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Volume 7, Issue 6 (Suppl)
J Gastrointest Dig Syst, an open access journal
ISSN: 2161-069X
Page 68
December 07-08, 2017 Madrid, Spain
&
13
th
International Conference on Clinical Gastroenterology & Hepatology
2
nd
International Conference on Digestive Diseases
CO-ORGANIZED EVENT
Acute-on-chronic liver failure: An update
Dong Joon Kim
Hallym University College of Medicine, South Korea
A
cute-on-chronic liver failure (ACLF) is an increasingly recognized distinct disease entity encompassing an acute
deterioration of liver function in patients with chronic liver disease. Although there are no widely accepted diagnostic
criteria for ACLF, the Asian–Pacific Association for the Study of the Liver (APASL) and the American Association for the
Study of Liver Disease and the European Association for the Study of the Liver (AASLD/EASL) consensus definitions are
commonly used. It is obvious that the APASL and the AASLD/EASL definitions are based on fundamentally different features.
Two different definitions in two different parts of the world hamper the comparability of studies. Recently, the EASL-Chronic
Liver Failure Consortium proposed new diagnostic criteria for ACLF based on analyses of patients with organ failure. There
are areas of uncertainty in defining ACLF, such as heterogeneity of ACLF, ambiguity in qualifying underlying liver disease,
argument for infection or sepsis as a precipitating event, etc. The two ACLF definitions result in differences in mortality and
patient characteristics among ACLF patients. Although the exact pathogenesis of ACLF remains to be elucidated, alteration
of host response to injury, infection, and unregulated inflammation play important roles. The predisposition, infection/
inflammation, response, organ failure (PIRO) concept used for sepsis might be useful in describing the pathophysiology and
clinical categories for ACLF. The mechanisms of ACLF were described recently. In 1/3 of cases of ACLF, inflammation develops
in response to bacterial infection. However, a significant number of cases are not related to obvious bacterial infection. In
these cases, the translocation of PAMPs without viable bacteria or the releases of DAMPs by dying cells are likely mechanisms
of the ‘sterile inflammation’. Finally, a decrease in the tolerance to inflammation could be involved. Treatment strategies are
limited to organ support, but better understanding of the pathophysiology is likely to lead to discovery of novel biomarkers
and therapeutic strategies in the future.
djkim@hallym.ac.krJ Gastrointest Dig Syst 2017, 7:6(Suppl)
DOI: 10.4172/2161-069X-C1-059