World Journal of Hepatology最新文献

A recent study in World Journal of Hepatology examined the use of intravascular ultrasound (IVUS) for transjugular intrahepatic portosystemic shunt (TIPS) creation. The study concluded that IVUS significantly reduces procedure time, radiation exposure, and the number of needle passes compared to conventional fluoroscopic guidance. IVUS offers real-time visualization of the portal vein, but challenges remain in terms of equipment costs and the operator learning curve. TIPS creation techniques vary widely in clinical practice, where methods, such as conventional fluoroscopy, three-dimensional image fusion, electromagnetic navigation, and IVUS, are commonly employed. In this editorial, we provide a comparative analysis of these methods based on clinical experience and the literature. By evaluating the strengths and limitations of each technique, we aim to inform clinical decision-making and enhance procedural outcomes. Future developments in TIPS creation are likely to focus on hybrid techniques that combine the strengths of IVUS, electromagnetic navigation, and real-time image fusion, potentially leading to more precise, cost-effective, and accessible methods.

Pediatric liver masses encompass a diverse spectrum of benign and malignant lesions, with distinct patterns based on patient age. Optimal imaging is critical for timely diagnosis, management, and prognosis. This pictorial minireview categorizes pediatric liver masses by age group to guide hepatology and radiology practice, with an emphasis on imaging characteristics. In children from birth to six years of age, the most common liver masses include hepatoblastoma, the most common primary hepatic malignancy in this age group; infantile hemangioma, a benign vascular tumor with a characteristic appearance on imaging; and mesenchymal hamartoma, a rare developmental lesion. For children older than six years, liver masses are distinct, with hepatocellular carcinoma being the predominant malignant lesion. Benign masses such as focal nodular hyperplasia and hepatocellular adenoma also emerge in this age range, often linked to hormonal influences or metabolic disorders. The masses observed across all pediatric age groups include hepatic cysts, choledochal cysts, hydatid cysts, pyogenic and amebic abscesses, tuberculosis, lymphoma, and metastases, each presenting with unique imaging features essential for differential diagnosis. This minireview provides a comprehensive, age-based overview of pediatric liver masses, focusing on clinical presentation and key imaging findings to support accurate diagnosis and optimize management strategies in clinical hepatology, particularly in low resource settings.

Portal hypertension is a critical determinant of prognosis in chronic liver disease and a key factor in evaluating candidates for liver transplantation. Traditional methods such as hepatic venous pressure gradient (HVPG) measurement have long been considered the gold standard for assessing portal pressure. However, these methods are invasive and carry procedural limitations. Recent advances in endoscopic ultrasound (EUS)-guided techniques have emerged as promising alternatives, offering direct and minimally invasive assessment of portal pressure. EUS-guided portal pressure gradient measurement enables real-time evaluation of haemodynamic through direct access to the portal system. This technique has shown to be as accurate as HVPG, and it has some extra benefits, like the ability to take liver biopsies and check collateral circulation all at the same time. Despite these benefits, the technique poses challenges such as operator dependence, procedural complexity, and limited standardization across centres. This minireview highlights the evolution of portal pressure measurement, focusing on the potential of EUS-guided techniques in pre-transplant assessment, risk stratification, and monitoring therapeutic outcomes. Furthermore, it discusses the technical challenges, clinical implications, and future directions for integrating these innovations into routine practice. Advances in portal pressure measurement hold significant promise for enhancing decision-making and outcomes in liver transplantation.

The liver is a central metabolic organ that regulates numerous physiological processes, including glucose and lipid metabolism, detoxification, and the synthesis of essential proteins and bile. Bile acids (BAs), synthesized from cholesterol in hepatocytes, not only facilitate the emulsification and absorption of dietary fats but also act as potent signaling molecules through receptors such as the farnesoid X receptor (FXR) and Takeda G-protein-coupled receptor 5. Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of chronic liver disease globally, closely linked with obesity, insulin resistance, and other components of metabolic syndrome. In MASLD, the metabolism of BAs is markedly disrupted, resulting in alterations in their synthesis, composition, and signaling activity. These changes contribute to hepatic steatosis, inflammation, and fibrosis, thereby exacerbating metabolic dysfunction and liver damage. The altered profiles and signaling activity of BAs in MASLD patients suggest that BAs act not only as biomarkers of disease severity, but also as active mediators of its pathogenesis. Modulators of BA signaling pathways, especially FXR agonists, are the focus of intense research for their potential to beneficially influence liver steatosis and inflammation in MASLD. Recent research has yielded promising results, indicating potential therapeutic application and the introduction of novel agents aimed at modulating BA homeostasis and function. This minireview outlines the physiological roles of BAs, seeks to advance the elucidation of the mechanisms by which their dysregulation contributes to MASLD progression, and highlights current and emerging therapeutic approaches. A deeper understanding of these complex interactions is essential for improving the diagnosis, prognosis and treatment of MASLD.

Background: There is increasing incidence of alcohol-associated liver disease in females. Despite this recent increased incidence, there is a paucity of research on the clinical course and outcomes of alcohol-associated hepatitis (AH) in females compared to males.

Aim: To assess if there may be sex differences in severity, outcomes, and healthcare utilization for patients hospitalized for AH.

Methods: This study used ICD-9-CM and ICD-10-CM codes to retrospectively identify inpatient encounters for AH at the University of Kentucky from 2012-2021 and obtained data on patient demographics and clinical outcomes. Encounters were cohorted by patient sex and differences in patient demographics and clinical outcomes were assessed. Multivariate logistic regression models were constructed to assess risk of mortality, sepsis, and mechanical ventilation during the encounter.

Results: Of 1386 subjects, 511 (36.9%) were female and 875 (63.1%) were male. Both sexes had similar baseline characteristics of race/ethnicity, discriminant function score, model of end-stage liver disease score, and length of hospital stay. However, the incidence of urinary tract infection, sepsis, and norepinephrine administration was significantly higher for females. Males had a significantly higher incidence of esophageal variceal bleed. On multivariate logistic regression analysis, females had higher odds of encounter sepsis (OR 1.41; 95%CI: 1.064-1.869) and mechanical ventilation (OR 1.352; 95%CI: 1.006-1.816). Odds of encounter mortality were significantly increased in encounters with sepsis (OR 2.309; 95%CI: 1.419-3.757) and mechanical ventilation (OR 9.301; 95%CI: 5.724-15.114).

Conclusion: This study shows sex-based differences in AH outcomes at the University of Kentucky. Future studies are warranted to assess whether tailoring treatments will improve clinical outcomes in females with AH.

Vitamin A is essential for vision, immunity, and cellular function, but excessive intake, known as hypervitaminosis A, leads to liver toxicity. Toxicity can be acute (from high single doses) or chronic (from prolonged overconsumption), causing symptoms like nausea, bone pain, and liver damage. The normal values of vitamin A in adults, measured as serum retinol, can range from 0.3 mg/L to 1.2 mg/L. The liver, which stores vitamin A in hepatic stellate cells, becomes overwhelmed, leading to retinoid accumulation, oxidative stress, and inflammation. Pathologically, vitamin A toxicity progresses from hepatic steatosis (fatty liver) to fibrosis and cirrhosis. Histological changes include hepatocellular ballooning, stellate cell activation, and perisinusoidal fibrosis. Molecular mechanisms involve oxidative stress from reactive oxygen species, apoptosis, and dysregulated pathways (tumor growth factor-beta, nuclear factor-kappa B), which drive fibrogenesis. Chronic toxicity also disrupts lipid metabolism, worsening liver injury. Clinically, management includes limiting vitamin A intake and exploring antioxidants (e.g., N-acetylcysteine) or anti-fibrotic therapies. Research gaps include the need for better biomarkers, personalized risk assessment, and refined dietary guidelines. Future studies should focus on therapeutic interventions and experimental models to improve outcomes. In conclusion, while vitamin A is vital, its toxicity poses serious hepatic risks. Understanding its mechanisms and developing targeted treatments are crucial for preventing liver damage and ensuring safe consumption.

Skeletal muscles perform important metabolic functions. Muscle mass wasting in sarcopenia is an urgent problem of modern medicine, the interest in which is related to its prognostic significance. The liver has numerous direct and indirect metabolic and immune connections with skeletal muscle and disruptions of these connections in liver disease are of clinical interest. A recent article by Liang et al emphasized potential biomarkers of sarcopenia in liver cirrhosis. Identification of biomarkers of sarcopenia in patients with cirrhosis has important diagnostic value. Common pathophysiologic mechanisms of sarcopenia and liver cirrhosis include disorders of protein and energy metabolism, disturbances in the structure of gut microbiota, inflammation and oxidative stress.

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, necessitating innovative treatment strategies. Surgical resection and liver transplantation continue to be the gold standards for early-stage HCC; however, advances in imaging and minimally invasive techniques have improved patient selection and outcomes. Additionally, the emergence of targeted therapies and immunotherapy has transformed the treatment landscape for advanced HCC. This review highlights the efficacy of agents such as tyrosine kinase inhibitors, alongside emerging options like immune checkpoint inhibitors, which have shown promise in clinical trials. Furthermore, the role of locoregional therapies, including ablation in the setting of combined treatment, transarterial chemoembolization and transarterial radioembolization with flow catheters, cone-beam computed tomography and 4D navigation guidance, is examined in the context of bridging therapies for patients awaiting surgical intervention. The integration of multidisciplinary care approaches and personalized treatment plans is crucial for optimizing outcomes. Future directions for HCC treatment are discussed, including the potential of novel biomarkers in prognosis and treatment response. This comprehensive overview aims to equip clinicians with the latest insights and foster collaborative efforts to improve HCC patient management and survival rates.

Targeting the gut-liver axis has emerged as a promising strategy in the treatment of metabolic dysfunction-associated steatotic liver disease (MASLD), a condition that currently represents the most common cause of chronic liver disease worldwide. Within this axis, the duodenum serves not only as a site of nutrient absorption but also as a metabolic sensor capable of influencing systemic and hepatic homeostasis. We have read with great interest the recent study by Yu et al, investigating the effects of duodenal mucosal ablation (DMA) by irreversible electroporation in a rat model of MASLD. The authors reported remarkable reductions in hepatic lipid content, improvements in serum lipid profiles, and both structural and functional changes in the intestinal mucosa, including alterations in enteroendocrine signaling. These results corroborate the pivotal role of the gut-liver axis in the pathogenesis of MASLD and highlight the potential of minimally invasive approaches targeting the proximal intestine. In this letter, we discuss the broader implications of these findings, emphasizing the translational relevance of intestinal modulation strategies in the comprehensive treatment of MASLD.

Background: Whether rtS106C+H126Y+D134E/rtS106C+H126Y+D134E+L269I (rtCYE/rtCYEI) mutations in the hepatitis B virus (HBV) reverse-transcriptase (RT) region are associated with tenofovir disoproxil fumarate (TDF) resistance is controversial.

Aim: To evaluate the presence of the rtCYE/rtCYEI mutations in a large cohort of Chinese patients with chronic HBV infection.

Methods: A total of 28236 patients who underwent drug resistance testing at the Fifth Medical Center of Chinese PLA General Hospital from 2007 to 2019 were enrolled. All patients received nucleoside/nucleotide analogues (NAs) therapy, and serum samples were collected for sequence analysis of the HBV RT domain with mutation analysis.

Results: The detection rates of a single mutation of rtS106C, rtH126Y, rtD134E, and rtL269I were 8.21%, 3.20%, 2.55% and 61.49% in 23718 genotype C patients, and 1.31%, 1.76%, 0.21%, and 92.33% in 4266 genotype B patients, respectively. The combined mutations of rtCYE/rtCYEI were only detected in 12 genotype C patients, accounting for 0.042% of all patients. These 12 patients had received NA treatments except TDF before testing. Among them, 6 patients had coexisting rtCYE/rtCYEI and lamivudine-resistance mutations, and 2 patients had coexisting rtCYE/rtCYEI and adefovir-resistance mutations. Compared with the wild-type (WT) strain, the replication capacity of rtCYE/rtCYEI mutants from representative patients decreased by 41.1%-71.8%, and TDF susceptibility reduced by less than 2-fold, but rtCYEI+rtA181V/N236T mutants exhibited a 6.2-/9.9-fold decrease in TDF susceptibility. Molecular modeling showed that rtCYE/rtCYEI mutants had a slight decrease in binding energy to TDF compared to the WT strain. In the clinic, emergence of the rtCYE/rtCYEI mutations was not specifically associated with TDF treatment.

Conclusion: HBV rtCYE/rtCYEI mutations have a limited effect on TDF susceptibility and are not sufficient to cause TDF resistance.