Acute-on-Chronic Liver Failure Is a Distinct Syndrome That Develops in Patients With Acute Decompensation of Cirrhosis

Moreau, Richard; Jalan, Rajiv; Ginès, Pere; Pavesi, Marco; Angeli, Paolo; Córdoba, Juan; Durand, François; Gustot, Thierry; Saliba, Faouzi; Domenicali, Marco; Gerbes, Alexander L.; Wendon, Julia; Alessandria, Carlo; Laleman, Wim; Zeuzem, Stefan; Trebicka, Jonel; Bernardi, Mauro; Arroyo, Vicente

doi:10.1053/j.gastro.2013.02.042

Cited by 2,466 publications

(4,016 citation statements)

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“…Among extrinsic factors, bacterial infections are frequent in hospitalized patients with cirrhosis, and often responsible for acute on chronic liver failure [69,70]. The condition may favor a hemorrhagic diathesis through a direct effect of bacterial products or the hyper-production of proinflammatory cytokines, causing defects in platelet aggregation [71], coagulation activation and hyperfibrinolysis [72][73][74], and release of endogenous heparinoids [75][76][77].…”

Section: Factors Tipping the Hemostatic Balance 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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Section: Factors Tipping the Hemostatic Balance 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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“…In selected patients, TIPS decompresses the portal venous system, successfully treats ascites and variceal bleeding, and improves survival 14, 15, 16, 17. However, AD of liver cirrhosis can progress and develop into acute‐on‐chronic liver failure (ACLF) with poor survival 18. While deposition of ECM in the course of liver fibrosis has been known for some time, the role of collagen in patients with advanced liver cirrhosis and AD19 remains unclear.…”

Section: Introductionmentioning

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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“…1). Similar to the study evaluating the outcome in the ICU of patients with cirrhosis, 6 we found that liver function was not the main determinant of outcome so that an organ failure score as the SOFA or the new chronic liver failure (CLIF)-SOFA score 7 could be more useful in predicting outcome, although not sufficient.…”

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confidence: 56%

Liver transplantation in patients with end‐stage liver disease requiring intensive care unit admission and intubation

et al. 2015

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Acute-on-Chronic Liver Failure Is a Distinct Syndrome That Develops in Patients With Acute Decompensation of Cirrhosis

Cited by 2,466 publications

References 30 publications

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

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

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

Liver transplantation in patients with end‐stage liver disease requiring intensive care unit admission and intubation

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