Chronic hepatitis B (CHB) remains a major global cause of liver cirrhosis and hepatocellular carcinoma (HCC), particularly in China. With ongoing advances in antiviral therapy, the therapeutic objective for CHB has evolved from sustained suppression of hepatitis B virus replication toward achievement of a functional cure, defined by hepatitis B surface antigen (HBsAg) loss with or without anti-HBs seroconversion. Increasing evidence suggests that HBsAg clearance is strongly associated with reduced hepatic inflammation, regression of fibrosis, and a substantially lower risk of HCC, thereby serving as a critical indicator of long-term clinical prognosis in patients with CHB. Drawing upon recent domestic and international advances, this review summarizes the biological characteristics and pathogenic significance of HBsAg, its dynamic changes during antiviral therapy, and its associations with virologic responses and clinical outcomes. Particular emphasis is placed on the integrated immunologic mechanisms underlying HBsAg decline and clearance, including the interplay between innate and adaptive immune responses, cytokine networks, and immune reconstitution during functional cure. In addition, emerging predictive models and potential therapeutic strategies targeting HBsAg clearance are discussed, together with future research directions aimed at advancing standardized management and precision treatment strategies for CHB.
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Currently, research on biopsy-proven acute drug-induced liver injury (DILI) remains limited. This study aimed to identify clinical characteristics and risk factors for significant hepatic inflammation in patients with acute DILI.
An ambispective cohort study was conducted on biopsy-proven acute DILI patients admitted to our hospital from 2012 to 2018. Using the Scheuer scoring system, patients were categorized into G0-2 or G3-4 groups and followed up for 12 months after first admission. Clinical characteristics and outcomes were retrieved from medical records.
The median age of the 157 enrolled patients (65.6% female) was 40.4 (interquartile range (IQR), 31.9–49.1) years. The median latency and length of hospitalization were 30.0 (IQR, 5.0–60.0) and 18.0 (IQR, 12.0–26.0) days. The proportions of patients in the G0-2 and G3-4 groups were 54.8% and 45.2%, respectively. Logistic regression analysis revealed that females (odds ratio (OR): 2.623, 95% confidence interval (CI): 1.169–5.887, p = 0.019), higher body mass index (OR: 1.168, 95% CI: 1.029–1.325, p = 0.016), higher total bilirubin (OR: 1.004, 95% CI: 1.000–1.007, p = 0.047), and lower prothrombin activity (OR: 0.976, 95% CI: 0,957–0.995, p = 0.013) were associated with significant hepatic inflammation. The predominance of the hepatocellular injury pattern (60.5%) at admission transformed into a predominance of the cholestatic pattern (60.5%) at discharge. During follow-up, 23 patients (14.6%) developed chronic DILI, with nine patients (5.7%) progressing to cirrhosis. Moreover, 15 female patients (9.6%) developed autoimmunity (3cases in the G0-2 group vs 12 cases in the G3-4 group, p < 0.05).
Acute DILI patients with high-risk factors were more likely to develop significant hepatic inflammation, and females with significant inflammation were at a higher risk of developing autoimmunity during follow-up.
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Nonalcoholic steatohepatitis (NASH), an inflammatory form of non-alcoholic fatty liver disease, can progress to advanced liver fibrosis, cirrhosis, and liver cancer. Metabolic syndrome (MetS) parallels the prevalence of non-alcoholic fatty liver disease/NASH and increases patients’ risk of advanced liver disease. This study aimed to determine whether MetS was associated with the histological progression of NASH.
Patients with liver biopsy-proven NASH were retrospectively screened and categorized into two groups for each histological feature: with (<2 points) or without (≥2 points) significant hepatic steatosis/inflammation/fibrosis. Multivariable logistic regression was used to explore the association between MetS and histological features.
In total, 386 patients with a median age of 33.0 years were enrolled; among them, 35.2% were female, and 41.2% had MetS. The proportion of significant hepatic fibrosis and steatosis in those with MetS was significantly higher than in those without MetS (p < 0.05). Multivariable logistic regression analyses showed that MetS remained significantly associated with significant hepatic fibrosis (adjusted odds ratio: 1.852, 95% confidence interval: 1.042–3.292, p = 0.036), and severe hepatic steatosis (adjusted odds ratio: 2.008, 95% confidence interval: 1.030–3.914, p = 0.041).
MetS was associated with significant hepatic fibrosis and steatosis in patients with NASH. Our results suggest that NASH patients with MetS should be closely monitored and given targeted intervention and treatment, which may help to prevent disease progression and mitigate the growing burden of NASH.
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