中华肝脏病杂志最新文献

Artificial intelligence (AI), a core technology of the Fourth Industrial Revolution, profoundly reshapes the landscape of modern medicine. AI can extract information from extensive datasets, optimizing trial design, and enhancing research efficiency. It is widely applied in field such as medical imaging, clinical decision support, precision medicine, and drug development. Notably, AI brings revolutionary opportunities to clinical research and practice; however, it also raises a series of serious ethical and regulatory challenges regarding data privacy, algorithmic bias, attribution of responsibility, and informed consent. This article systematically discusses the current applications of AI at various stages of clinical research, deeply analyzes the core ethical dilemmas arising from these applications, and outlines corresponding ethical governance frameworks and response strategies. In addition, we advocated establishment of a collaborative governance system that is people-oriented and technology-driven, emphasizing strict adherence to ethical principles throughout the entire process of technological development to ensure the scientific, fair, and safe nature of clinical research, ultimately resulting in the coordinated progress of artificial intelligence technology and medical ethics.

In recent years, the European Society for Vascular Surgery has proposed the concept of porto-sinusoidal vascular disease (PSVD) based on idiopathic non-cirrhotic portal hypertension (INCPH), thereby expanding the scope of these disease conditions and creating understanding for their natural history. However, research on the pathogenesis of this disease has progressed slowly due to the lack of corresponding animal models. A review of previous animal models that meet the definition of porto-sinusoidal vascular disease reveals that none of these models have progressed to develop cirrhosis. Nine models exhibited elevated portal vein pressure, while sixteen models showed histological manifestations related to portal hypertension. This summary aims to lay the foundation for future research.

Currently, the commonly used antiviral drugs for hepatitis B virus (HBV) primarily include nucleos(t)ide analogues and interferons, which effectively suppress viral replication but typically have difficulty achieving clinical cure of chronic hepatitis B (CHB). Recent clinical trials have demonstrated that small-molecule nucleic acid drugs have favorable safety profiles for CHB treatment. Thus, these drugs have the potential to become a novel breakthrough point in CHB and demonstrate promising prospects in terms of clinical cure by inducing the degradation of viral RNA and activating the body's immune response to clear hepatitis B surface antigen. This review summarized the current clinical research advances for small-molecule nucleic acid drugs in the treatment of CHB.

Objective: To evaluate the efficacy of the Baveno VI criteria in the diagnosis of clinically significant portal hypertension (CSPH) under two conditions: non-etiological control and complete etiological control. Methods: A cross-sectional study was conducted. Clinical data were collected from 232 cases with compensated advanced chronic liver disease who underwent hepatic venous pressure gradient measurement and had liver stiffness measurement (LSM) ≥10 kPa at Nanfang Hospital, Southern Medical University, between July 2019 and December 2024. Patients were categorized into the etiological control group (78 cases) and the non-etiological control group (154 cases) according to the definition of etiological control. Patients meeting the criteria for etiological control or near-control, with alanine transaminase≤upper limit of normal (ULN) were further defined into the near-etiological control group (110 cases). Intergroup comparisons of normally distributed and skewed quantitative data were performed using the independent sample t-test and the Mann-Whitney U test, respectively. Categorical variables were compared using χ² tests. The diagnostic performance of LSM in predicting CSPH under controlled and uncontrolled conditions was evaluated based on sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). Results: The PPVs of LSM≥25 kPa for diagnosing CSPH in the overall population, the subgroups of the etiological-control, non-control, and nearly control were 82.8%, 93.3%, 79.6%, and 92.0%, respectively, with specificities of 89.3%, 96.3%, 86.8%, and 95.3%. The PPVs of LSM≥25 kPa for diagnosing CSPH were 90.0% and 76.9%, respectively, with the specificities of 93.8% and 85.0% in the non-control group with ALT≤ULN and ALT>ULN. LSM≥25 kPa demonstrated PPVs of 90.0% and 76.9% for diagnosing CSPH in populations with ALT≤ULN and ALT>ULN, respectively, with specificities of 93.8% and 85.0% in the non-etiological control group. The sensitivity and NPV for excluding CSPH using LSM≤15 kPa combined with platelet count (PLT)≥150×10⁹/L in the etiological-control group, the non-control group, and the near-control group were 100% in the overall population. The combined model of LSM≥25 kPa and LSM≤15 kPa+PLT ≥150×10⁹/L for diagnosing and excluding CSPH yielded gray zone rates of 60.3%, 67.9%, 56.5%, and 64.6% in the overall population and subgroups, respectively. The combined model of LSM≥25 kPa and LSM≤15 kPa+PLT≥110×10⁹/L yielded gray zone rates of 50.8%, 59.0%, 46.8%, and 58.2% in the overall population and subgroups, respectively. Conclusion: The Baveno VI criteria reliably and effectively identify CSPH in patients with cACLD with well-controlled etiologies but remain to be validated in the non-controlled etiology group.

Objective: To analyze the antiviral efficacy and its influencing factors in pediatric patients with hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (CHB). Methods: Thirty-eight initially treated pediatric patients with HBeAg-negative CHB who visited the Department of Hepatology of the Fifth Medical Center of the General Hospital of the People's Liberation Army (PLA) from June 2010 to June 2019 were retrospectively enrolled, and the clinical medications included interferon alpha (IFN-α) and nucleos(t)ide analogs (NAs). The antiviral efficacy and safety profile were assessed at 96 weeks. Pediatric patients were categorized into a cure group [quantitative HBsAg (qHBsAg)<0.05 IU/mL], a low HBsAg group (0.05 IU/mL≤qHBsAg ≤ 1 500.00 IU/mL), and a high HBsAg group (qHBsAg>1 500.00 IU/ mL) according to different levels of hepatitis B surface antigen (HBsAg). The antiviral efficacy and its influencing factors were analyzed using the Kaplan-Meier method and generalized estimating equations in pediatric patients. Results: Clinical cure was achieved in 13% (5/38) at 96 weeks in pediatric patients. Young age at baseline and high B-lymphocyte count levels were the characteristics of pediatric patients who achieved clinical cure. Further analysis indicated that the HBsAg-negative conversion rate was significantly higher in children aged 1-<3 years than that in children aged 3-<7 and 7-12 years [33% (4/12), 5% (1/20), and 0 (0/6) in the three groups, respectively, P=0.025]. No serious adverse reactions were observed during treatment and follow-up. Conclusion: Antiviral therapy efficacy and safety profile are superior for HBeAg-negative CHB children, and some children can achieve clinical cure.Younger age at baseline and higher B-lymphocyte count level might be important factors favoring the clinical cure in children.

Objective: This study systematically assessed the latest epidemiological model and changing trends of metabolic-associated fatty liver disease (MAFLD)-associated cirrhosis at the global and regional levels based on the updated 2021 Global Burden of Disease (GBD2021) database, with the aim to provide important reference to make decisions in patients. Methods: Global and regional data on MAFLD-associated cirrhosis were extracted from the GBD 2021 database. Prevalence, incidence rate, and total years lived with disability (YLD), as well as age-standardized rates per 100 000 population, were analyzed according to year, age, and gender. Estimated results were presented with uncertainty intervals (UIs) to ensure the robustness of the statistical findings. Results: The global age-standardized prevalence of MAFLD-associated cirrhosis was 15,017.5 (95% UI 13 755.8-16 360.8) per 100 000 population, the incidence rate was 876.5 (95% UI 862.2-890.0) per 100 000 population, and the YLD rate was 0.4 (95% UI 0.2-0.6) per 100 000 population in 2021. The highest age-standardized prevalence was observed in North Africa and the Middle East, Central Latin America, and Tropical Latin America among the regions. The lowest age-standardized prevalence was observed in high-income North America, Australia, and high-income Asia-Pacific. The highest age-standardized prevalence was observed in Kuwait, Egypt, and Qatar, while the lowest was observed in Japan, Finland, and Canada among 204 countries. Gender analysis revealed that the prevalence rate was significantly higher in males than females, with a peaked prevalence rate in the 45-49 age group for males and the 50-54 age group for females. The incidence rates peaked in the 15-19 and 20-24 age groups, respectively. Conclusion: MAFLD-associated cirrhosis is a global health problem. The highest incidence rates are found in North Africa and the Middle East, central Latin America, and southern sub-Saharan Africa, while the lowest rates are found in high-income North America, Australia, and the Asia-Pacific region. The prevalence, incidence, and YLD and their corresponding age-standardized rates were higher in males than in females between 2010 and 2021. Therefore, understanding the epidemiological characteristics and evolving trends will aid in formulating preventive and treatment strategies to reduce the global burden of MAFLD-associated cirrhosis.

Artificial intelligence (AI) has shown great potential in the field of hepatology, and it is gradually revolutionizing novel research for liver diseases. However, its full integration into real-world diagnostic and treatment processes still faces significant challenges. This article analyzed the application progress of AI in key areas such as big data analysis, translational research, and imaging and pathological interpretation. Physicians need to integrate massive amounts of multimodal data (medical history, physical signs, laboratory data, imaging, and pathology) to make informed decisions in clinical practice. Although AI has gradually shown a preliminary auxiliary application role in certain liver disease diagnosis and treatment scenarios, current machine learning and deep learning technologies are far from being able to effectively support clinical decision-making in real-world settings. The core pain points are as follows: firstly, AI tools are not yet mature enough to truly independently and reliably assist in complex clinical evaluation; secondly, even if assistance is provided, the ultimate responsibility for medical decisions still clearly belongs to the physician, failing to reduce their workload effectively; finally, due to the different specialties and data characteristics of various medical centers, individually trained AI models are often relatively independent and personalized, fragmented, and difficult to integrate into a widely applicable and scalable multi-center general model, limiting their universal value. In the future, enhancing clinicians' understanding of AI and building multidisciplinary collaborative networks will be crucial to accelerating the development of AI-driven decision support tools for specific liver diseases. At the same time, ethical, legal, and talent development challenges, and others must be carefully addressed to bridge the gap and safely and eppectively apply AI in clinical practice.

Objective: To investigate the effect of Kupffer cells on liver regeneration with metabolic associated fatty liver disease (MAFLD) induced by a methionine-choline-deficient (MCD) diet in mice. Methods: Eight-week-old C57BL/6J male mice were randomly divided into three groups: control (normal diet), MAFLD model (MCD feeding), and MAFLD remission (MCD feeding followed by a normal diet after 5 weeks). Liver biochemical indices were detected. Liver tissue pathological morphology was analyzed. Kupffer cells infiltration and hepatocyte proliferation conditions were detected by immunofluorescence staining. Statistical analyses were performed using the t-test, one-way ANOVA, Tukey test, Dunnett test, or Two-way ANOVA test according to different data. Results: The MAFLD model group mice had severe liver lipid accumulation and delayed hepatocyte proliferation. The serum alanine aminotransferase, aspartate aminotransferase, and triglyceride content in the MAFLD model group were increased by 8.10 times, 4.69 times, and 7.32 times, respectively, in comparison to the control group, as indicated by the results of biochemical index detection following five weeks, and this phenomenon was accompanied by a decrease in Kupffer cells. The MAFLD model group had an approximate reduction of 50% in Kupffer cells count compared to the control group. The addition of Kupffer cells had restored the normalized hepatocyte proliferation capacity and alleviated liver steatosis in vitro or through dietary change. Conclusion: The proliferation of hepatocytes has a certain stimulating effect with the supplementation of Kupffer cells in MCD-induced MAFLD mice.

Objective: To construct Slc27a5 gene knockout mice and investigate changed conditions in the serum lipidomics. Methods: Liver tissues and serum samples were collected from wild-type and Slc27a5 gene knockout mice at different time points. Hematoxylin-eosin staining was used to observe hepatic pathological changes. Immunofluorescence staining was used to detect the expression of α-smooth muscle actin and F4/80 proteins. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to analyze changes in serum lipid composition. The comparison of quantitative data was performed using the t-test between groups. Results: The percentage area of α-smooth muscle actin staining (7.33% ± 3.08% vs. 1.14% ± 0.30%, t=3.996, P<0.01) and F4/80 staining area (2.48% ± 0.71% vs. 0.76% ± 0.19%, t=4.683, P<0.01) was significantly higher in Slc27a5 gene-deficient mice than in wild-type mice in liver tissue at 24 months of age. The results of the serum lipidomics analysis indicated significant alterations in lipid composition of Slc27a5 gene-deficient mice. Compared with wild-type mice, the serum of Slc27a5 gene-deficient mice had increased levels of 19 types of phosphatidylinositols and 14 types of phosphatidylcholines and decreased levels of 17 types of phosphatidylethanolamines. Conclusion: Spontaneous liver fibrosis induced by Slc27a5 deficiency in a mouse model is accompanied by significant remodeling of the serum lipid profiles.