The CLIF Consortium Acute Decompensation score (CLIF-C ADs) for prognosis of hospitalised cirrhotic patients without acute-on-chronic liver failure

Jalan, Rajiv; Pavesi, Marco; Saliba, Faouzi; Amorós, Àlex; Fernández, Javier; Holland-Fischer, Peter; Sawhney, Rohit; Mookerjee, Rajeshwar P.; Caraceni, Paolo; Moreau, Richard; Ginès, Pere; Durand, François; Angeli, Paolo; Alessandria, Carlo; Laleman, Wim; Trebicka, Jonel; Samuel, Didier; Zeuzem, Stefan; Gustot, Thierry; Gerbes, Alexander L.; Wendon, Julia; Bernardi, Mauro; Arroyo, Vicente; Investigators, Canonic Study

doi:10.1016/j.jhep.2014.11.012

Cited by 295 publications

(331 citation statements)

References 25 publications

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“…It was found that SBP alone accounts for 31%, almost one-third cases of acute deterioration in type I ACLF. A similar finding was reported by a Western study done by Jalan et al 6 Could hepatocellular carcinoma (HCC) be a cause of acute deterioration? The answer is HCC can lead to acute worsening.…”

Section: Cause Of Acute Deteriorationsupporting

confidence: 82%

Metabolic Syndrome with Double Hit, Nonproteinuric Diabetic Nephropathy and Nonalcoholic Steatohepatitis-related Cirrhosis: Autopsy Findings

Taneja¹,

Duseja²,

Bhatia³

et al. 2017

Journal of Postgraduate Medicine, Education and Research

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Section: Cause Of Acute Deteriorationsupporting

confidence: 82%

Metabolic Syndrome with Double Hit, Nonproteinuric Diabetic Nephropathy and Nonalcoholic Steatohepatitis-related Cirrhosis: Autopsy Findings

Taneja¹,

Duseja²,

Bhatia³

et al. 2017

Journal of Postgraduate Medicine, Education and Research

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“…4C). Indeed, patients with higher chronic liver failure‐C (CLIF‐C) AD score, reflecting a high risk of ACLF,27 also had a higher deposition ratio (Fig. 4D).…”

Section: Resultsmentioning

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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“…This hypothesis gains considerable support by recent studies in patients with cirrhosis and SBP reporting that combined treatment with intravenous albumin and an antibiotic reduces the risk for renal dysfunction/failure and mortality in comparison to therapy with a single antibiotic [39]. Last but not least, clinical investigations, which clearly identified white blood cell count and C-reactive protein (CRP) as independent predictors of in-hospital survival, add great evidence to the prognosis-relevant role of SI [64,65]. More information on 'immune dysregulation' is given by Lange and Moreau [66] in this focus issue of Visceral Medicine.…”

Section: Immune Dysfunctionmentioning

confidence: 93%

“…In addition, a 'leaky gut' favoring translocation of bacteria towards the bloodstream along with a gradually impaired hepatic clearance capacity for bacterial antigens, such as lipopolysaccharide (LPS) or endotoxin, may induce activation of toll-like receptor (TLR) pathways, and, thus, further enhance SI that accelerates fibrogenesis and progression to liver cirrhosis [63]. This, in turn, boosts cytokine secretion along with an ongoing synthesis of reactive oxygen species (ROS), thereby forming a vicious circle in the development of intestinal inflammation and tissue hyperpermeability [64,65]. In this light, it is reasonable to assume that some beneficial effects of albumin administration in cirrhotic patients with SBP and/or type-1 HRS might be largely attributable to its anti-inflammatory and antioxidative stress properties [36].…”

Section: Immune Dysfunctionmentioning

confidence: 99%

Intensive Care Therapy for Patients with Advanced Liver Diseases

Katsounas

Canbay

2018

Visc Med

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Decompensated cirrhosis is characterized by high hospitalization rates and costs, frequent readmissions, and poor short-term survival. Patients admitted to the hospital with acute variceal bleeding and/or hepatic encephalopathy and/or renal dysfunction are at serious risk for developing infection and/or sepsis; in turn, this renders them highly susceptible to the development of multi-system organ failure. The lack of standardized intensive care unit management protocols in patients with cirrhosis along with only few data reports from longitudinal clinical trials makes it difficult for hepatologists and critical care specialists to provide uniform evidence for clinical practice that could safely consolidate favorable outcomes such as lower hospitalization rates and/or mortality. Based on a rigorous online search of the scientific literature as well as a longtime clinical experience of the authors in the field of hepatology and critical care medicine, this work represents a focused effort to elucidate the specific bio-morbidity of advanced liver diseases in relation to the aforementioned challenges in clinical management. Further meta-analyses and/or systematic reviews are needed to enable clinicians to develop more effective strategies to bridge patients with decompensated liver disease to recompensation or liver transplantation.

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The CLIF Consortium Acute Decompensation score (CLIF-C ADs) for prognosis of hospitalised cirrhotic patients without acute-on-chronic liver failure

Abstract: The new CLIF-C ADs is more accurate than other liver scores in predicting prognosis in hospitalised cirrhotic patients without ACLF. CLIF-C ADs therefore may be used to identify a high-risk cohort for intensive management and a low-risk group that may be discharged early.

Cited by 295 publications

References 25 publications

Metabolic Syndrome with Double Hit, Nonproteinuric Diabetic Nephropathy and Nonalcoholic Steatohepatitis-related Cirrhosis: Autopsy Findings

Metabolic Syndrome with Double Hit, Nonproteinuric Diabetic Nephropathy and Nonalcoholic Steatohepatitis-related Cirrhosis: Autopsy Findings

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

Intensive Care Therapy for Patients with Advanced Liver Diseases

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