World Journal of Hepatology最新文献

Background: Laparoscopic surgery is increasingly used for complex hepatolithiasis; however, data on laparoscopic vs open surgery remain limited. This study was undertaken to test the hypothesis that laparoscopic surgery offers comparable safety and efficacy to open surgery, with added benefits in recovery outcomes.

Aim: To compare clinical outcomes between laparoscopic and open approaches in complex hepatolithiasis.

Methods: This retrospective cohort study was conducted at Ningde Municipal Hospital, a tertiary care center, and included 80 patients with complex hepatolithiasis treated between January 2020 and August 2024. Patients were non-randomly allocated to laparoscopic (n = 40) or open surgery (n = 40) groups based on the treatment period. Clinical, intraoperative, and postoperative data were analyzed using appropriate parametric or non-parametric tests; categorical data were analyzed using χ ² or Fisher's exact test.

Results: Laparoscopic surgery was associated with a longer median operative time (250.0 minutes vs 207.0 minutes, P = 0.003) but shorter postoperative hospital stay (9.0 days vs 14.0 days, P < 0.001) compared to open surgery. Wound infection rates were significantly less frequent in the laparoscopic group (5.0% vs 22.5%, P = 0.023). Stone clearance rates and overall complications were comparable. One case of perioperative mortality occurred in the open surgery cohort.

Conclusion: Laparoscopic surgery is a feasible and safe alternative to open surgery for complex hepatolithiasis, offering faster recovery and reduced wound-related complications.

In this editorial, author specifically focuses upon metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver diseases (ALD) in the current era. This editorial article is inspired by the observational study by Harris et al in the recent issue. Alcohol and metabolic dysfunction cause steatotic changes in the hepatic parenchyma. The ALD and MASLD are major cause of chronic liver disease. Liver cirrhosis (LC) is a result of chronic liver inflammation with many causes (e.g., viral hepatitis, drug, alcohol and metabolic disorder). Metabolic dysfunction-associated steatohepatitis and alcohol-associated hepatitis can lead to liver fibrosis and LC. LC leads to hepatic dysfunction and can progress to eventual liver failure and death. Though chronic viral hepatitis is considered a main cause of LC for a long time, other etiologies (i.e., ALD, MASLD) has significantly increased in the current era. From the viewpoint of carcinogenesis, LC frequently causes hepatocellular carcinoma (HCC), and HCC is the most common type of primary liver cancer worldwide. As regards major causes of HCC, chronic viral hepatitis is gradually outweighed by ALD and MASLD. Note that patients coexisting with ALD and metabolic dysfunction-associated steatohepatitis show higher occurrence of HCC. Impact of ALD and MASLD upon the development of chronic liver disease, liver fibrosis, LC, and HCC is drastically increased in the current era. Establishments of diagnostic and therapeutic strategies to overcome these hepatic disorders are still required.

Metabolic dysfunction-associated steatotic liver disease (MASLD) requires accurate liver fibrosis assessment for management. While liver biopsy remains the gold standard, its invasiveness drives demand for non-invasive biomarkers. This review evaluates blood biomarkers for MASLD fibrosis staging. Established scores (fibrosis-4, non-alcoholic fatty liver disease fibrosis score) offer accessible screening but exhibit variable performance influenced by age, obesity, and comorbidities. Patented panels (e.g., enhanced liver fibrosis test, FibroMeter) improve accuracy by integrating extracellular matrix or metabolic markers, though context-specific thresholds are essential. Emerging biomarkers like propeptide of type 3 collagen, Mac-2 binding protein glycosylation isomer, epigenetic markers (proliferator-activated receptor-γ methylation), and angiopoietin-like proteins a family of eight glycoproteins show promise but require large-scale validation. Genetic risk scores and multi-omics approaches face generalizability challenges. Integration strategies, such as combining serum biomarkers with liver stiffness measurement via Agile scores, enhance diagnostic precision and reduce indeterminate classifications. Current tools aid risk stratification, but no single biomarker replicates biopsy-level precision. Future efforts must prioritize MASLD-specific diagnostic frameworks, standardized protocols, and multi-modal integration to enhance clinical utility and address MASLD's growing burden.

The evolving nomenclature from non-alcoholic fatty liver disease (NAFLD) to metabolic dysfunction-associated steatotic liver disease (MASLD) aims to better encompass the metabolic context of the disease. This change has significant implications for patients with type 2 diabetes mellitus (T2DM), given the frequent overlap between these conditions. This minireview explores the rationale behind the change, compares diagnostic criteria, and evaluates the impact of the MASLD framework on disease prevalence, characterization, and outcomes in T2DM patients. The updated MASLD criteria include all individuals with T2DM and hepatic steatosis, emphasizing metabolic dysfunction as the primary driver. In contrast, the NAFLD definition necessitates excluding other chronic liver diseases and verifying the absence of significant alcohol consumption, leading to a narrower diagnostic framework. Both metabolic dysfunction-associated fatty liver disease and MASLD identify a higher prevalence of steatotic liver disease, particularly among T2DM patients, compared to NAFLD. Notably, the MASLD framework introduces metabolic and alcohol-associated liver disease to account for dual etiologies involving alcohol use, which is common in T2DM populations but previously excluded under NAFLD criteria. While the new definitions enhance clinical relevance and inclusivity, they also highlight challenges such as unrecognized medication-induced steatosis and the need for reclassification in ongoing T2DM clinical trials. Emerging evidence supports enhanced screening strategies (e.g., fibrosis-4) and metabolic-targeted treatments for MASLD in T2DM patients. The successful integration of MASLD into clinical practice will require system-wide reeducation, standardization, and multidisciplinary collaboration to improve outcomes for T2DM patients.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease, affecting more than 30% of adults and 7%-14% of youths globally. MASLD and its advanced form of metabolic dysfunction-associated steatohepatitis (MASH) can progress to liver cirrhosis and hepatocellular carcinoma. Despite its growing burden, effective therapies for MASLD and MASH remain limited. Accumulating evidence indicates that short-chain fatty acids (SCFAs) modulate the activation of hepatic innate and adaptive immune cells, influencing liver inflammation and fibrosis. Moreover, SCFAs modulate liver lipid and glucose metabolism and insulin sensitivity, affecting MASLD progression. This review summarizes the cellular and molecular mechanisms through which SCFAs impact liver inflammation, fibrosis, and energy metabolism. Several key molecular signaling pathways are discussed. Clinical trials aiming to modulate SCFA production through different treatments are reviewed. Collectively, emerging evidence supports that targeting SCFA-mediated function represents a promising therapeutic strategy for MASLD and MASH.

Hypertransaminasemia - acute elevation of alanine aminotransferase and aspartate aminotransferase - is prevalent in non-cirrhotic adults admitted to the intensive care unit (ICU) and often signals extra-hepatic pathophysiology rather than intrinsic liver disease. To synthesise contemporary evidence on aetiology-driven diagnosis, management and emerging biomarkers of hypertransaminasemia in critically ill patients. We performed a structured search of PubMed, EMBASE and CENTRAL (January 2010-June 2025). The search was restricted to full-text articles that were published in English in peer-reviewed journals. Hypoxic liver injury is the leading cause of hypertransaminasemia in non-cirrhotic ICU patients and is characterized by a ≥ 50% alanine aminotransferase/aspartate aminotransferase fall within 72 hours after haemodynamic stabilisation. Idiosyncratic drug-induced liver injury remains uncommon yet explains about 13% of acute liver-failure cases in Western registries. Sepsis-associated liver injury presents mainly as conjugated hyperbilirubinaemia with modest transaminase rise, whereas parenteral-nutrition-associated liver disease is dominated by cholestasis after > 2 weeks of parenteral feeding. Early optimisation of macro-/micro-circulation, rational deprescribing of hepatotoxins, rapid source control of infection and prompt transition to enteral nutrition are outcome-modifying interventions across all phenotypes. In the ICU, aminotransferase elevation should be interpreted as a dynamic biomarker of systemic distress. A pattern-recognition algorithm integrating clinical context, enzyme kinetics and novel biomarkers (glutamate dehydrogenase, microRNA-122, high-mobility group box-1) can expedite aetiology-specific therapy and deserves prospective validation.

Beyond its traditional role in calcium and bone metabolism, vitamin D has emerged as a critical regulator of liver health. Its active form, calcitriol [1α,25(OH)₂D], signals through the vitamin D receptor (VDR), which is expressed in hepatic stellate cells, Kupffer cells, and cholangiocytes. Through this pathway, vitamin D modulates fibrosis, inflammation, oxidative stress, bile acid homeostasis, and immune responses. This review explores the growing body of evidence linking vitamin D deficiency to chronic liver diseases, including autoimmune hepatitis, primary biliary cholangitis, alcoholic liver disease, viral hepatitis B and C, and metabolic-associated steatotic liver disease. Low vitamin D levels are frequently observed in these conditions and are associated with disease severity, complications (such as spontaneous bacterial peritonitis, sarcopenia, and hepatic encephalopathy), and increased mortality. Mechanistically, vitamin D-VDR signaling inhibits profibrotic TGF-β1/SMAD pathways, downregulates proinflammatory cytokines, enhances regulatory T cell differentiation, and improves insulin sensitivity. Although preclinical studies support its protective effects, clinical trials of vitamin D supplementation have produced mixed results. Overall, vitamin D appears to influence multiple pathways in liver disease pathophysiology, and correcting its deficiency may offer clinical benefits. However, its integration into clinical care will depend on identifying responsive patient subgroups and defining optimal dosing strategies to maximize therapeutic benefit.

Steatotic liver disease (SLD) encompasses a group of disorders characterized by the excessive accumulation of fat in the liver. It is classified into four categories based on clinical manifestations: Metabolic dysfunction-associated SLD (MASLD), metabolic-alcohol-associated liver disease (ALD), ALD, and cryptogenic SLD. In the United States, its prevalence stands at 34.2%, making it the most common cause of cirrhosis and hepatocellular carcinoma (HCC). In addition to factors related to endocrine, nutrition, and medications, several genetic markers have been implicated in the disease's pathogenesis. Notable genes include PNPLA3, TM6SF2, GCKR, MBOAT7 and HSD17B13. These genetic polymorphisms can significantly impact prognosis and disease outcomes. For example, PNPLA3 is the most frequently associated gene with MASLD, increasing the risk of HCC by 12-fold and liver-related mortality by 18-fold. Furthermore, certain genetic markers are more prevalent in specific ethnic groups; for instance, PNPLA3 is common among Hispanics, while TM6SF2 is linked to higher fat content in African Americans. With a better understanding of the genetic factors involved in the pathogenesis of SLD, significant advancements have been made in diagnostics and therapeutics. This review explores the role of genetic factors in the disease's development, discusses current advancements in non-invasive diagnostic modalities, and examines therapeutic improvements based on these genetic insights to achieve better outcomes.

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease, represents a growing global health burden, contributing significantly to liver-related morbidity and mortality. Early detection and timely intervention are essential to prevent disease progression. Conventional diagnostic methods, which rely on specialized imaging and invasive liver biopsies, underscore the need for non-invasive, cost-effective alternatives. Artificial intelligence-particularly machine learning and deep learning-has emerged as a transformative tool in MASLD diagnostics, offering improved accuracy in risk prediction, imaging interpretation, and disease stratification. This review synthesizes recent advancements in AI-based MASLD diagnostics, highlighting key models, performance metrics, and clinical applications, while addressing ongoing challenges such as data standardization, interpretability, and clinical validation.

Hepatocellular carcinoma (HCC) is imposing a growing global health burden, with China accounting for nearly half of incident cases and mortality worldwide. Early screening is critical to improving survival in high-burden regions. However, the global standardized screening rate for high-risk populations is less than 24%, and HCC screening currently faces severe challenges. We synthesize recent advances in HCC screening, including optimized serum biomarkers, evolving imaging techniques, and validated models. Emerging liquid biopsy technologies and artificial intelligence further demonstrate considerable promise for enhancing noninvasive detection efficacy. Multifaceted collaboration among policymakers, healthcare systems, and communities is essential to implement effective screening programs and ultimately improve survival outcomes.