Acute-on-chronic liver failure (ACLF) is increasingly recognized as a distinct disease entity associated with acute deterioration of liver function in patients with chronic liver disease. Although no widely accepted diagnostic criteria for ACLF are yet available, the definitions of the Asian-Pacific Association for the Study of the Liver (APASL) ACLF Research Consortium (AARC) and the European Association for the Study of the Liver (EASL) Chronic Liver Failure Consortium (CLIF-C) are commonly employed. However, the AARC and CLIF-C criteria are based on fundamentally different features, rendering among-study comparisons difficult. The areas of uncertainty include the definition and extent of heterogeneity of ACLF, ambiguities in terms of the underlying liver disease, and whether infection or sepsis may precipitate the condition. Although the detailed pathogenesis of ACLF remains to be elucidated, changes in host responses to injury, infection, and uncontrolled inflammation play important roles. The “predisposition, infection/inflammation, response, organ failure” (PIRO) concept used to evaluate sepsis may be valuable when it is sought to describe the pathophysiology and clinical features of ACLF. Currently, treatment is limited to organ support but a better understanding of the pathophysiology is likely to lead, in future, to the discovery of novel biomarkers and the development of new therapeutic strategies.
Acute-On-Chronic Liver Failure* ; Biomarkers ; End Stage Liver Disease ; Humans ; Inflammation ; Liver ; Liver Cirrhosis ; Liver Diseases ; Liver Failure ; Population Characteristics ; Sepsis ; Uncertainty

Objective: To investigate the ABC prognostic classification and the updated version of Model for End-stage Liver Disease (MELD) score 3.0 and Chinese Group on the Study of Severe Hepatitis B ACLF Ⅱ score (COSSH-ACLF Ⅱ score) to evaluate the prognostic value in acute-on-chronic liver failure (ACLF). Methods: ABC classification was performed on a 1 409 follow-up cohorts. The area under the receiver operating characteristic curve (AUROC) was used to analyze MELD, MELD 3.0, COSSH-Ⅱ and COSSH-Ⅱ score after 3 days of hospitalization (COSSH-Ⅱ-3d). The prognostic predictive ability of patients were evaluated for 360 days, and the prediction differences of different classifications and different etiologies on the prognosis of ACLF were compared. Results: The survival curve of 1 409 cases with ACLF showed that the difference between class A, B, and C was statistically significant, Log Rank (Mantel-Cox) χ²=80.133, P<0.01. Compared with class A and C, χ²=76.198, P<0.01, the difference between class B and C, was not statistically significant χ²=3.717, P>0.05. AUROC [95% confidence interval (CI)] analyzed MELD, MELD 3.0, COSSH-Ⅱ and COSSH-Ⅱ-3d were 0.644, 0.655, 0.817 and 0.839, respectively (P<0.01). COSSH-Ⅱ had better prognostic predictive ability with class A ACLF and HBV-related ACLF (HBV-ACLF) for 360-days, and AUROC (95% CI) were 0.877 and 0.881, respectively (P<0.01), while MELD 3.0 prognostic predictive value was not better than MELD. Conclusion: ACLF prognosis is closely related to ABC classification. COSSH-Ⅱ score has a high predictive value for the prognostic evaluation of class A ACLF and HBV-ACLF. COSSH-Ⅱ score has a better prognostic evaluation value after 3 days of hospitalization, suggesting that attention should be paid to the treatment of ACLF in the early stage of admission.
Humans ; Acute-On-Chronic Liver Failure ; Prognosis ; End Stage Liver Disease/complications* ; Retrospective Studies ; Severity of Illness Index

Liver transplant is an unreplaceable method for benign end-stage liver disease. The risk evaluation for the waiting list recipients and for post-transplant survival could provide practical indication for organ allocation. In recent years, there are two major kinds of evaluation scores. The first kind of evaluation scores is based on model for end-stage liver disease(MELD) score,including SOFT/P-SOFT score,UCLA-FRS score and BAR score. The other evaluation system is based on the concept of acute-on-chronic liver failure,including CLIF-C-ACLF score,TAM score,AARC-ACLF score and COSSH-ACLF score. The scores based on ACLF have been shown superior power in predicting waiting list survival and post-transplant prognosis than MELD. This article reviews the two kinds of evaluation scores,aiming for the better allocation policy and the better prognosis of benign end-stage liver disease.
Acute-On-Chronic Liver Failure ; End Stage Liver Disease/surgery* ; Humans ; Liver Transplantation ; Prognosis ; Retrospective Studies ; Severity of Illness Index

OBJECTIVETo observe the clinical characteristics and short-term survival of patients with splenomegaly and acute-on-chronic liver failure related to chronic HBV infection.

METHODSElectronic medical records of patients with acute-on-chronic liver failure were collected to analyze the clinical parameters and 4-week survival of patients with or without splenomegaly.

RESULTSOf the 149 patients enrolled, the overall 28-day mortality rate was 48.3%, which was lower in patients with enlarged spleen than those without (34.2% vs 54.1%, P=0.034). Compared with patients without splenomegaly, patients with splenomegaly had lower platelet counts (P=0.001), lower ALT levels (P=0.005) and lower PT-INR (P=0.010). Although the occurrence of hepatic encephalopathy was comparable between patients with or without splenomegaly, severe conditions were more frequent in those without splenomegaly. Hepatic encephalopathy grades, serum creatinine levels, neutrophil percentages over 70%, PT-INR and splenomegaly were independent factors associated with the 28-day survival, and this novel model was superior to model of end-stage of liver disease in predicting the 4-week survival (P=0.017).

CONCLUSIONPatients with splenomegaly that evolves into acute-on-chronic liver failure have unique clinical characteristics and further clinical observations are warranted.

Acute-On-Chronic Liver Failure ; mortality ; physiopathology ; Chronic Disease ; Hepatic Encephalopathy ; physiopathology ; Humans ; Splenomegaly ; mortality ; physiopathology

PURPOSE: To evaluate the clinical significance of T1 high signal intensity on the globus pallidus as a predictor of severe hepatic encephalopathy in patients with acute-on-chronic liver failure (ACLF), which is a distinct syndrome characterized by multi-organ dysfunction including cerebral failure. MATERIALS AND METHODS: From January 2002 to April 2014, we retrospectively reviewed the magnetic resonance imaging (MRI) findings and clinical and magnetic resonance (MR) features of 74 consecutive patients (44 men and 30 women; mean age, 59.5 years) with liver cirrhosis. The chronic liver failure-sequential organ failure assessment score was used to diagnose ACLF. The pallidal index (PI), calculated by dividing the mean signal intensity of the globus pallidus by that of the subcortical frontal white matter were compared according to ACLF. The PI was compared with the Model for End-Stage Liver Disease (MELD) score in predicting the development of ACLF. RESULTS: Fifteen patients who were diagnosed with ACLF had higher hepatic encephalopathy grades (initial, P = 0.024; follow-up, P = 0.002), MELD scores (P < 0.001), and PI (P = 0.048). In the ACLF group, the mean PI in patients with cerebral failure was significantly higher than that in the patients without cerebral failure (1.33 vs. 1.20, P = 0.039). In patients with ACLF, the area under the curve (AUC) for PI was 0.680 (95% confidence intervals [CI], 0.52–0.85), which was significantly lower than that for the MELD score (AUC, 0.88; 95% CI, 0.77–0.99) (P = 0.04). CONCLUSION: The PI can be an ancillary biomarker for predicting the development of ACLF and severe hepatic encephalopathy.
Acute-On-Chronic Liver Failure ; Female ; Follow-Up Studies ; Globus Pallidus ; Hepatic Encephalopathy* ; Humans ; Liver Cirrhosis ; Liver Diseases* ; Liver* ; Magnetic Resonance Imaging ; Male ; Retrospective Studies ; White Matter

PURPOSE: To evaluate the clinical significance of T1 high signal intensity on the globus pallidus as a predictor of severe hepatic encephalopathy in patients with acute-on-chronic liver failure (ACLF), which is a distinct syndrome characterized by multi-organ dysfunction including cerebral failure. MATERIALS AND METHODS: From January 2002 to April 2014, we retrospectively reviewed the magnetic resonance imaging (MRI) findings and clinical and magnetic resonance (MR) features of 74 consecutive patients (44 men and 30 women; mean age, 59.5 years) with liver cirrhosis. The chronic liver failure-sequential organ failure assessment score was used to diagnose ACLF. The pallidal index (PI), calculated by dividing the mean signal intensity of the globus pallidus by that of the subcortical frontal white matter were compared according to ACLF. The PI was compared with the Model for End-Stage Liver Disease (MELD) score in predicting the development of ACLF. RESULTS: Fifteen patients who were diagnosed with ACLF had higher hepatic encephalopathy grades (initial, P = 0.024; follow-up, P = 0.002), MELD scores (P < 0.001), and PI (P = 0.048). In the ACLF group, the mean PI in patients with cerebral failure was significantly higher than that in the patients without cerebral failure (1.33 vs. 1.20, P = 0.039). In patients with ACLF, the area under the curve (AUC) for PI was 0.680 (95% confidence intervals [CI], 0.52–0.85), which was significantly lower than that for the MELD score (AUC, 0.88; 95% CI, 0.77–0.99) (P = 0.04). CONCLUSION: The PI can be an ancillary biomarker for predicting the development of ACLF and severe hepatic encephalopathy.
Acute-On-Chronic Liver Failure ; Female ; Follow-Up Studies ; Globus Pallidus ; Hepatic Encephalopathy* ; Humans ; Liver Cirrhosis ; Liver Diseases* ; Liver* ; Magnetic Resonance Imaging ; Male ; Retrospective Studies ; White Matter

Acute-On-Chronic Liver Failure ; diagnosis ; Humans

Acute-on-chronic liver failure (ACLF) is a form of complex syndrome with acute deterioration of liver function that occurs on the basis of chronic liver disease, and is accompanied by hepatic and extrahepatic organ failure with high mortality rate. The short-term mortality rate of comprehensive internal medicine treatment is as high as 50%-90%. This paper summarizes the current common definitions and diagnostic criteria, early-warning prediction models, and pathogenesis of ACLF.
Acute-On-Chronic Liver Failure/therapy* ; Humans ; Prognosis

In cases of acute liver failure or acute or chronic liver failure, extracorporeal albumin dialysis utilizing a Molecular Adsorbent Recirculating System has been used to treat liver failure and to reduce serum total bilirubin concentrations as a bridge therapy until either liver transplantation or spontaneous recovery. However, the procedure is expensive and is not easily administered in clinical practice. Recently, single pass albumin dialysis (SPAD) using continuous renal replacement therapy was introduced, but information is scarce regarding its efficacy in controlling serum bilirubin. The authors report a case of acute hepatitis A, in which SPAD was performed to correct severe hyperbilirubinemia.
Bilirubin ; Dialysis ; End Stage Liver Disease ; Formaldehyde ; Hepatitis ; Hepatitis A ; Hyperbilirubinemia ; Liver Failure ; Liver Failure, Acute ; Liver Transplantation ; Polymers ; Renal Dialysis ; Renal Replacement Therapy ; Resorcinols

Heart failure is a recognized, although uncommon, cause of massive liver cell necrosis, the clinical consequence of which are intermingled with those of cardiac insufficiency in most case. But, hepatic coma is rerely caused by hepatic congestion only. We report the three cases with heart failure resulted in massive liver cell necrosis and fulminant hepatic failure. The manifestations of fulminant hepatic failure were hepatic encephalopathy, jaundice, marked increase of prothrombin time and serum transaminase and there were no evidences of viral hepatitis and toxic hepatitis as a cause of liver failure.
Drug-Induced Liver Injury ; Estrogens, Conjugated (USP)* ; Heart Failure* ; Hepatic Encephalopathy ; Hepatitis ; Jaundice ; Liver ; Liver Failure ; Liver Failure, Acute* ; Necrosis ; Prothrombin Time