The Model for End-Stage Liver Disease （MELD） score is currently used to prioritize liver allocation for cirrhotic patients awaiting liver transplantation in the world. With the application of MELD score in transplantation for patients with severe conditions， several models have been proposed to refine and improve MELD score. MELD score has also been used for the management of non-transplantation patients with chronic liver disease. This article briefly reviews the background of these models and believes that the original intention of MELD is to determine the priority of organ allocation for liver transplantation. The expanded application of MELD score beyond liver transplantation assessment should be performed with reference to clinical practice， and different MELD models should be selected rationally based on individual conditions， in order to help patients achieve optimal prognosis assessment， intervention measures， and benefits.

The American College of Gastroenterology published the clinical guideline on alcohol-associated liver disease(ALD)in January 2024 in American Journal of Gastroenterology.This guideline elaborates on the epidemiology and disease burden of ALD and alcohol use disorder,the risk factors for ALD,the diagnosis and treatment of alcohol use disorder,the disease spectrum of ALD,the management of ALD,and public policy and prevention.This article gives an excerpt of the recommendations and key points/statements in this guideline.

There are gradual increases in the incidence rates of metabolic associated fatty liver disease （MAFLD） and type 2 diabetes mellitus （T2DM）， with close relationship and mutual interaction between the two diseases， but the specific mechanism is still unclear. Studies have shown that T2DM and MAFLD may cause aggravation of each other through insulin resistance， inflammation， some hepatocyte factors， and cellular senescence and protect each other through some hepatocyte factors. Further research on the association between T2DM and MAFLD and the mechanism of comorbidity is of great significance for the clinical prevention and treatment of the two diseases.

Alcoholic hepatitis is a severe and life-threatening systemic inflammatory response syndrome, which has a high incidence and mortality rate worldwide. The severity ranges from asymptomatic liver biochemical disturbances to fulminant liver failure or death; however, there are few effective therapeutic interventions. Maddrey discriminant function not only predicts short-term mortality, but it also guides clinicians to choose appropriate alcoholic hepatitis-specific treatments. Alcohol abstinence, nutritional support, psychological counseling, and infection prevention remain the cornerstones for alcoholic hepatitis treatment. Corticosteroids remain the mainstay of treatment when patients have a good appetite and normal serum creatinine levels, but early liver transplantation is the only life-saving option for steroid-unresponsive patients. New studies have found that gut microbiota is an important therapeutic targets in patients with alcohol hepatitis, and N-acetylcysteine, granulocyte colony-stimulating factor, and metadoxine as adjunctive therapy have a positive effect on patient survival.

Objective:To explore the relationship between triglyceride-glucose index (TyG) and non-alcoholic fatty liver disease (NAFLD).Methods:25 535 cases who participated in the health check-ups at the First Hospital of China Medical University from January 2019 to December 2019 were selected as the eligible subjects. Logistic regression analysis and receiver operating characteristic curve were used to analyze the relationship between TyG index and NAFLD risk and its diagnostic value for NAFLD.Results:NAFLD prevalence was gradually increased with the increase of the TyG index. After adjusting for other potential influencing factors, compared with the first quarter of TyG in patient with NAFLD, the OR (95% CI) in the second, third, and fourth quarter were 1.677 (1.495 ~ 1.881), 2.707 (2.397 ~ 3.057) and 4.049 (3.482 ~ 4.710), respectively. Receiver operating characteristic curve analysis showed that the best cut-off value of TyG index for the diagnosis of NAFLD was 6.9, and the area under the curve was 0.816. The sensitivity and specificity were 77.66% and 70.51%, respectively. The combined application of TyG and ALT levels had higher diagnostic value. Conclusion:TyG, as a simple and convenient biosynthetic index, is closely related to the NAFLD. In addition, when the TyG index is ≥6.9, it has a high diagnostic value for NAFLD.

Objective:To explore the current status of alcoholic hepatitis diagnosis by clinicians’ in China.Methods:Clinical data of inpatients confirmed with alcohol-associated liver disease diagnosed at Tongliao Infectious Disease Hospital of Inner Mongolia from June 1, 2018 to May 31, 2019 were retrospectively analyzed. The consistency of clinical diagnosis of alcoholic hepatitis was judged according to the diagnostic criteria recommended by the National Institute of Alcohol Abuse and Alcoholism (USA), and then the alcoholic hepatitis severity assessment model recommended by international guidelines, including Maddrey discriminant function, Model for end-stage liver disease, and Glasgow alcoholic hepatitis score and ABIC scores (age, total bilirubin, international normalized ratio and creatinine) were applied to evaluate this group of cases.Results:Among 79 cases with alcohol-associated liver disease, 75 were males and 4 were females, age ranged between 27~75 (51.1±8.8) years. Alcohol consumption varied from 60 g/d to 600g/d, with an average consumption of 148.8 ± 76.6 g/d. The alcohol consumption duration ranged from 4 to 50 [average (23.9 ± 9.6)] years. According to the initial discharge diagnosis, there were 47 and 32 cases in alcoholic hepatitis and alcoholic liver cirrhosis group, respectively. The mean erythrocyte volume, serum alanine aminotransferase, aspartate aminotransferase and total bilirubin were increased in alcoholic liver cirrhosis than alcoholic hepatitis group, while albumin and total cholesterol were lowered in alcoholic liver cirrhosis than alcoholic hepatitis group, and coagulation indexes were significantly extended. Alpha-fetoprotein of both groups were in the normal range; however, it was significantly higher in the alcoholic hepatitis group than the alcoholic cirrhosis group. The 10 cases in the alcoholic cirrhosis group met the definition and diagnosis of alcoholic hepatitis defined by the National Institute of Alcohol Abuse and Alcoholism (USA), but there was no case in the alcoholic hepatitis group. Among the 10 diagnosed cases of alcoholic hepatitis, 5, 6, 1 and 3 cases met the diagnostic criteria of Maddrey discriminant function, Model for end-stage liver disease, Glasgow alcoholic hepatitis score, and ABIC score for severe alcoholic hepatitis, respectively. The Maddrey discriminant function, ABIC score, and Glasgow alcoholic hepatitis score within the Model for end-stage liver disease scores> 20 points had 5, 1, and 3 cases, respectively.Conclusion:Alcoholic hepatitis is over-diagnosed by clinicians. Alcoholic hepatitis patients have the base of liver cirrhosis who meet the diagnostic criteria of National Institute of Alcohol Abuse and Alcoholism (USA). Patients with Model for end-stage liver disease score > 20 points have good consistency with Maddrey discriminant function score ≥ 32 points, and both can be used to evaluate the alcoholic hepatitis patient clinical severity.

Gilbert’s syndrome is a kind of benign inherited disease of bilirubin binding disorder, mainly due to the homozygous polymorphism A(TA)7TAA in the promoter of the gene for uridine diphosphate -glucuronosyltransferase 1A1 (UGT1A1), which is a TA insertion into the promoter, designated as UGT1A1*28, with UGT activity reduction to 30% of the normal value. Therefore, circulating fat-soluble unconjugated bilirubin cannot be converted into water-soluble conjugated bilirubin, leading to unconjugated hyperbilirubinemia. Bilirubin has a strong affinity for erythrocyte phospholipids, which interferes with membrane composition and dynamics, resulting in increased erythrocytes fragility, easy rupture, and gradual shortening of survival time. However, there are no obvious sign of hemolysis or abnormal iron metabolism, erythrocytes and bone marrow morphology. A small amount of chronic hemolysis stimulates extramedullary (normal bone marrow morphology) hematopoiesis, ensuing compensatory increase in circulating erythrocytes and hemoglobin. Hyperbilirubinemia may also weaken gastrointestinal motility, increase passive diffusion and absorption across the intestinal mucosal epithelium by 1.5 to 2 times, thereby aggravating or worsening hyperbilirubinemia mainly with unconjugated bilirubin circulation, which indicates that there is a causal relationship between the circulating bilirubin concentration and rapid erythrocytes turnover and hemolysis rate in patients with Gilbert’s syndrome. Interestingly, bilirubin also has significant antioxidant and anti-mutagenic activities, and the potential health benefits of mild hyperbilirubinemia in Gilbert's syndrome include reduced prevalence of cardiovascular disease, type 2 diabetes mellitus (and related risk factors), certain cancers, and cardiovascular-related and all-cause mortality. Exogenous bilirubin and biliverdin supplements in intestinal epithelial cells can be absorbed and may increase circulating concentration of these antioxidant compounds. With this information, we hope to raise awareness of the potentially harmful and beneficial effects of benign hyperbilirubinemia, and explore and develop beneficial medical interventions.

Alcoholic hepatitis (AH) is a severe alcohol-associated liver disease with a mortality rate as high as 40%. A recent study reveals that the exotoxin (cytolysin)-secreting gut bacterium Enterococcus faecalis is a critical factor for AH, which can be eliminated by bacteriophages, and therefore, the use of bacteriophages for the treatment of AH provide a new treatment option for AH. This article introduces this pioneering study and the knowledge of bacteriophages and cytolysin, so as to provide a theoretical basis for the clinical research on AH.

Non-alcoholic fatty liver disease and alcohol (ethanol)-related liver disease is a global epidemic of chronic liver disease and the main cause of fatty liver. Non-alcoholic fatty liver patients sometimes ingest different types of alcohol. Therefore, when obesity coexist with alcohol consumption, it is more difficult to diagnose the cause of fatty liver. The amount of alcohol consumption and alcohol drinking pattern and chronic liver injury, type 2 diabetes mellitus, cardiovascular disease and other metabolic-related diseases may have J-type correlation; that is to say, a light to moderate amount of alcohol consumption may bring certain benefits to the above diseases, but excessive alcohol consumption may promote the development of obesity, aggravate liver disease, metabolic abnormalities, and increase the risk of tumors. Screening for metabolic-related disease risk should be considered in addition to the assessment of changing liver lesions when obesity coexists with alcohol consumption. Changing bad living habits, losing weight and abstaining from alcohol are still the basis of treating fatty liver and metabolic disorders. Carefully selecting patients and communicating with them about the risk and benefit of drugs are important indicators of drug therapy. Patients with end-stage liver disease can be considered for liver transplantation and postoperative lifestyle improvement should be emphasized.

Alcoholic hepatitis (AH) is a non-infectious inflammatory injury of the liver and often occurs on the basis of chronic liver disease including fatty liver disease and liver cirrhosis. Acute exacerbation of liver disease due to heavy drinking within a short period of time is a severe manifestation of AH. The prognosis of AH depends on treatment timing and methods, and liver function can quickly recover or rapidly deteriorate into multiple organ failure. Many clinicians lack the experience in early identification and timely treatment of AH, due to a lack of typical clinical manifestations and specific auxiliary examinations, which affects clinical treatment, delays treatment, and exposes some AH patients to the risk of death. Therefore, it is imperative to conduct more clinical studies on AH, summarize real-world data, and develop expert consensus.