World Journal of Gastroenterology最新文献

Hemorrhoids are a common and painful condition, with conventional treatments such as endoscopic rubber band ligation (ERBL) and injection sclerotherapy often falling short due to high recurrence rates and significant post-operative pain. A clinical trial by Qu et al introduces a novel approach called endoscopic poli-docanol foam sclerobanding (EFSB). This multicenter randomized trial involved 195 patients with grade II and III internal hemorrhoids and demonstrated that EFSB significantly reduced recurrence rates and post-procedural pain while improving symptom relief and patient satisfaction compared to ERBL. The study's strengths include its robust design, comprehensive outcome evaluation, and patient-centered approach. Despite limitations such as the single-blind design and relatively short follow-up period, the findings suggest that EFSB could enhance clinical practice by offering a more effective and patient-friendly treatment option. Further research is needed to validate these results and explore the long-term benefits and cost-effectiveness of EFSB.

Background: Surgical resection and liver transplantation (LT) are the most effective curative options for hepatocellular carcinoma (HCC). However, few patients with huge HCC (> 10 cm in diameter), especially those with portal vein tumor thrombus (PVTT), can receive these treatments. Selective internal radiation therapy (SIRT) can be used as a conversion therapy for them because it has the dual benefit of shrinking tumors and increasing residual hepatic volume. However, in patients with huge HCC, high lung absorbed dose often prevents them from receiving SIRT.

Case summary: A 35-year-old man was admitted because of emaciation and pain in the hepatic region for about 1 month. The computed tomography scan showed a 20.2 cm × 19.8 cm tumor located in the right lobe-left medial lobes with right portal vein and right hepatic vein invasion. After the pathological type of HCC was confirmed by biopsy, two conversions were presented. The first one was drug-eluting bead transarterial chemoembolization plus hepatic arterial infusion chemotherapy and lenvatinib and sintilimab, converted to SIRT, and the second one was sequential SIRT with continued systemic treatment. The tumor size significantly decreased from 20.2 cm × 19.8 cm to 16.2 cm × 13.8 cm, then sequentially to 7.8 cm × 6.8 cm. In the meantime, the ratio of spared volume to total liver volume increased gradually from 34.4% to 55.7%, then to 62.9%. Furthermore, there was visualization of the portal vein, indicating regression of the tumor thrombus. Finally, owing to the new tumor in the left lateral lobe, the patient underwent LT instead of resection without major complications.

Conclusion: Patients with inoperable huge HCC with PVTT could be converted to SIRT first and accept surgery sequentially.

In recent years, with the extensive application of immunotherapy in clinical practice, it has achieved encouraging therapeutic effects. While enhancing clinical efficacy, however, it can also cause autoimmune damage, triggering immune-related adverse events (irAEs). Reports of immunotherapy-induced gastritis have been increasing annually, but due to its atypical clinical symptoms, early diag-nosis poses a certain challenge. Furthermore, it can lead to severe complications such as gastric bleeding, elevating the risk of adverse outcomes for solid tumor patients if immunotherapy is interrupted. Therefore, gaining a thorough under-standing of the pathogenesis, clinical manifestations, diagnostic criteria, and treatment of immune-related gastritis is of utmost importance for early identification, diagnosis, and treatment. Additionally, the treatment of immune-related gastritis should be personalized according to the specific condition of each patient. For patients with grade 2-3 irAEs, restarting immune checkpoint inhibitors (ICIs) therapy may be considered when symptoms subside to grade 0-1. When restarting ICIs therapy, it is often recommended to use different types of ICIs. For grade 4 irAEs, permanent discontinuation of the medication is necessary.

This letter emphasizes the need to expand discussions on gut microbiome's role in inflammatory bowel disease (IBD) and colorectal cancer (CRC) by including the often-overlooked non-bacterial components of the human gut flora. It highlights how viral, fungal and archaeal inhabitants of the gut respond towards gut dys-biosis and contribute to disease progression. Viruses such as bacteriophages target certain bacterial species and modulate the immune system. Other viruses found associated include Epstein-Barr virus, human papillomavirus, John Cunningham virus, cytomegalovirus, and human herpes simplex virus type 6. Fungi such as Candida albicans and Malassezia contribute by forming tissue-invasive filaments and producing inflammatory cytokines, respectively. Archaea, mainly metha-nogens are also found altering the microbial fermentation pathways. This corres-pondence, thus underscores the significance of considering the pathological and physiological mechanisms of the entire spectrum of the gut microbiota to develop effective therapeutic interventions for both IBD and CRC.

Background: This study examines the complex relationships among the neuroendocrine axis, gut microbiome, inflammatory responses, and gastrointestinal symptoms in patients with irritable bowel syndrome (IBS). The findings provide new insights into the pathophysiology of IBS and suggest potential therapeutic targets for improving patient outcomes.

Aim: To investigate the interactions between the neuroendocrine axis, gut microbiome, inflammation, and gastrointestinal symptoms in patients with IBS.

Methods: Patients diagnosed with IBS between January 2022 and January 2023 were selected for the study. Healthy individuals undergoing routine check-ups during the same period served as the control group. Data were collected on neuroendocrine hormone levels, gut microbiome profiles, inflammatory biomarkers, and gastrointestinal symptomatology to analyze their interrelations and their potential roles in IBS pathogenesis.

Results: IBS patients exhibited significant dysregulation of the neuroendocrine axis, with altered levels of cortisol, serotonin, and neuropeptides compared to healthy controls. The gut microbiome of IBS patients showed reduced diversity and specific alterations in bacterial genera, including Bifidobacterium, Lactobacillus, and Faecalibacterium, which were associated with neuroendocrine disturbances. Additionally, elevated levels of inflammatory markers, such as C-reactive protein, interleukin-6, and tumor necrosis factor-α, were observed and correlated with the severity of gastrointestinal symptoms like abdominal pain, bloating, and altered bowel habits.

Conclusion: The findings suggest that targeting the neuroendocrine axis, gut microbiome, and inflammatory pathways may offer novel therapeutic strategies to alleviate symptoms and improve the quality of life in IBS patients.

This editorial examines the therapeutic potential of traditional Chinese medicine (TCM) for aggressive cancers, particularly liver cancer. It highlights the study by Huang et al, which shows how Calculus bovis, a component of the TCM Pien Tze Huang, suppresses liver cancer by inhibiting M2 macrophage polarization via the Wnt/β-catenin pathway. This research emphasizes the importance of transitioning from effective TCM formulations to isolating active components and understanding their mechanisms. While the study provides valuable insights, it primarily focuses on the Wnt/β-catenin pathway and does not delve deeply into the mechanisms of individual components. Future research should aim to comprehensively study these components, explore their interactions, and validate findings through clinical trials. This approach will integrate traditional wisdom with modern scientific validation, advancing the development of innovative cancer treatments based on TCM formulations.

In this editorial, we examine a paper by Koizumi et al, on the role of peroxisome proliferator-activated receptor (PPAR) agonists in alcoholic liver disease (ALD). The study determined whether elafibranor protected the intestinal barrier and reduced liver fibrosis in a mouse model of ALD. The study also underlines the role of PPARs in intestinal barrier function and lipid homeostasis, which are both affected by ALD. Effective therapies are necessary for ALD because it is a critical health issue that affects people worldwide. This editorial analyzes the possibility of PPAR agonists as treatments for ALD. As key factors of inflammation and metabolism, PPARs offer multiple methods for managing the complex etiology of ALD. We assess the abilities of PPARα, PPARγ, and PPARβ/δ agonists to prevent steatosis, inflammation, and fibrosis due to liver diseases. Recent research carried out in preclinical and clinical settings has shown that PPAR agonists can reduce the severity of liver disease. This editorial discusses the data analyzed and the obstacles, advantages, and mechanisms of action of PPAR agonists for ALD. Further research is needed to understand the efficacy, safety, and mechanisms of PPAR agonists for treating ALD.

In this editorial, we comment on an article published in the recent issue of the World Journal of Gastroenterology. Celiac disease (CeD) is a disease occurring in genetically susceptible individuals, which is mainly characterized by gluten intolerance in the small intestine and clinical symptoms such as abdominal pain, diarrhea, and malnutrition. Therefore, patients often need a lifelong gluten-free diet, which greatly affects the quality of life and expenses of patients. The gold standard for diagnosis is intestinal mucosal biopsy, combined with serological and genetic tests. At present, the lack of safe, effective, and satisfactory drugs for CeD is mainly due to the complexity of its pathogenesis, and it is difficult to find a perfect target to solve the multi-level needs of patients. In this editorial, we mainly review the pathological mechanism of CeD and describe the current experimental and improved drugs for various pathological aspects.

In this editorial, we comment on the recent article by Huang et al. The editorial focuses specifically on the molecular mechanisms of hepatocellular carcinoma (HCC), mechanism of Wnt/β-catenin pathway in HCC, and protective mechanism of Calculus bovis (CB) in HCC. Liver cancer is the fourth most common cause of cancer-related deaths globally. The most prevalent kind of primary liver cancer, HCC, is typically brought on by long-term viral infections (hepatitis B and C), non-alcoholic steatohepatitis, excessive alcohol consumption, and other conditions that can cause the liver to become chronically inflamed and cirrhotic. CB is a well-known traditional remedy in China and Japan and has been used extensively to treat a variety of diseases, such as high fever, convulsions, and stroke. Disturbances in lipid metabolism, cholesterol metabolism, bile acid metabolism, alcohol metabolism, and xenobiotic detoxification lead to fatty liver disease and liver cirrhosis. Succinate, which is a tricarboxylic acid cycle intermediate, is vital to energy production and mitochondrial metabolism. It is also thought to be a signaling molecule in metabolism and in the development and spread of liver malignancies. The Wnt/β-catenin pathway is made up of a group of proteins that are essential for both adult tissue homeostasis and embryonic development. Cancer is frequently caused by the dysregulation of the Wnt/β-catenin signaling pathway. In HCC liver carcinogenesis, Wnt/β-catenin signaling is activated by the expression of downstream target genes. Communication between the liver and the gut exists via the portal vein, biliary tract, and systemic circulation. This "gut-liver axis" controls intestinal physiology. One of the main factors contributing to the development, progression, and treatment resistance of HCC is the abnormal activation of the Wnt/β-Catenin signaling pathway. Therefore, understanding this pathway is essential to treating HCC. Eleven ingredients of CB, particularly oleanolic acid, ergosterol, and ursolic acid, have anti-primary liver cancer properties. Additionally, CB is important in the treatment of primary liver cancer through pathways linked to immune system function and apoptosis. CB also inhibits the proliferation of cancer stem cells and tumor cells and controls the tumor microenvironment. In the future, clinicians may be able to recommend one of many potential new drugs from CB ingredients to treat HCC expression, development, and progress.

Fusobacterium nucleatum (F. nucleatum) is a Gram-negative anaerobic bacterium that plays a key role in the development of oral inflammation, such as periodontitis and gingivitis. In the last 10 years, F. nucleatum has been identified as a prevalent bacterium associated with colorectal adenocarcinoma and has also been linked to cancer progression, metastasis and poor disease outcome. While the role of F. nucleatum in colon carcinogenesis has been intensively studied, its role in gastric carcinogenesis is still poorly understood. Although Helicobacter pylori infection has historically been recognized as the strongest risk factor for the development of gastric cancer (GC), with recent advances in DNA sequencing technology, other members of the gastric microbial community, and F. nucleatum in particular, have received increasing attention. In this review, we summarize the existing knowledge on the involvement of F. nucleatum in gastric carcinogenesis and address the potential translational and clinical significance of F. nucleatum in GC.