Systematic review: portal vein thrombosis in cirrhosis

Tsochatzis, Emmanuel; Senzolo, Marco; Germani, Giacomo; Gatt, Alex; Burroughs, Andrew K.

doi:10.1111/j.1365-2036.2009.04182.x

Cited by 276 publications

(218 citation statements)

References 83 publications

(170 reference statements)

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“…Continuous liver injury leads to ECM remodeling in response to tissue injury and to development of progressive fibrosis in affected patients 28, 29, 30, 31. Development of ascites and acute decompensation are decisive events in patients with liver cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Acute decompensation boosts hepatic collagen type III deposition and deteriorates experimental and human cirrhosis

Praktiknjo

Lehmann

Nielsen

et al. 2018

Hepatology Communications

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Patients with end‐stage liver disease develop acute decompensation (AD) episodes, which become more frequent and might develop into acute‐on‐chronic liver failure (ACLF). However, it remains unknown how AD induces acceleration of liver disease. We hypothesized that remodeling of collagen type III plays a role in the acceleration of liver cirrhosis after AD and analyzed its formation (Pro‐C3) and degradation (matrix metalloproteinase‐degraded type III collagen [C3M]) markers in animal models and human disease. Bile duct ligation induced different stages of liver fibrosis in rats. Fibrosis development (hydroxyprolin content, sirius red staining, α‐smooth muscle actin immunohistochemistry, messenger RNA of profibrotic cytokines), necroinflammation (aminotransferases levels), fibrolysis (matrix metalloproteinase 2 expression and activity, C1M, C4M), and Pro‐C3 and C3M were analyzed 2, 3, 4, 5, and 6 weeks after bile duct ligation (n = 5 each group). In 110 patients with decompensated liver cirrhosis who underwent a transjugular intrahepatic portosystemic shunt procedure for AD, clinical and laboratory parameters as well as Pro‐C3 and C3M were measured in blood samples from portal and hepatic veins and were collected just before the transjugular intrahepatic portosystemic shunt placement and 1‐3 weeks later. Animal studies showed increased markers of collagen type III deposition with fibrosis, necroinflammation, and decompensation of liver cirrhosis, defined as ascites development. Higher Pro‐C3 levels were associated with injury, disease severity scores (Model for End‐Stage Liver Disease, Child‐Pugh, chronic liver failure‐C AD), ACLF development, and mortality. C3M decreased with AD and the chronic liver failure‐C AD score. Collagen type III deposition ratio increased with the risk of ACLF development and mortality. Conclusion: We show for the first time that AD boosts collagen type III deposition in experimental and human cirrhosis, possibly contributing to the worsened outcome in patients with decompensated cirrhosis. (Hepatology Communications 2018;2:211–222)

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Section: Discussionmentioning

confidence: 99%

Acute decompensation boosts hepatic collagen type III deposition and deteriorates experimental and human cirrhosis

Praktiknjo

Lehmann

Nielsen

et al. 2018

Hepatology Communications

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“…Slow portal blood flow, vessel wall damage and hypercoagulability are risk factors for PVT in patients with cirrhosis [191][192][193]. Other risk factors include male sex, previous abdominal surgery, encephalopathy, ascites, a low platelet count and a history of bleeding varices [35,184,[194][195][196][197][198].…”

Section: Portal Vein Thrombosis In Cirrhosismentioning

confidence: 99%

Hemostatic balance in patients with liver cirrhosis: Report of a consensus conference

Andriulli

Tripodi

Angeli

et al. 2016

Digestive and Liver Disease

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a b s t r a c tPatients with cirrhosis present with hemostatic alterations secondary to reduced availability of procoagulant and anti-coagulant factors. The net effect of these changes is a rebalanced hemostatic system. The Italian Association of the Study of the Liver (AISF) and the Italian Society of Internal Medicine (SIMI) promoted a consensus conference on the hemostatic balance in patients with cirrhosis. The consensus process started with the review of the literature by a scientific board of experts and ended with a formal consensus meeting in Rome in December 2014. The statements were graded according to quality of evidence and strength of recommendations, and approved by an independent jury. The statements presented here highlight strengths and weaknesses of current laboratory tests to assess bleeding and thrombotic risk in cirrhotic patients, the pathophysiology of hemostatic perturbations in this condition, and outline the optimal management of bleeding and thrombosis in patients with liver cirrhosis.

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“…However, in this particular situation, there is no consensus on whether nonselective beta-blockers, endoscopic variceal ligation (EVL), or combination therapy is better for variceal bleed prophylaxis. 29,63,75,76 In case EVL is being performed (generally for large varices with red color signs or in patients with past history of variceal bleeding), it is recommended to delay initiation of anticoagulation therapy for atleast 2 weeks after the last EVL so as to allow post EVL ulcers to heal completely. 52 In the published studies most patients have been on nonselective beta-blockers with or without EVL prior to initiating anticoagulation.…”

Section: Complications Of Anticoagulation and Prophylaxis Of Varicealmentioning

confidence: 99%

Portal Vein Thrombosis in Cirrhosis

Raja

Jacob

Asthana

2014

Journal of Clinical and Experimental Hepatology

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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. ( J CLIN EXP HEPATOL 2013;4:320-331)

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Systematic review: portal vein thrombosis in cirrhosis

Cited by 276 publications

References 83 publications

Acute decompensation boosts hepatic collagen type III deposition and deteriorates experimental and human cirrhosis

Acute decompensation boosts hepatic collagen type III deposition and deteriorates experimental and human cirrhosis

Hemostatic balance in patients with liver cirrhosis: Report of a consensus conference

Portal Vein Thrombosis in Cirrhosis

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