World Journal of Gastroenterology最新文献

Neurosurgical patients, including those with severe traumatic brain injury, spinal cord injury, stroke, or raised intracranial pressure, are at heightened risk for stress ulcers and aspiration pneumonitis, leading to significant morbidity and mortality. These patients are typically managed through both pharmacological interventions [e.g., proton pump inhibitors (PPIs), histamine 2 (H2) antagonists, sucralfate] and non-pharmacological measures (e.g., nasogastric decompression, patient positioning) to mitigate adverse outcomes. The pathogenesis of stress ulcers in neurosurgical patients is multifactorial, but the routine use of stress ulcer prophylaxis remains controversial. While gastric acid suppression with H2 receptor antagonists and PPIs is commonly employed, concerns have arisen regarding the association between elevated gastric pH, bacterial colonization, and ventilator-associated pneumonia. The lack of comprehensive data on gastroprotection in critically ill neurosurgical patients, who face a greater risk than non-neurosurgical counterparts, further complicates this issue. Recent studies, such as one by Gao et al on the efficacy of vonoprazan-amoxicillin dual therapy in elderly patients, highlight the potential of novel therapies, but the influence of pre-existing conditions like Helicobacter pylori infection remains unclear. Non-pharmacological interventions, including nasogastric decompression and early enteral nutrition, are critical in improving outcomes but require further research to refine strategies. This editorial underscores the need for tailored approaches and encourages further investigation into optimal gastroprotective strategies for neurosurgical patients.

This paper highlights the innovative approach and findings of the recently published study by Xu et al, which underscores the integration of radiomics and clinicoradiological factors to enhance the preoperative prediction of microvascular invasion in patients with hepatitis B virus-related hepatocellular carcinoma (HBV-HCC). The study's use of contrast-enhanced computed tomography radiomics to construct predictive models offers a significant advancement in the surgical planning and management of HBV-HCC, potentially transforming patient outcomes through more personalized treatment strategies. This editorial commends the study's contribution to precision medicine and discusses its implications for future research and clinical practice.

In this manuscript, we provide critical commentary on the systematic review by Augustin et al, which investigated acute pancreatitis induced by primary hyperparathyroidism during pregnancy. Although this is an infrequent complication, it poses severe risks to both maternal and fetal health. Due to its infrequent occurrence in clinical practice, this review is based on an analysis of individual case reports over the past 55 years. While this is not the first study to utilize this sampling method for primary hyperparathyroidism-induced acute pancreatitis, it is unique in that it has a sufficiently large sample size with statistically significant results. Our discussion focuses on the diagnostic challenges associated with this condition, which are grounded in the mechanisms of parathyroid hormone secretion and variations in serum calcium levels. We also address the limitations of the current review and suggest potential strategies to increase diagnostic accuracy and improve health outcomes for both mothers and fetuses during pregnancy.

Background: Excessive endoplasmic reticulum (ER) stress in intestinal epithelial cells can lead to damage to the intestinal mucosal barrier, activate the signal transducer and activator of transcription 3 (STAT3)/nuclear factor kappa B (NF-κB) signaling pathway, and exacerbate the inflammatory response, thus participating in the pathogenesis of ulcerative colitis (UC). Mesalazine is a commonly used drug in the clinical treatment of UC. However, further studies are needed to determine whether mesalazine regulates the ER stress of intestinal epithelial cells, down-regulates the STAT3/NF-κB pathway to play a role in the treatment of UC.

Aim: To study the therapeutic effects of mesalazine on spontaneous colitis in interleukin-10 (IL-10)^-/- mice.

Methods: The 24-week-old IL-10^-/- mice with spontaneous colitis were divided into the model group and the 5-amino salicylic acid group. Littermates of wild-type mice of the same age group served as the control. There were eight mice in each group, four males and four females. The severity of symptoms of spontaneous colitis in IL-10^-/- mice was assessed using disease activity index scores. On day 15, the mice were sacrificed. The colon length was measured, and the histopathological changes and ultrastructure of colonic epithelial cells were detected. The protein expressions of STAT3, p-STAT3, NF-κB, IκB, p-IκB, and glucose-regulated protein 78 were identified using Western blotting. The STAT3 and NF-κB mRNA expressions were identified using real-time polymerase chain reaction. The glucose-regulated protein 78 and C/EBP homologous protein expressions in colon sections were detected using immunofluorescence.

Results: Mesalazine reduced the symptoms of spontaneous colitis in IL-10 knockout mice and the histopathological damage of colonic tissues, and alleviated the ER stress in epithelial cells of colitis mice. Western blotting and quantitative real-time polymerase chain reaction results showed that the STAT3/NF-κB pathway in the colon tissue of model mice was activated, suggesting that this pathway was involved in the pathogenesis of UC and might become a potential therapeutic target. Mesalazine could down-regulate the protein expressions of p-STAT3, NF-κB and p-IκB, and down-regulate the mRNA expression of STAT3 and NF-κB.

Conclusion: Mesalazine may play a protective role in UC by reducing ER stress by regulating the STAT3/NF-κB signaling pathway.

Functional constipation (FC) is the most common gastrointestinal disorder in children, with a global prevalence of 14.4% based on Rome IV criteria. This editorial explores the multifactorial pathogenesis and diagnostic complexity of FC, emphasizing the importance of early and accurate diagnosis. Effective management of FC hinges on child-oriented toilet training and the use of osmotic laxatives, particularly polyethylene glycol. Emerging therapies, including probiotics, serotonin 5-HT4 receptor agonists, chloride channel activators, and herbal remedies, offer promising options but require further research. Lifestyle modifications, such as adequate fiber and fluid intake and physiotherapy, are crucial in supporting pharmacological treatments. For intractable cases, a multidisciplinary approach involving pediatric specialists, nutritionists, physiotherapists, and psychologists is essential. This comprehensive strategy aims to improve the quality of life for children with FC and their families through continuous research, education, and collaborative care.

Helicobacter pylori (H. pylori) infection plays a critical role in gastric diseases, impacting the microbiota structure in gastric and duodenal ulcers. In their study, Jin et al utilized metagenomic sequencing to analyze mucosal samples from patients with ulcers and healthy controls, revealing significant changes in microbial diversity and composition. This article reviews their findings, emphasizing H. pylori's role in gastric ulcers and the need for further research on its impact on duodenal ulcers. We evaluate the study's strengths and limitations, suggesting future research directions to enhance our understanding of H. pylori's contribution to ulcerative diseases.

Background: Fungal esophagitis (FE) is caused by fungal invasion of the esophageal mucosa. Under endoscopy, the esophageal mucosa shows edema, congestion, erosion, and ulceration, and bleeds easily when touched, and the surface of the mucosa is covered with small white spots like "bean curd residue". Clinical cases showing typical FE under endoscopic imaging but negative esophageal mucosal brush (referred to as suspected FE) have increased the difficulty and challenge of clinical diagnosis and treatment. At present, the esophageal fungal flora of suspected case has not been thoroughly studied.

Aim: To characterize the fungal flora in FE, suspected FE, and the esophageal normal controls (NCs), and to identify marker species to improve detection of FE.

Methods: This was a case-control study. A total of 19 patients with FE, 16 with suspected FE, and 10 NCs were selected by endoscopy. The esophageal cell brush samples of each group were sequenced by internal transcribed spacer (ITS) 1 and analyzed by bioinformatics.

Results: In FE and suspected FE patients, species richness, species diversity and species evenness, as measured by the Chao1 index, Shannon index and Pielou index, were lower than in the NCs, and the comparison between the FE and NCs was the most significant (P < 0.05). Compared with the NCs, the relative abundance of Candida in FE and suspected FE patients was significantly increased (P < 0.001), while the relative abundance of Yarrowia was significantly decreased (P < 0.05). Moreover, Yarrowia abundance in the FE group was significantly lower than in the NCs and suspected FE groups (P < 0.001). The area under the curve for Candida in FE and suspected FE patients was 99.5% (P < 0.05) and 81.3% (P < 0.05), respectively. Finally, compared with FE patients, the relative abundance of Ascomycota and Candida in the esophageal flora of suspected FE patients was decreased, while the relative abundance of Yarrowia, Thermomyces and Pichia was increased.

Conclusion: ITS showed that composition of the fungal community was similar in the FE and suspected FE groups. ITS can be used as an auxiliary diagnostic method for FE and provide a theoretical basis for follow-up diagnosis and treatment.

This letter comments on the recently published manuscript by Yu et al, in which the authors revealed a novel mechanism by which the m6A-modified long noncoding RNA kinesin family member 9-antisense RNA 1 promotes stemness and sorafenib resistance of hepatocellular carcinoma (HCC) through ubiquitin-specific peptidase 1-mediated deubiquitination of oncogene short stature homeobox 2. Given the high mortality rate and poor prognosis of HCC, the findings by Yu et al open a new avenue for overcoming HCC burden by focusing on kinesin family member 9-antisense RNA 1 and short stature homeobox 2 as prognostic markers and therapeutic targets.

With the widespread use of upper gastrointestinal endoscopy, more and more gastric polyps (GPs) are being detected. Traditional management strategies often rely on histopathologic examination, which can be time-consuming and may not guide immediate clinical decisions. This paper aims to introduce a novel classification system for GPs based on their potential risk of malignant transformation, categorizing them as "good", "bad", and "ugly". A review of the literature and clinical case analysis were conducted to explore the clinical implications, management strategies, and the system's application in endoscopic practice. Good polyps, mainly including fundic gland polyps and inflammatory fibrous polyps, have a low risk of malignancy and typically require minimal or no intervention. Bad polyps, mainly including hyperplastic polyps and adenomas, pose an intermediate risk of malignancy, necessitating closer monitoring or removal. Ugly polyps, mainly including type 3 neuroendocrine tumors and early gastric cancer, indicate a high potential for malignancy and require urgent and comprehensive treatment. The new classification system provides a simplified and practical framework for diagnosing and managing GPs, improving diagnostic accuracy, guiding individualized treatment, and promoting advancements in endoscopic techniques. Despite some challenges, such as the risk of misclassification due to similar endoscopic appearances, this system is essential for the standardized management of GPs. It also lays the foundation for future research into biomarkers and the development of personalized medicine.

Background: The CRAFITY score is mainly utilized for hepatocellular carcinoma (HCC) patients receiving atezolizumab and bevacizumab, with little investigation in its predictive capacity for alternative regimens, such as lenvatinib and programmed cell death protein 1 (PD-1) inhibitors, which are widely utilized in Chinese clinical practice.

Aim: To look at the predictive significance of the CRAFITY score in HCC patients taking lenvatinib and PD-1 inhibitors.

Methods: The retrospective investigation consisted of 192 patients with incurable HCC who received lenvatinib and PD-1 inhibitors between January 2018 and January 2022. Patients were stratified according to CRAFITY score (based on baseline alpha-fetoprotein and C-reactive protein levels) into CRAFITY-low, CRAFITY-intermediate, and CRAFITY-high groups. Overall survival (OS) and progression-free survival (PFS) were assessed using Kaplan-Meier analysis, and independent prognostic factors were identified through Cox regression analysis. Nomograms were created to forecast survival for a year.

Results: The median PFS and OS were the longest for patients in the CRAFITY-low group, followed by those in the CRAFITY-intermediate and CRAFITY-high groups (median PFS: 8.4 months, 6.0 months, and 3.1 months, P < 0.0001; median OS: 33.4 months, 19.2 months, and 6.6 months, P < 0.0001). Both the objective response rate (5%, 19.6%, and 22%, P = 0.0669) and the disease control rate (50%, 76.5%, and 80%, P = 0.0023) were considerably lower in the CRAFITY-high group. The findings from the multivariate analysis showed that a nomogram which included the tumor number, prior transarterial chemoembolization history, and CRAFITY score predicted 12-month survival with an area under the curve of 0.788 (95% confidence interval: 0.718-0.859), which was in good agreement with actual data.

Conclusion: The CRAFITY score is a valuable predictor of survival and treatment outcomes in patients receiving lenvatinib and PD-1 inhibitors.