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• W3124865463 abstract "See Article, pages 670–685 See Article, pages 670–685 When I started my training in hepatology in 1980, survival after a first episode of gastrointestinal (GI) bleeding due to ruptured oesophageal varices was below 50%, while it was below 30% after a first episode of spontaneous bacterial peritonitis (SBP). Before the 2000s, survival in patients with hepatorenal syndrome (HRS) type 1 and anuria was close to zero at 28 days and most patients were not admitted to the intensive care unit (ICU) because of their poor spontaneous prognosis. Several factors have led to a major improvement in survival in patients with end-stage cirrhosis: first, a better comprehension of the pathophysiology of portal hypertension and liver failure in patients with cirrhosis; second, the advent of new technologies such as emergency gastroduodenal endoscopic variceal sclerotherapy, banding ligation, and emergency transjugular intrahepatic portosystemic shunt in patients with active GI bleeding due to portal hypertension;[1]De Franchis R. Faculty Baveno VI. Expanding consensus in portal hypertension: report of the Baveno VI Consensus Workshop: stratifying risk and individualizing care for portal hypertension.J Hepatol. 2015; 63: 743-752Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar third, the advent and exponential development of liver transplantation, which has become a life-saving procedure for many patients with end-stage liver disease. However, nothing would have been possible without the better comprehension of the pathophysiology of liver diseases. The mechanisms of portal hypertension have been dissected, revealing the role of vascular resistance in the cirrhotic liver, of the splanchnic portal flow and of endothelial involvement; this has enabled major therapeutic advances, including the use of β-blockers, somatostatin and vasopressin (and its derivate terlipressin).[1]De Franchis R. Faculty Baveno VI. Expanding consensus in portal hypertension: report of the Baveno VI Consensus Workshop: stratifying risk and individualizing care for portal hypertension.J Hepatol. 2015; 63: 743-752Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar Better understanding of the role of the angiotensin-aldosterone system and of hypoalbuminemia in the occurrence of ascites has led to the introduction of effective diuretic therapy and to the use of iterative paracentesis with albumin supplementation, which has been of major importance for the long-term management of patients with refractory ascites. Understanding the role of bacterial translocation in the development of SBP, leading to the use of prophylactic and therapeutic anti-gram negative non-nephrotoxic antibiotics alongside albumin perfusion, has led to a major improvement in survival in patients with SBP. Finally, the use of terlipressin to reverse the fatal HRS type 1 has led to a dramatic improvement in survival of patients responding to this therapy.[2]European Association for the Study of the Liver. Electronic address: [email protected], European Association for the Study of the LiverEASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis.J Hepatol. 2018; 69: 406-460Abstract Full Text Full Text PDF PubMed Scopus (678) Google Scholar,[3]Angeli P. Gines P. Wong F. Bernardi M. Boyer T.D. Gerbes A. et al.Diagnosis and management of acute kidney injury in patients with cirrhosis: revised consensus recommendations of the International Club of Ascites.Gut. 2015; 64: 531-537Crossref PubMed Scopus (188) Google Scholar For many years, decompensated cirrhosis was defined by the occurrence of one of the following complications (increasing in severity): GI bleeding, ascites responding to diuretics, refractory ascites, SBP, and HRS. More recently, the concept of acute-on-chronic liver failure (ACLF) has emerged, initially within the classification of decompensated cirrhosis but progressively as an independent entity.[4]Moreau R. Jalan R. Gines P. Pavesi M. Angeli P. Cordoba J. et al.Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis.Gastroenterology. 2013; 144: 1426-1437Abstract Full Text Full Text PDF PubMed Scopus (1373) Google Scholar,[5]Jalan R. Yurdaydin C. Bajaj J.S. Acharya S.K. Arroyo V. Lin H.-C. et al.Toward an improved definition of acute-on-chronic liver failure.Gastroenterology. 2014; 147: 4-10Abstract Full Text Full Text PDF PubMed Scopus (168) Google Scholar For many years it has been known that patients with cirrhosis develop severe complications after an acute event (GI bleeding, acute alcoholic hepatitis, HBV reactivation, sepsis, overuse of diuretics ..) and for this reason the distinction between acute decompensation of cirrhosis and ACLF was not so clear for many of us. The EASL definition of ACLF according to the European CLIF consortium has progressively emerged as the occurrence of ≥1 organ failure(s) with elevated short-term mortality in a patient with acute decompensation of cirrhosis. “Classical” acute decompensation is associated with an acceptable 28-day and 3-month mortality (around 5% and 15% respectively) and is defined by the absence of organ failures (OFs). The median model for end-stage liver disease (MELD) score of patients hospitalized in this setting is around 15-17. Patients with very high MELD scores are more likely to be admitted in the context of ACLF. APASL defined ACLF as a syndrome in patients with chronic liver disease, characterized by acute hepatic decompensation resulting in liver failure (jaundice and prolongation of the international normalized ratio) and ≥1 extrahepatic OFs associated with increased mortality within a period of 28 days.[6]Sarin S.K. Kumar A. Almeida J.A. Chawla Y.K. Fan S.T. Garg H. et al.Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific Association for the Study of the Liver (APASL).Hepatol Int. 2009; 3: 269-282Crossref PubMed Scopus (606) Google Scholar,[7]Sarin S.K. Kedarisetty C.K. Abbas Z. Amarapurkar D. Bihari C. Chan A.C. et al.Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific Association for the Study of the Liver (APASL) 2014.Hepatol Int. 2014; 8: 453-471. 2Crossref PubMed Scopus (360) Google Scholar According to NACSELD, ACLF is defined by ≥2 extrahepatic OFs among the following: circulatory failure defined by shock, grade III/IV hepatic encephalopathy, renal failure requiring renal replacement therapy, and respiratory failure requiring mechanical ventilation.[8]O’Leary J.G. Reddy K.R. Garcia-Tsao G. Biggins S.W. Wong F. Fallon M.B. et al.NACSELD Acute-on-Chronic Liver Failure (NACSELD-ACLF) score predicts 30-day survival in hospitalized patients with cirrhosis.Hepatology. 2018; 67: 2367-2374Crossref PubMed Scopus (100) Google Scholar The main difference between this latter definition and EASL-CLIF consortium definition is the stringent definition of renal failure restricted to requirements of renal replacement therapy and the absence of liver-related variables (i.e. bilirubin and international normalized ratio). In a position paper on ACLF published in this issue by Arroyo and colleagues,[9]Arroyo V. Angeli P. Moreau R. Jalan R. Claria J. Trebicka J. et al.The Systemic Inflammation Hypothesis: towards a new paradigm of acute decompensation and multiorgan failure in cirrhosis.J Hepatol. 2021; 74: 670-685Abstract Full Text Full Text PDF Scopus (20) Google Scholar the CLIF consortium have tried to define different stages of decompensation leading to ACLF: stable decompensated cirrhosis, unstable decompensated cirrhosis (UDC), pre-ACLF and the classical ACLF-1 to 3, according to number of OFs. At this point, the border line between UDC and pre-ACLF has still to be defined and remains unclear. Improving short-term prognostic scores is an important aspect of current research into ACLF. Since the year 2000, the MELD score has emerged as a better score than the classical Child-Pugh score for determining 1-year prognosis in patients with cirrhosis.[10]Kamath P.S. Wiesner R.H. Malinchoc M. Kremers W. Therneau T.M. Kosberg C.L. et al.A model to predict survival in patients with end-stage liver disease.Hepatology. 2001; 33: 464-470Crossref PubMed Scopus (3376) Google Scholar However, the utility of the MELD score in predicting short-term mortality is limited in patients with ACLF, particularly those in the ICU. In patients with ACLF, prognosis is more closely associated with the number of OFs than with liver failure per se.[11]Levesque E. Hoti E. Azoulay D. Ichaï P. Habouchi H. Castaing D. et al.Prospective evaluation of the prognostic scores for cirrhotic patients admitted to an intensive care unit.J Hepatol. 2012; 56: 95-102Abstract Full Text Full Text PDF PubMed Scopus (130) Google Scholar,[12]Levesque E. Saliba F. Ichaï P. Samuel D. Outcome of patients with cirrhosis requiring mechanical ventilation in ICU.J Hepatol. 2014; 60: 570-578Abstract Full Text Full Text PDF PubMed Scopus (82) Google Scholar In patients with cirrhosis admitted to the ICU, scores such as the sequential organ failure assessment (SOFA) are better predictors of mortality than the MELD.[13]Vincent J.L. Moreno R. Takala J. Willatts S. De Mendonça A. Bruining H. et al.The SOFA (Sepsis-related organ failure assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on sepsis-related problems of the European society of intensive care medicine.Intensive Care Med. 1996; 22: 707-710Crossref PubMed Scopus (6127) Google Scholar Using the CANONIC European cohort and other European cohorts the CLIF consortium developed the CLIF-SOFA score[14]Jalan R. Pavesi M. Saliba F. Amorós A. Fernandez J. Holland-Fischer P. et al.The CLIF Consortium Acute Decompensation score (CLIF-C ADs) for prognosis of hospitalised cirrhotic patients without acute-on-chronic liver failure.J Hepatol. 2015; 62: 831-840Abstract Full Text Full Text PDF PubMed Scopus (163) Google Scholar,[15]Jalan R. Saliba F. Pavesi M. Amoros A. Moreau R. Gines P. et al.Development and validation of a prognostic score to predict mortality in patients with acute-on-chronic liver failure.J Hepatol. 2014; 61: 1038-1047Abstract Full Text Full Text PDF PubMed Scopus (444) Google Scholar and then the CLIF-C OF score,[15]Jalan R. Saliba F. Pavesi M. Amoros A. Moreau R. Gines P. et al.Development and validation of a prognostic score to predict mortality in patients with acute-on-chronic liver failure.J Hepatol. 2014; 61: 1038-1047Abstract Full Text Full Text PDF PubMed Scopus (444) Google Scholar identifying ACLF grade 1, 2, and 3 patients, with 28-day mortality rates of 22% 32% and 76.7%, respectively. This classification is very important in determining when to perform liver transplantation, either at the stage of ACLF-3 or ACLF-1/2. Recent studies have shown that liver transplantation in patients with ACLF-3 without severe respiratory failure is associated with good post-transplant survival and confers a significantly better prognosis than no transplantation.16Gustot T. Fernandez J. Garcia E. Morando F. Caraceni P. Alessandria C. et al.Clinical Course of acute-on-chronic liver failure syndrome and effects on prognosis.Hepatology. 2015; 62: 243-252Crossref PubMed Scopus (305) Google Scholar, 17Artru F. Louvet A. Ruiz I. Levesque E. Labreuche J. Ursic-Bedoya J. et al.Liver transplantation in the most severely ill cirrhotic patients: a multicenter study in acute-on-chronic liver failure grade 3.J Hepatol. 2017; 67: 708-715Abstract Full Text Full Text PDF PubMed Scopus (130) Google Scholar, 18Sundaram V. Jalan R. Wu T. Volk M.L. Asrani S.K. Klein A.S. et al.Factors associated with survival of patients with severe acute-on-chronic liver failure before and after liver transplantation.Gastroenterology. 2019; 156 (e1383): 1381-1391Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar, 19Thuluvath P.J. Thuluvath A.J. Hanish S. Savva Y. Liver transplantation in patients with multiple organ failures: feasibility and outcomes.J Hepatol. 2018; 69: 1047-1056https://doi.org/10.1016/j.jhep.2018.07.007Abstract Full Text Full Text PDF PubMed Scopus (60) Google Scholar Therefore, the concept of ACLF based on the number of OFs and on the type of OF is important in determining who could be transplanted and when. In this Position paper, Arroyo and colleagues have introduced 2 new concepts: that systemic inflammation drives the development of decompensation and that the increased incidence of infections in patients with cirrhosis is the result of immunoparesis. The authors developed the hypothesis that acute decompensation of cirrhosis, including GI bleeding, is driven by systemic inflammation and they try to explain all the complications of cirrhosis within this entity. It looks like an attempt to square the circle! The role of systemic inflammation has been well described in patients with ACLF[4]Moreau R. Jalan R. Gines P. Pavesi M. Angeli P. Cordoba J. et al.Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis.Gastroenterology. 2013; 144: 1426-1437Abstract Full Text Full Text PDF PubMed Scopus (1373) Google Scholar,[14]Jalan R. Pavesi M. Saliba F. Amorós A. Fernandez J. Holland-Fischer P. et al.The CLIF Consortium Acute Decompensation score (CLIF-C ADs) for prognosis of hospitalised cirrhotic patients without acute-on-chronic liver failure.J Hepatol. 2015; 62: 831-840Abstract Full Text Full Text PDF PubMed Scopus (163) Google Scholar and systemic inflammation certainly plays an important role in this syndrome. However, the role of systemic inflammation has not been so well described in patients with complications of cirrhosis outside ACLF. Systemic inflammation has been associated with the development or severity of encephalopathy and of renal failure.[2]European Association for the Study of the Liver. Electronic address: [email protected], European Association for the Study of the LiverEASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis.J Hepatol. 2018; 69: 406-460Abstract Full Text Full Text PDF PubMed Scopus (678) Google Scholar,[3]Angeli P. Gines P. Wong F. Bernardi M. Boyer T.D. Gerbes A. et al.Diagnosis and management of acute kidney injury in patients with cirrhosis: revised consensus recommendations of the International Club of Ascites.Gut. 2015; 64: 531-537Crossref PubMed Scopus (188) Google Scholar However, the role of systemic inflammation in the occurrence of ascites or GI bleeding has still to be demonstrated. What is missing here is the connection between the systemic inflammation hypothesis and the classical pathophysiological concepts of ascites, HRS, and GI bleeding. Leaving open the question of what is driving the development of these complications. The authors have also suggested that immunoparesis could be the driver of infections in patients with cirrhosis. It is known that patients with cirrhosis have defects in cellular immunity. This has been shown in patients with acute alcoholic hepatitis, explaining the occurrence of opportunistic infections even in the absence of steroid therapy. The question is whether immunoparesis is responsible for the occurrence of bacterial infections and of SBP or if it occurs secondarily. The concept of immunoparesis is interesting but more immunological investigations in patients with cirrhosis are required. In addition, this concept still has to be connected with the concept of bacterial translocation well described in patients with cirrhosis.[20]Fernández J. Acevedo J. Wiest R. Gustot T. Amoros A. Deulofeu C. et al.Bacterial and fungal infections in acute-on-chronic liver failure: prevalence, characteristics and impact on prognosis.Gut. 2018; 67: 1870-1880Crossref PubMed Scopus (192) Google Scholar In conclusion, the authors have to be congratulated for the huge work done in defining the concept of ACLF and the role of systemic inflammation in ACLF. In the future this may lead to the use of anti-inflammatory therapies. However, a lot of work must still be done to determine whether systemic inflammation and immunoparesis are drivers or complications of decompensated cirrhosis. The author received no financial support to produce this manuscript. The author declares no conflicts of interest that pertain to this work. Please refer to the accompanying ICMJE disclosure forms for further details. The following is/are the supplementary data to this article: Download .pdf (1.2 MB) Help with pdf files Multimedia component 1 The systemic inflammation hypothesis: Towards a new paradigm of acute decompensation and multiorgan failure in cirrhosisJournal of HepatologyVol. 74Issue 3PreviewAcute decompensation (AD) of cirrhosis is defined by the development of ascites, hepatic encephalopathy and/or variceal bleeding. Ascites is traditionally attributed to splanchnic arterial vasodilation and left ventricular dysfunction, hepatic encephalopathy to hyperammonaemia, and variceal haemorrhage to portal hypertension. Recent large-scale European observational studies have shown that systemic inflammation is a hallmark of AD. Here we present a working hypothesis, the systemic inflammation hypothesis, suggesting that systemic inflammation through an impairment of the functions of one or more of the major organ systems may be a common theme and act synergistically with the traditional mechanisms involved in the development of AD. Full-Text PDF Open Access" @default.
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• W3124865463 title "Systemic inflammation and liver cirrhosis complications: Driving or secondary event? How to square the circle?" @default.
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