Drug-induced liver injury (DILI) is caused by the direct toxicity of drugs and/or their metabolites or the body-specific heterogeneous response to drugs. Since 2019, the European Association for the Study of the Liver, the American College of Gastroenterology, and the Asia Pacific Association of Study of Liver have successively updated previously published guidelines on DILI. Based on the above 3 updated guidelines and in combination with Chinese Diagnosis and Treatment Guideline on Drug-Induced Liver Injury, the Guideline for Primary Care of Drug-Induced Liver Injury (2019), and the relevant literature at home and abroad in recent years, we review the progress on the diagnosis and treatment of DILI in this paper, aiming to help the diagnosis and treatment of DILI in clinic.

Chronic HBV infection can generally be divided into four stages according to the natural course of disease. Clinically, the determination of different natural stages of chronic HBV infection is crucial for patients to start antiviral therapy and to avoid missing the antiviral opportunity and progressing to cirrhosis. In particular, it is a challenge for clinicians to distinguish the immune control stage from the reactive stage. As a novel marker of HBV, the quantitative detection of HBV core-associated antigen (HBcrAg) is of value for the identification of the HBV infection stages. This article reviews the research progress of HBcrAg in the identification of different stages of chronic HBV infection.

Drug-induced liver injury (DILI) is caused by the direct toxicity of drugs and/or their metabolites or the body-specific heterogeneous response to drugs. Since 2019, the European Association for the Study of the Liver, the American College of Gastroenterology, and the Asia Pacific Association of Study of Liver have successively updated previously published guidelines on DILI. Based on the above 3 updated guidelines and in combination with Chinese Diagnosis and Treatment Guideline on Drug-Induced Liver Injury, the Guideline for Primary Care of Drug-Induced Liver Injury (2019), and the relevant literature at home and abroad in recent years, we review the progress on the diagnosis and treatment of DILI in this paper, aiming to help the diagnosis and treatment of DILI in clinic.

ObjectiveTo investigate the effect of entecavir (ETV) alone or combined with interferon (IFN) on the risk of hepatocellular carcinoma (HCC) in patients with chronic hepatitis B (CHB). MethodsA retrospective analysis was performed for 409 patients with CHB who were admitted to Beijing Ditan Hospital from January 2008 to December 2014, and according to their antiviral therapy, they were divided into ETV+IFN group with 169 patients (IFN treatment for ≥6 months) and ETV group with 240 patients (ETV treatment for ≥12 months). The patients were followed up to June 2019, and the development of HCC was the outcome event. The Mann-Whitney U test was used for comparison of continuous variables between two groups, and the chi-square test was used for comparison of categorical variables between two groups. The propensity score matching (PSM) method was used to eliminate baseline differences between groups, the Kaplan-Meier method and the log-rank test were used to compare the incidence rate of HCC between groups, and the Cox proportional-hazards regression model analysis was used to investigate the risk factors for the development of HCC. ResultsThe median follow-up time in this study was 5.4 years (IQR: 4.9-7.9). There was no significant difference in the cumulative incidence rate of HCC between the two groups before and after PSM (before PSM: 1.2% vs 2.8%, χ2=1.423, P=0.233; after PSM: 1.7% vs 4.1%, χ2=1.676, P=0.195), and the subgroup analysis also showed no significant difference in the cumulative incidence rate of HCC between the two groups in the non-high risk population (1.3% vs 1.5%, χ2=0.335, P=0.563). The Cox proportional-hazards regression model showed that age was an independent risk factor for HCC (hazard ratio=1.107, 95% confidence interval: 1.005-1.219, P=0.038). ConclusionFor CHB patients without a high risk of cancer, compared with ETV monotherapy, ETV combined with IFN for at least 6 months does not significantly reduce the risk of HCC.

HBV can interact with alcohol in various ways to cause liver damage. Heavy drinking can accelerate the progression of chronic hepatitis B and lead to a poorer prognosis; meanwhile, it can also affect the outcome and compliance in patients receiving antiviral therapy. The epidemiology of drinking in patients with chronic hepatitis B in China remains unclear, and further studies are needed to clarify the mechanism of interaction between alcohol and HBV. Drinking management should be strengthened in patients with chronic hepatitis B in clinical practice, in order to alleviate liver injury induced by alcohol.

Normal intestinal microflora and microecology are essential for normal physiological functions in human body. Intestinal microflora imbalance is often observed in patients with alcoholic liver disease and manifests as abnormal number and constituent ratio of intestinal microflora, dysfunction of intestinal mucosal barrier, bacterial translocation, and intestinal endotoxemia, and it plays an important role in the development and progression of alcoholic liver disease. In addition, intestinal microflora also has influence on alcohol metabolism. Probiotics or fecal microbiota transplantation can regulate intestinal microflora and may play an active role in the treatment of alcoholic liver disease. Further studies are needed to discuss the standardized use of microecologics, dose selection, dosage form, and course of treatment during the prevention and treatment of alcoholic liver disease.

Cholestatic liver diseases (CHD) refers to a kind of liver disease in which accumulation of excessive bile due to various causes from inside and outside of the liver blocks the formation, secretion and excretion of bile, and thereby induce the normal bile flow unable to enter the duodenum. During the occurrence and development of CHD, intestinal microflora plays an important role in regulating bile acid metabolism, and immune response. In addition, CHD affects the composition, abundance and function of intestinal microflora, which in turn affects the synthesis and metabolism of bile acids. Hence, bile acids being an important signaling molecule for the occurrence and development of CHD plays role in the pathophysiological processes through bile acid transporters and nuclear receptors, such as farnesoid receptors. This paper briefly introduces the relationship between intestinal microecology and cholestatic liver disease based on the interrelationship among bile acid, intestinal flora and cholestatic liver disease, with a view to provide assistance in the treatment of cholestatic liver disease.

Clinically, hepatocellular carcinoma (HCC) is one of the most common malignant tumors with a high rate of morbidity and mortality. Hepatitis B virus infection is the main cause of hepatocellular carcinoma in China and it is a serious threat to people's health. Antiviral drugs such as nucleos(t)ide analogues and interferon can inhibit viral replication and liver fibrosis progression and reduce the occurrence of hepatitis B-related HCC. This article reviews the effects of different antiviral therapy on the occurrence of hepatitis B-related hepatocellular carcinoma in recent years.

Objective To investigate the correlation between hepatitis B virus (HBV)drug -resistance gene mutations and hepatocellular carcinoma (HCC).Methods The clinical data of treatment -experienced patients,who underwent examination for HBV drug -resistance gene mutations in Beijing Ditan Hospital from January 1 to December 31,2013,and still had detectable HBV DNA after being treated with nucleos(t)ide analogues,were collected.All the patients were followed up,and the development of HCC was considered as the clinical out-come.The correlation between drug -resistance gene mutations and the development of HCC in patients with HBV infection was analyzed. The chi -square test was used for comparison of categorical between groups,the t -test was used for comparison of continuous data between two groups,and the log -rank test was used for comparison of the incidence of HCC between two groups.Results A total of 227 patients were enrolled in this study.According to the results of the detection of HBV drug -resistance gene mutations,103 patients (103 /227, 45.37%)had no drug -resistance gene mutations and 124 (124 /227,54.63%)had drug -resistance gene mutations.There were no sig-nificant differences between the mutation group and the non -mutation group in HBV DNA load (5.19 ±1.60 log10 IU /ml vs 5.44 ±1.75 log10 IU /ml,t =-1.134,P =0.258)and the percentage of patients with liver cirrhosis (24.19% (30 /124)vs 16.50% (17 /103),χ2 =2.026,P =0.155).The median follow -up was 28 months (range 4 -58 months),and the incidence of HCC was 7.49% (17 /227).A-mong the patients with HBV drug -resistance gene mutations,12 (12 /124,9.68%)developed HCC,and among those without HBV drug-resistance gene mutations,5 (5 /103,4.85%)developed HCC.Among the patients who developed HCC,70.59% (12 /17)had HBV drug -resistance gene mutations at baseline;among the patients who did not develop HCC,53.33% (112 /210)had HBV drug -resistance gene mutations at baseline.Conclusion The patients with poor control of HBV DNA during antiviral therapy have a comparable incidence of HCC to those not treated with antiviral therapy,with a relatively high risk of developing HCC;the treated patients with HBV drug -resist-ance gene mutations may have a higher risk of HCC than those without such mutations,which needs to be confirmed by the studies with a longer follow -up period and a larger sample size.