of portal vein thrombosis in patients with liver cirrhosis.J Hepatol. 2004; 40: 736-741Abstract Full Text Full Text PDF PubMed Scopus (418) Google Scholar Some interesting in-vitro evidence also supports these clinical findings. The ratio of the most powerful procoagulant (factor VIII) and anticoagulant (protein C) in plasma showed a balance strongly in favor of factor VIII, which indicates hypercoagulability.16Tripodi A. Primignani M. Chantarangkul V. et al.An imbalance of pro- vs anti-coagulation factors in plasma from patients with cirrhosis.Gastroenterology. 2009; 137: 2105-2111Abstract Full Text Full Text PDF PubMed Scopus (404) Google Scholar Factor VIII concentrations have been reported to be higher in patients with worse Child-Pugh grade.16Tripodi A. Primignani M. Chantarangkul V. et al.An imbalance of pro- vs anti-coagulation factors in plasma from patients with cirrhosis.Gastroenterology. 2009; 137: 2105-2111Abstract Full Text Full Text PDF PubMed Scopus (404) Google Scholar A recent study reported that high levels of factor VIII were independently associated with cirrhotic PVT, with odds ratio for thrombosis being 6.0 if factor VIII levels were above 129 IU/dl.28Martinelli I. Primignani M. Aghemo A. et al.High levels of factor VIII and risk of extra-hepatic portal vein obstruction.J Hepatol. 2009; 50: 916-922Abstract Full Text Full Text PDF PubMed Scopus (55) Google Scholar While in non-cirrhotic patients, PVT is related to prothrombotic states (myeloproliferative diseases and/or inherited coagulation disorders) in a significant percentage of patients, in cirrhotic patients portal hemodynamics also plays an important role in the development of PVT.29DeLeve L.D. Valla D.C. Garcia-Tsao G. Vascular disorders of the liver.Hepatology. 2009; 49: 1729-1764Crossref PubMed Scopus (673) Google Scholar Portal flow is reduced in cirrhotic livers due to increased intrahepatic vascular resistance and this phenomenon is further pronounced as liver disease progresses.30Shah V. Molecular mechanisms of increased intrahepatic resistance in portal hypertension.J Clin Gastroenterol. 2007; 41: S259-S261Crossref PubMed Scopus (26) Google Scholar, 31Zocco M.A. Di Stasio E. De Cristofaro R. et al.Thrombotic risk factors in patients with liver cirrhosis: correlation with MELD scoring system and portal vein thrombosis development.J Hepatol. 2009; 51: 682-689Abstract Full Text Full Text PDF PubMed Scopus (344) Google Scholar This may be another reason to explain the increased prevalence of PVT in advanced cirrhotics as compared to early cirrhotics with well compensated disease. In one prospective study, reduced portal flow velocity below 15 cm/s was the only independent variable that correlated with the risk of developing PVT at 1 year of follow-up.31Zocco M.A. Di Stasio E. De Cristofaro R. et al.Thrombotic risk factors in patients with liver cirrhosis: correlation with MELD scoring system and portal vein thrombosis development.J Hepatol. 2009; 51: 682-689Abstract Full Text Full Text PDF PubMed Scopus (344) Google Scholar Patients who develop PVT have also been reported to have low portal flow volumes and high collateral vessel flow velocity and flow volume.9Maruyama H. Okugawa H. Takahashi M. Yokosuka O. De novo portal vein thrombosis in virus-related cirrhosis: predictive factors and long-term outcomes.Am J Gastroenterol. 2013; 108: 568-574Crossref PubMed Scopus (148) Google Scholar Another independent risk factor for PVT is the degree of thrombocytopenia.9Maruyama H. Okugawa H. Takahashi M. Yokosuka O. De novo portal vein thrombosis in virus-related cirrhosis: predictive factors and long-term outcomes.Am J Gastroenterol. 2013; 108: 568-574Crossref PubMed Scopus (148) Google Scholar, 31Zocco M.A. Di Stasio E. De Cristofaro R. et al.Thrombotic risk factors in patients with liver cirrhosis: correlation with MELD scoring system and portal vein thrombosis development.J Hepatol. 2009; 51: 682-689Abstract Full Text Full Text PDF PubMed Scopus (344) Google Scholar This seems paradoxical since low platelet count should logically predispose to bleeding. Possibly as cirrhosis and portal hypertension progresses, the resultant decrease in portal flow possibly outweighs a protective effect of low platelet count against thrombosis and the paradoxical finding of increased PVT with lower platelet counts may be thus related to decreased portal flows that occurs with progression of portal hypertension.32Lisman T. Porte R.J. The role of platelets in liver inflammation and regeneration.Semin Thromb Hemost. 2010; 36: 170-174Crossref PubMed Scopus (42) Google Scholar Although limited, but some studies do report a thrombophilic genotype in up to 70% of patients with cirrhosis and PVT. Polymorphisms TT677 of methylene-tetrahydrofolate reductase (MTHFR) and G20210A in the prothrombin gene were significantly more frequent in this group compared with that in controls.8Amitrano L. Brancaccio V. Guardascione M.A. et al.Inherited coagulation disorders in cirrhotic patients with portal vein thrombosis.Hepatology. 2000; 31: 345-348Crossref PubMed Scopus (214) Google Scholar, 12Amitrano L. Guardascione M.A. Brancaccio V. et al.Risk factors and clinical presentation of portal vein thrombosis in patients with liver cirrhosis.J Hepatol. 2004; 40: 736-741Abstract Full Text Full Text PDF PubMed Scopus (418) Google Scholar, 33Mangia A. Villani M.R. Cappucci G. et al.Causes of portal venous thrombosis in cirrhotic patients: the role of genetic and acquired factors.Eur J Gastroenterol Hepatol. 2005; 17: 745-751Crossref PubMed Scopus (71) Google Scholar Apart from gene mutations, it is actually difficult to detect underlying prothrombotic condition in these patients due to the non-specific decrease in both coagulation factors and inhibitors.29DeLeve L.D. Valla D.C. Garcia-Tsao G. Vascular disorders of the liver.Hepatology. 2009; 49: 1729-1764Crossref PubMed Scopus (673) Google Scholar Among other factors that may increase the risk of PVT is endotoxemia.34Violi F. Ferro D. Basili S. et al.Ongoing prothrombotic state in the portal circulation of cirrhotic patients.Thromb Haemost. 1997; 77: 44-47PubMed Google Scholar Endotoxemia is common" @default.
• W2053646670 created "2016-06-24" @default.
• W2053646670 creator A5003595725 @default.
• W2053646670 creator A5009027475 @default.
• W2053646670 creator A5068786980 @default.
• W2053646670 date "2014-12-01" @default.
• W2053646670 modified "2023-09-27" @default.
• W2053646670 title "Portal Vein Thrombosis in Cirrhosis" @default.
• W2053646670 cites W155891895 @default.
• W2053646670 cites W1738779651 @default.
• W2053646670 cites W1753709933 @default.
• W2053646670 cites W1923113404 @default.
• W2053646670 cites W1970902654 @default.
• W2053646670 cites W1972486471 @default.
• W2053646670 cites W1974708718 @default.
• W2053646670 cites W1986644481 @default.
• W2053646670 cites W1986963195 @default.
• W2053646670 cites W1989713925 @default.
• W2053646670 cites W1990192396 @default.
• W2053646670 cites W1992235530 @default.
• W2053646670 cites W1992618503 @default.
• W2053646670 cites W1994892190 @default.
• W2053646670 cites W1995608256 @default.
• W2053646670 cites W1996755789 @default.
• W2053646670 cites W1997376075 @default.
• W2053646670 cites W1999337145 @default.
• W2053646670 cites W2003559187 @default.
• W2053646670 cites W2004595908 @default.
• W2053646670 cites W2005403960 @default.
• W2053646670 cites W2006916640 @default.
• W2053646670 cites W2009594394 @default.
• W2053646670 cites W2011557656 @default.
• W2053646670 cites W2013077431 @default.
• W2053646670 cites W2014780671 @default.
• W2053646670 cites W2015413115 @default.
• W2053646670 cites W2016191890 @default.
• W2053646670 cites W2016572253 @default.
• W2053646670 cites W2019725414 @default.
• W2053646670 cites W2019743060 @default.
• W2053646670 cites W2025389760 @default.
• W2053646670 cites W2027114285 @default.
• W2053646670 cites W2028213315 @default.
• W2053646670 cites W2031935034 @default.
• W2053646670 cites W2032537572 @default.
• W2053646670 cites W2033918989 @default.
• W2053646670 cites W2038287002 @default.
• W2053646670 cites W2040826870 @default.
• W2053646670 cites W2046305607 @default.
• W2053646670 cites W2048441761 @default.
• W2053646670 cites W2050690194 @default.
• W2053646670 cites W2051427787 @default.
• W2053646670 cites W2054312277 @default.
• W2053646670 cites W2054668384 @default.
• W2053646670 cites W2063668704 @default.
• W2053646670 cites W2070298490 @default.
• W2053646670 cites W2072212394 @default.
• W2053646670 cites W2072289402 @default.
• W2053646670 cites W2072330219 @default.
• W2053646670 cites W2076429273 @default.
• W2053646670 cites W2079551812 @default.
• W2053646670 cites W2088638588 @default.
• W2053646670 cites W2089422120 @default.
• W2053646670 cites W2092879097 @default.
• W2053646670 cites W2093904358 @default.
• W2053646670 cites W2094486696 @default.
• W2053646670 cites W2097256068 @default.
• W2053646670 cites W2113917646 @default.
• W2053646670 cites W2114729715 @default.
• W2053646670 cites W2116419942 @default.
• W2053646670 cites W2119768870 @default.
• W2053646670 cites W2121077197 @default.
• W2053646670 cites W2121504015 @default.
• W2053646670 cites W2135361119 @default.
• W2053646670 cites W2136002789 @default.
• W2053646670 cites W2139090396 @default.
• W2053646670 cites W2139398552 @default.
• W2053646670 cites W2140237998 @default.
• W2053646670 cites W2142011623 @default.
• W2053646670 cites W2145598693 @default.
• W2053646670 cites W2145791480 @default.
• W2053646670 cites W2147335115 @default.
• W2053646670 cites W2150451639 @default.
• W2053646670 cites W2151886152 @default.
• W2053646670 cites W2155112010 @default.
• W2053646670 cites W2157769987 @default.
• W2053646670 cites W2158268405 @default.
• W2053646670 cites W2160633420 @default.
• W2053646670 cites W2166018647 @default.
• W2053646670 cites W2170740817 @default.
• W2053646670 cites W2172060670 @default.
• W2053646670 cites W2209834821 @default.
• W2053646670 cites W2413454704 @default.
• W2053646670 cites W2466191110 @default.
• W2053646670 cites W4242342831 @default.
• W2053646670 doi "https://doi.org/10.1016/j.jceh.2013.12.003" @default.
• W2053646670 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4298635" @default.
• W2053646670 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25755579" @default.
• W2053646670 hasPublicationYear "2014" @default.

• next