World Journal of Gastroenterology最新文献

This article reviews of the original research published by Wu et al in the World Journal of Gastroenterology, delving into the pivotal role of the gut microbiota in the pathogenesis of Crohn's disease (CD). Insights were gained from fecal microbiota transplantation (FMT) in mouse models, revealing the intricate interplay between the gut microbiota, mesenteric adipose tissue (MAT), and creeping fat. The study uncovered the characteristics of inflammation and fibrosis in the MAT and intestinal tissues of patients with CD; moreover, through the FMT mouse model, it observed the impact of samples from healthy patients and those with CD on symptoms. The pathogenesis of CD is complex, and its etiology remains unclear; however, it is widely believed that gut microbiota dysbiosis plays a significant role. Recently, with the development and application of next-generation sequencing technology, research on the role of fungi in the pathogenesis and chronicity of CD has deepened. This editorial serves as a supplement to the research by Wu et al who discussed advances related to the study of fungi in CD.

Liver cancer is associated with a few factors, such as viruses and alcohol consumption, and hepatectomy is an important treatment for patients with liver cancer. However, post-hepatectomy liver failure (PHLF) is the most serious complication and has a high mortality rate. Effective prediction of PHLF allows for the adjustment of clinical treatment strategies and is critical to the long-term prognosis of patients. Many factors have been associated with the development of PHLF, so there is an increasing interest in the development of predictive models for PHLF, such as nomograms that integrate intra-operative factors, imaging and biochemical characteristics of the patient. Ultrasound, as a simple and important examination method, plays an important role in predicting PHLF, especially the Nomogram established based on ultrasound measurements of liver stiffness and spleen area provides a more convenient way to predict the occurrence of PHLF.

Considering the bidirectional crosstalk along the gut-liver axis, gut-derived microorganisms and metabolites can be released into the liver, potentially leading to liver injury. In this editorial, we comment on several studies published in the recent issue of the World Journal of Gastroenterology. We focus specifically on the roles of gut microbiota in selected gastrointestinal (GI) diseases that are prevalent, such as inflammatory bowel disease, metabolic dysfunction-associated steatotic liver disease, and hepatitis B virus-related portal hypertension. Over the past few decades, findings from both preclinical and clinical studies have indicated an association between compositional and metabolic changes in the gut microbiota and the pathogenesis of the aforementioned GI disorders. However, studies elucidating the mechanisms underlying the host-microbiota interactions remain limited. The purpose of this editorial is to summarize current findings and provide insights regarding the context-specific roles of gut microbiota. Ultimately, the discovery of microbiome-based biomarkers may facilitate disease diagnosis and the development of personalized medicine.

Esophageal squamous cell carcinoma (ESCC) is the most common histological type of esophageal cancer with a poor prognosis. Early diagnosis and prognosis assessment are crucial for improving the survival rate of ESCC patients. With the advancement of artificial intelligence (AI) technology and the proliferation of medical digital information, AI has demonstrated promising sensitivity and accuracy in assisting precise detection, treatment decision-making, and prognosis assessment of ESCC. It has become a unique opportunity to enhance comprehensive clinical management of ESCC in the era of precision oncology. This review examines how AI is applied to the diagnosis, treatment, and prognosis assessment of ESCC in the era of precision oncology, and analyzes the challenges and potential opportunities that AI faces in clinical translation. Through insights into future prospects, it is hoped that this review will contribute to the real-world application of AI in future clinical settings, ultimately alleviating the disease burden caused by ESCC.

A recently published article in the World Journal of Gastroenterology clarified that elafibranor, a dual peroxisome proliferator activated receptor α/δ (PPARα/δ) agonist, reduced inflammation and fibrosis in alcohol-associated liver disease (ALD). This letter aims to discuss the findings presented in that article. ALD is a global health problem, and no effective drugs has been approved by the Food and Drug Administration to cure it. Thus, finding targeted therapies is of great urgency. Herein, we focus on the pathogenesis of ALD and the role of PPARα/δ in its development. Consistent with the conclusion of the article of interest, we think that elafibranor may be a promising therapeutic option for ALD, due to the pivotal involvement of PPARα/δ in the pathogenesis of the disease. However, its treatment dose, timing, and side effects need to be further investigated in future studies.

As a research hotspot in the field of molecular biology, N6-methyladenosine (m6A) modification has made progress in the treatment of colorectal cancer (CRC), leukemia and other cancers. Numerous studies have demonstrated that the tumour microenvironment (TME) regulates the level of m6A modification in the host and activates a series of complex epigenetic signalling pathways through interactions with CRC cells, thus affecting the progression and prognosis of CRC. However, with the diversity in the composition of TME factors, this action is reciprocal and complex. Encouragingly, some studies have experimentally revealed that the intestinal flora can alter CRC cell proliferation by directly acting on m6A and thereby altering CRC cell proliferation. This review summarizes the data, supporting the idea that the intestinal flora can influence host m6A levels through pathways such as methyl donor metabolism and thus affect the progression of CRC. We also review the role of m6A modification in the diagnosis, treatment, and prognostic assessment of CRC and discuss the current status, limitations, and potential clinical value of m6A modification in this field. We propose that additional in-depth research on m6A alterations in CRC patients and their TME-related targeted therapeutic issues will lead to better therapeutic outcomes for CRC patients.

We have read the article by Qu et al with great interest, as it presents an integration of endoscopic polidocanol foam sclerotherapy with rubber band ligation in patients with Grade II-III internal hemorrhoids. The authors conducted a prospective, multicenter, randomized study to evaluate the long-term symptomatic and endoscopic efficacy of this combined intervention. In this discussion, we focus on the procedural steps of this combined strategy and suggest potential avenues for future research.

Helicobacter pylori (H. pylori) infection affects a substantial proportion of the global population and causes various gastric disorders, including gastric cancer. Recent studies have found an inverse relationship between H. pylori infection and esophageal cancer (EC), suggesting a protective role against EC. This editorial focuses on the possible mechanisms underlying the role of H. pylori infection in EC and explores the role of gut microbiota in esophageal carcinogenesis and the practicality of H. pylori eradication. EC has two major subtypes: Esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC), which have different etiologies and risk factors. Gut microbiota can contribute to EC via inflammation-induced carcinogenesis, immunomodulation, lactagenesis, and genotoxin production. H. pylori infection is said to be inversely related to EAC, protecting against EAC by inducing atrophic gastritis, altering serum ghrelin levels, and triggering cancer cell apoptosis. Though H. pylori infection has no significant association with ESCC, COX-2-1195 polymorphisms and endogenous nitrosamine production can impact the risk of ESCC in H. pylori-infected individuals. There are concerns regarding a plausible increase in EC after H. pylori eradication treatments. However, H. pylori eradication is not associated with an increased risk of EC, making it safe from an EC perspective.

The challenge of diagnosis delay in inflammatory bowel disease (IBD) has emerged as a significant concern for both patients and healthcare professionals. The widely accepted notion that there is an extended time frame from the onset of symptoms to the definitive diagnosis is often attributed to the heterogeneity of IBD and the non-specificity of clinical manifestations. Specific to patients with Crohn's disease, the issue of delayed diagnosis appears to be more pronounced across different regions globally. The intricate interplay of real-world factors has led to debates regarding the primary contributors to these diagnostic delays. Drawing a comparison solely between patients and physicians and implicating the latter as the predominant influence factor may fall into a simplistic either-or logical trap that may obscure the truth. This letter, grounded in published evidence, explores areas for improvement in a forthcoming paper within the field, hoping to pinpoint the culprit behind the diagnosis delay issue for IBD patients rather than simply attributing it to so-called "physician-dependent factors". Our objective is to motivate healthcare providers and policymakers in relevant fields to reflect on strategies for addressing this problem to reduce diagnostic delays and enhance patient outcomes.

Background: The incidence of oesophageal adenocarcinoma (OAC) has been reported to be increasing in many countries. Alongside this trend, an increase in incidence of early-onset OAC, defined as OAC in adults aged under 50 years, has been observed. It is unclear whether survival outcomes for early-onset OAC patients differ from older age groups.

Aim: To investigate survival outcomes in early-onset OAC patients.

Methods: Ovid Medline and Embase were searched from inception to January 2022 for relevant studies relating to early-onset OAC and survival outcomes. Results regarding the overall five-year survival and risk of death of younger and older patients with OAC were extracted and pooled using meta-analyses to produce pooled estimates and 95%CIs where possible.

Results: Eleven studies which compared survival of early-onset OAC, defined as age at diagnosis of < 50 years, with older patients were included. A narrative review of median and mean survival demonstrated conflicting results, with studies showing early-onset OAC patients having both better and worse outcomes compared to older age groups. A meta-analysis of five-year survival demonstrated similar outcomes across age groups, with 22%-25% of patients in the young, middle and older age groups alive after five years. A meta-analysis of four studies demonstrated that early-onset OAC patients did not have a significantly increased risk of death compared to middle-aged patients (hazard ratio 1.12, 95%CI: 0.85-1.47).

Conclusion: Results suggest that early-onset OAC patients do not have a significantly different survival compared to older patients, but further population-based research, taking into account stage and treatment, is required.