World Journal of Hepatology最新文献

Background: The immune response following radiofrequency ablation (RFA) is characterized by a dynamic interaction between proinflammatory and anti-inflammatory factors. An elevated ratio of interleukin (IL)-6 to IL-10 may serve as a key indicator of post-RFA immune dysregulation.

Aim: To evaluate the prognostic relevance of the IL-6/IL-10 ratio as a surrogate indicator of immune dysregulation in patients with malignant liver tumors treated by RFA.

Methods: We enrolled 91 patients undergoing RFA for hepatic malignancies were prospectively enrolled. Serum levels of IL-6 and IL-10 were measured both prior to the procedure and within 7 days post-RFA. Statistical analyses were conducted to assess the association between the IL-6/IL-10 ratio and clinical outcomes.

Results: The study population consisted predominantly of males (74.73%), with a mean age of 60.88 ± 9.03 years. Most participants presented with ≤ 2 hepatic lesions (91.21%) and well-preserved hepatic function, as indicated by Child-Pugh class A status (98.9%). The mean lesion diameter was 26.27 ± 13.8 mm, and 78.02% had a documented history of hepatitis B virus infection. Post-procedural cytokine profiling revealed a marked and rapid surge in IL-6 concentrations peaking within 24 hours after RFA, whereas IL-10 exhibited only a modest elevation. Consequently, the IL-6/IL-10 ratio remained persistently elevated throughout the 7-day monitoring period (all P < 0.05). Multivariate logistic regression analysis identified the IL-6/IL-10 ratio as an independent prognostic indicator for adverse post-ablation outcomes (odds ratio = 1.11 per unit increment, 95%CI: 1.033-1.204, P = 0.006), with higher ratios signifying increased inflammatory burden. In contrast, elevated serum albumin levels conferred a protective effect (odds ratio = 0.81, 95%CI: 0.668-0.961, P = 0.021).

Conclusion: The IL-6/IL-10 ratio may constitute a clinically relevant biomarker indicative of immune dysregulation after RFA, with potential implications for understanding inflammation-driven outcomes and tailoring post-RFA management.

Background: Ziziphus spina-christi leaf extract (ZSCLE) can be used to treat hepatic schistosomiasis. However, its role as an anti-inflammatory and anti-proliferative agent remains unexplored.

Aim: To assess the therapeutic potential of ZSCLEs in hamsters infected with Schisto som mansoni (S. mansoni) undergoing 50% liver resection (LR).

Methods: Fifty hamsters were divided into five groups (10 hamsters each), with group I serving as the control; group II received ZSCLE treatment only; group III was infected with S. mansoni but was untreated; group IV was infected with S. mansoni and received ZSCLE treatment; group V was infected with S. mansoni and underwent ZSCLE treatment and 50% LR. Each group was analyzed using DNA flow cytometry, and oxidative stress (nitric oxide levels), inflammatory markers (tumor necrosis factor-α and interferon-γ), and liver biomarkers were assessed. Histopathological examination was conducted for all groups.

Results: Compared with the infected untreated group, the ZSCLE-treated group showed a significant 70.2% reduction in hepatic tissue egg load (3459.5 ± 191.3 vs 1032 ± 25.1, P < 0.001), and the ZSCLE-treated group that underwent surgical resection showed a 71.8% decrease (2021.7 ± 190.2 vs 7193.3 ± 103.4, P < 0.001). Alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and bilirubin levels were higher in group III than in group I, group IV, and group V (P < 0.0001). The liver regeneration rate (%) was significantly higher in group IV and group V than in group III (median values: 45.18%, 47.93% vs 28.31%). Pathological examination revealed fewer granulomas in group V.

Conclusion: ZSCLE-LR is a potent agent against schistosomiasis-induced hepatic damage, exhibiting a significant role in promoting hepatic regeneration. Further molecular-level studies are warranted to investigate the phytochemical properties of ZSCLE and its potential applications in managing schistosomiasis-induced hepatic fibrosis.

Unexplained liver disease in infants and children remains a significant diagnostic challenge as the spectrum of noninfectious pediatric liver disease expands. Timely, accurate etiologic assignment remains central to optimal care and resource allocation. Advances in next-generation sequencing, particularly whole-exome sequencing (WES), have transformed evaluation by enabling rapid identification of monogenic disorders that previously eluded standard algorithms. In this editorial, we synthesize recent evidence showing that comprehensive genetic testing substantially improves etiologic diagnosis in pediatric hepatology. WES markedly increases diagnostic yield in infants with cholestasis and in children with cryptogenic aminotransferase elevations, directly influencing management and outcomes. We compare yields across international reports from Asia, North America, and Europe, illustrating how WES and broad gene panels uncover heterogeneous genetic contributors to pediatric liver disease. We also address practical issues, including decreasing costs, faster turnaround times, and the importance of integrating conventional investigations with modern genomics. Finally, we emphasize that while WES is a powerful tool to "decode" unexplained disease and guide precision therapies, it must complement, not replace, careful clinical assessment and, in selected cases, liver biopsy. An integrated approach is essential for navigating heterogeneity, avoiding unnecessary procedures, and advancing personalized medicine in pediatric hepatology worldwide to improve outcomes and equity.

Background: Hepatitis B Virus (HBV) remains a global public health challenge, affecting over 296 million people, many of whom are asymptomatic. Incidentally diagnosed carriers provide a critical window for early intervention and prevention. Understanding their hematological profile and viral burden can help inform risk assessment and clinical management.

Aim: To evaluate hematological parameters and HBV viral load in incidentally detected asymptomatic hepatitis B surface antigen positive patients during routine health screenings.

Methods: A cross-sectional observational study was conducted from June 2024 to March 2025 at Dr. D. Y. Patil Medical College, Hospital and Research Centre a tertiary care hospital in Pune, Maharashtra, India, involving 100 hepatitis B surface antigen-positive patients and 20 healthy controls. Hematological and liver function parameters were assessed, and quantitative HBV DNA analysis was performed using real-time polymerase chain reaction. Statistical analysis was conducted using GraphPad Prism v8.0.

Results: Marked variations were detected in hemoglobin levels (P < 0.0001), percentage of neutrophils (P = 0.0006), percentage of lymphocytes (P = 0.0031), serum glutamic-oxaloacetic transaminase activity (P = 0.0013), and alanine aminotransferase levels (P = 0.0001) when comparing HBV-infected individuals with the control group. Conversely, differences in total leukocyte count, percentage of monocytes, percentage of eosinophils, platelet count, total bilirubin, and serum glutamic-pyruvic transaminase values were not statistically significant. Viral load > 2000 IU/mL was found in 17 patients, and < 2000 IU/mL in 24 patients. Viral load positively correlated with conjugated bilirubin, serum glutamic-oxaloacetic transaminase, serum glutamic-pyruvic transaminase, and alkaline phosphatase, and negatively with albumin and the albumin-globulin ratio.

Conclusion: Incidentally detected HBV infections present an opportunity for early disease detection. Hematological and viral markers can guide clinical decisions. Routine screening and contact tracing are essential strategies to control HBV transmission and progression.

Background: Autoantibodies, including anti-nuclear antibodies (ANA), are typically present in autoimmune hepatitis (AIH), but may be detected in other liver conditions, including metabolic dysfunction-associated steatotic liver disease (MASLD), even in the absence of an autoimmune disorder.

Aim: To identify predictive factors for the non-confirmation of AIH diagnosis in patients with liver dysfunction of unknown etiology and positive autoantibodies.

Methods: A retrospective cohort study was conducted in a university-affiliated hospital, including consecutive adult patients with liver dysfunction of unknown etiology and positive autoantibodies typically present in hepatic autoimmune disorders, who underwent liver biopsy, between June 2016 and August 2023. Patients with other known liver diseases or contraindications to liver biopsy were excluded, as well as those who underwent liver biopsy and had a poor specimen quality.

Results: A total of 81 patients were included, of whom 53.1% were diagnosed with AIH and 46.9% with MASLD. ANA had a high sensitivity (83.7%) in diagnosing AIH but the lowest specificity (18.4%). In patients with ANA positivity, male, diabetic and obese individuals were more likely to have a non-confirmed AIH (P = 0.022, P = 0.039 and P = 0.046, respectively). Higher controlled attenuation parameter (CAP) values in patients with ANA positivity were associated with non-confirmed AIH diagnosis (288 ± 56 vs 244 ± 60, P = 0.012). In multivariate analysis, male gender and higher CAP values were independent predictive factors for non-confirmed AIH diagnosis (P = 0.011 and P = 0.034, respectively).

Conclusion: AIH was not confirmed in 47% of patients with liver dysfunction and positive autoantibodies. Multivariate analysis identified male gender and elevated CAP values as independent predictive factors for a non-confirmed diagnosis of AIH in patients with liver dysfunction and ANA positivity. Further prospective and multicenter validation is required in order to corroborate our findings.

Contemporary treatment approaches have resulted in excellent cure rates for childhood cancer; however, these therapeutic advances are accompanied by adverse, long-term health outcomes, commonly referred to as late effects. Among these, late hepatic toxicity remains an underrecognized yet potentially serious consequence. Unlike acute liver injury, long-term hepatotoxicity often develops insidiously, with potential progression to severe morbidity or even life-threatening conditions. This review focuses on late hepatic adverse effects in childhood cancer survivors, highlighting the role of specific therapeutic exposures that compromise liver health. Early identification, monitoring, and timely intervention are essential to mitigate risk. Furthermore, long-term, multidisciplinary follow-up remains critical to improve quality of life in this growing population of survivors. Greater awareness and dedicated research are needed to address the burden of late therapy-related liver complications and to optimize survivorship care.

Accurate assessment of hepatic steatosis is essential for diagnosing, staging, and monitoring metabolic dysfunction-associated steatotic liver disease. This review comprehensively overviews conventional and emerging hepatic steatosis evaluation methods. Noninvasive imaging techniques such as ultrasound, controlled attenuation parameter, and magnetic resonance imaging-derived proton density fat fraction are discussed alongside invasive reference standards such as liver biopsy. The review also highlights the role of blood-based biomarkers, including fibroblast growth factor 21, cytokeratin-18, type III procollagen peptide, and Mac-2 binding protein glycosylation isomer, as well as novel approaches such as epigenetic markers, artificial intelligence-assisted imaging, and digital pathology. Each method is presented with consideration of its diagnostic performance, clinical utility, and limitations. By integrating these modalities into multimodal assessment strategies and incorporating dynamic endpoints such as magnetic resonance imaging-derived proton density fat fraction (known as magnetic resonance imaging-derived proton density fat fraction)-based fat reduction as a therapeutic response marker, clinicians can improve diagnostic accuracy, risk stratification, and therapeutic guidance.

Background: Progressive familial intrahepatic cholestasis type 3, caused by mutations in the ABCB4 gene, is a rare genetic disorder. Although severe phenotypes due to biallelic mutations are well described, emerging data seem to suggest the clinical relevance of monoallelic variants.

Aim: To describe the clinical spectrum and genotype-phenotype correlation of ABCB4 mutations in children in a cohort of North Indian children.

Methods: This is a retrospective analysis of a prospectively maintained database from a single tertiary care centre. Children (≤ 18 years) with ABCB4 mutations between January 2021 and March 2025 were analysed. The clinical presentation, laboratory investigations, genetic sequencing and outcomes were recorded. Patients were stratified into group 1 (homozygous/compound heterozygous) and group 2 (heterozygous). Variant pathogenicity was assessed using the American College of Medical Genetics guidelines and available predictive tools.

Results: Of the 26 patients, 16 had biallelic mutations, and 10 had monoallelic mutations. Group 1 exhibited higher rates of positive family history (75% vs 30%, P = 0.04), ascites (43.2% vs 0%, P = 0.02), larger varices (40% vs 0%, P = 0.009), higher gamma glutamyl transferase levels (171 U/L vs 38 U/L, P = 0.007), and lower platelet counts (162 × 10⁹/L vs 415 × 10⁹/L, P = 0.007). Notably, two-thirds of patients in group 1 experienced disease progression, and one-third died during follow-up. Certain missense variants (e.g., c.2860T>C) and all nonsense variants were linked to rapid deterioration. Most children in group 2 had transient cholestasis with a good outcome, but two older children succumbed.

Conclusion: Mutations in the ABCB4 gene contribute significantly to pediatric chronic liver disease. Patients with severe biallelic mutations frequently experience a progressive disease course, whereas those with monoallelic mutations may progress slowly. Genetic testing for ABCB4 should be considered in children with cryptogenic chronic liver disease, especially those with high gamma-glutamyltransferase cholestasis and portal hypertension.

Artificial intelligence (AI) has made remarkable strides, becoming an essential tool in modern medicine. As AI continues to evolve, it is crucial to redefine its scope, classifications, and subtypes to better align with its clinical applications and potential. With a growing number of sophisticated models, AI is now widely used in gastroenterology and hepatology, offering new ways to enhance patient care. In gastroenterology, AI helps doctors identify lesions during endoscopy, detect gastrointestinal bleeding, and support the diagnosis and treatment of conditions like inflammatory bowel disease and gastrointestinal cancers. In hepatology, it aids in staging liver fibrosis, tracking disease progression, and predicting hepatocellular carcinoma risks. Machine learning further personalizes treatment plans, helping physicians make more informed decisions. However, despite its promise, AI still faces hurdles, including biases in data, ethical considerations, regulatory challenges, and the need for better transparency. Moving forward, refining these models, conducting extensive validation studies, and integrating AI seamlessly into clinical practice will be crucial in fully realizing its benefits for gastroenterology and hepatology.

A study by Twohig et al evaluated the impact of an educational video module (EVM) on the treatment of alcohol use disorder (AUD) in hospitalized patients with alcohol-related liver disease (ALD). This single-center prospective study involved 42 patients, and the results were compared with those of a retrospective control group. EVM increased the rates of pharmacological (50% vs 22%, P = 0.0008) and psychosocial (73.8% vs 44%, P = 0.001) treatments within 30 days post-treatment. The rate of alcohol relapse decreased significantly (7.9% vs 35.6%, P = 0.003) after the intervention. All the participants recommended the EVM. These findings suggest that standardized educational interventions can address knowledge gaps and improve treatment engagement for AUD in patients with ALD.