World Journal of Gastroenterology最新文献

Small cell lung cancer (SCLC) is a common type of primary lung cancer that contributes to approximately 15% of cases. It is closely associated with tobacco risk factors. It is also known as a type of lung cancer that has a high mortality rate within a short time due to its rapid growth rate (with tumor doubling time of 30 days) and its tendency to metastasize early in the disease process. The primary sites of metastasis in SCLC are similar to those in other primary lung cancers and often include the brain, bones, adrenal glands, liver, and lymph nodes. However, there are a few clinical reports of uncommon metastases, such as gastric metastasis from SCLC. Although the incidence of this clinical presentation is very low, reported cases have generally resulted in early mortality due to inadequate treatment. The purpose of this letter is to discuss the knowledge related to gastric metastasis from SCLC and remind clinical doctors not to miss atypical symptoms, thereby providing the right attitude to improve the prognosis for these patients.

Background: Submucosal invasion in early-stage gastric cancer (GC) is a critical determinant of prognosis and treatment strategy, significantly influencing the risk of lymph node metastasis and recurrence. Identifying risk factors associated with submucosal invasion is essential for optimizing patient management and improving outcomes.

Aim: To comprehensively analyze clinical, imaging, and endoscopic characteristics to identify predictors of submucosal invasion in patients with early-stage differentiated GC.

Methods: A retrospective study was conducted at our institution from January 2019 to January 2023, including 268 patients diagnosed with early-stage differentiated GC who underwent surgical resection or endoscopic submucosal dissection. Data were collected on demographic, clinical, imaging, and endoscopic characteristics, with endoscopic images reviewed independently by two gastroenterologists. Statistical analysis included univariate and multivariate logistic regression to identify significant predictors of submucosal invasion, and receiver operating characteristic (ROC) curve analysis to evaluate the predictive value of continuous variables.

Results: A total of 268 patients were included, with 178 males and 90 females, and a mean age of 61.5 ± 9.8 years. Univariate analysis showed that male gender, history of alcohol consumption, smoking, and computed tomography-detected gastric wall thickening were more prevalent in patients with submucosal invasion. Significant endoscopic predictors included tumor location in the upper two-thirds of the stomach, depressed morphology, marginal elevation, and high color differences on white-light endoscopy (WLE) and linked color imaging (LCI). Multivariate analysis identified upper stomach location [odds ratio (OR): 5.268], depressed type (OR: 5.841), marginal elevation (OR: 4.132), and LCI color difference ≥ 18.1 (OR: 4.479) as significant predictors. ROC analysis showed moderate predictive value for lesion diameter, WLE, and LCI color differences (area under the curve: 0.630, 0.799, and 0.760, respectively).

Conclusion: Depressed-type lesions, marginal elevation, location in the upper two-thirds of the stomach, and significant color differences on LCI are high-risk indicators for submucosal invasion. These findings suggest that such lesions warrant more aggressive intervention to prevent disease progression and improve patient outcomes.

Background: Helicobacter pylori (H. pylori) infection exhibits a familial clustering phenomenon.

Aim: To investigate the prevalence of H. pylori infection, identify associated factors, and analyze patterns of transmission within families residing in the community.

Methods: From July 2021 to September 2021, a total of 191 families (519 people) in two randomly chosen community health service centers in the Chengguan District of Lanzhou in Gansu Province, were recruited to fill out questionnaires and tested for H. pylori infection. Individuals were followed up again from April 2023 and June 2023 to test for H. pylori infection. The relationship between variables and H. pylori infection was analyzed using logistic regression and generalized linear mixed models.

Results: In 2021, the individual-based H. pylori infection rate was found to be 47.0% (244/519), which decreased to 38.1% (177/464) in 2023. Additionally, the rate of individual-based H. pylori new infection was 22.8% (55/241). The family-based H. pylori infection rate in 2021 was 76.9% (147/191), which decreased to 67.1% (116/173) in 2023, and the rate of family-based H. pylori new infection was 38.6% (17/44). Individual H. pylori infection was positively correlated with age, body mass index (BMI), eating food that was excessively hot, frequent acid reflux, bloating, and halitosis symptoms, and negatively correlated with family size and nut consumption. New individual H. pylori infection was positively correlated with BMI, other types of family structures, drinking purified water, and frequent heartburn symptoms, while negatively correlated with the use of refrigerators and following a regular eating schedule. A larger living area was an independent protective factor for H. pylori infection in households. Frequently consuming excessively hot food and symptoms of halitosis were independent risk factors for H. pylori infection in individuals; frequent consumption of nuts was an independent protective factor for H. pylori infection. Other types of family structure, drinking purified water, and frequent heartburn symptoms were independent risk factors for new individual H. pylori infection; the use of a refrigerator was an independent protective factor for new H. pylori infections.

Conclusion: The household H. pylori infection rate in Lanzhou is relatively high and linked to socio-demographic factors and lifestyles. Eradication efforts and control of related risk factors are recommended in the general population.

A recent study published in the World Journal of Gastroenterology, suggests that transplanting the gut microbiota from healthy donors can alleviate the pathological processes linked to inflammatory bowel disease (IBD), particularly Crohn's disease. In addition, that paper illustrates the effect of changes in the gut microbiota on IBD and points out that altered mesenteric adipose tissue caused by the gut microbiota and creeping fat lead to increased inflammation, which exacerbates IBD. Moreover, recent research has shown that the interaction between Helicobacter pylori (H. pylori) and the gut microbiota is mediated through immune mechanisms, resulting in a synergistic impact on IBD. Therefore, in this manuscript, we will focus on the role of the gut microbiota and H. pylori in the immune response to IBD, as well as the possible impact of H. pylori on the gut microbiota. We will also explore their individual and synergistic immune effects on IBD and look at future therapeutic perspectives for IBD.

This manuscript focused on the surgical challenge of urinary and sexual dysfunction after rectal cancer surgery based on the interesting results demonstrated by the observational study of Chen et al, which was published in the World Journal of Gastrointestinal Surgery. Urinary dysfunction occurs in one-third of patients treated for rectal cancer. Surgical nerve damage is the main cause of urinary dysfunction. Radiotherapy seems to exacerbate sexual dysfunction. The role of Denonvilliers' fascia preservation vs resection when performing total mesorectal excision (TME), the impact of robotic and transanal TME, alternatives to open and laparoscopic TME, as well as intraoperative pelvic neuromonitoring are discussed in this report. In conclusion, exact knowledge of the highly complex pelvic neuroanatomy and the use of novel surgical techniques can lead to a reduction in urinary and sexual dysfunction after rectal cancer surgery.

Background: Metabolic dysfunction-associated fatty liver disease (MAFLD) is one of the main chronic liver diseases. However, the roles of mitochondrial carnitine palmitoyl transferase-II (CPT-II) downregulation and liver cancer stem cell (LCSC) activation remain to be identified.

Aim: To investigate the dynamic alterations in CPT-II inactivity and LCSC activation during the malignant progression of MAFLD.

Methods: Dynamic models of mouse MAFLD were generated via the consumption of a high-fat diet or the addition of 2-fluorenylacetamide for hepatocarcinogenesis. The mice were divided into groups on the basis of hematoxylin and eosin staining. Biochemistries, CPT-II, intrahepatic T cells, and LCSCs were determined and confirmed in clinical samples. The mitochondrial membrane potential (MMP) was analyzed. Differentially expressed genes were screened via RNA sequencing and enriched in KEGG pathways or GO functions.

Results: Dynamic models of MAFLD malignant transformation were successfully generated on the basis of pathological examination. Hepatic lipid accumulation was associated with the loss of mitochondrial CPT-II activity and alterations in the MMP, with decreases in liver CD3+ or CD4+ T cells and increased AFP levels. In the lipid accumulation microenvironment, mitochondrial CPT-II was inactivated, followed by aberrant activation of CD44+ or CD24+ LCSCs, as validated in MAFLD or hepatocellular carcinoma patient samples. In terms of mechanism, the biological process category focused mainly on the metabolic regulation of cells in response to external stimuli. The enriched molecular functions included protein binding, cell apoptosis, and cell proliferation.

Conclusion: CPT-II inactivity promotes the malignant progression of MAFLD via the loss of innate immune function and abnormal LCSC activation.

In this article, we comment on the article by Qu and Li, focusing specifically on the non-invasive diagnostic approaches for metabolic dysfunction-associated steatotic liver disease (MASLD). MASLD is the most common chronic liver disease in children. Nearly half of pediatric MASLD cases progress to metabolic dysfunction-associated steatohepatitis at diagnosis, often with comorbidities like renal disease, hypertension, type 2 diabetes, and mental health disorders. Early diagnosis and continuous intervention are crucial for managing this "silent organ" disease. Screening is recommended for children aged nine and older with obesity. Liver biopsy remains the diagnostic gold standard; however, due to its invasiveness, non-invasive methods - biomarkers, anthropometric algorithms, serum tests, and imaging - are increasingly vital. This editorial provides an overview of the current non-invasive diagnostic approaches for pediatric MASLD or liver fibrosis.

Background: Human leukocyte antigen (HLA) class II molecules are cell surface receptor proteins found on antigen-presenting cells. Polymorphisms and mutations in the HLA gene can affect the immune system and the progression of hepatitis B.

Aim: To study the relation between rs2856718 of HLA-DQ, rs3077, and rs9277535 of HLA-DP, hepatitis B virus (HBV)-related cirrhosis, and hepatocellular carcinoma (HCC).

Methods: In this case-control study, the genotypes of these single nucleotide polymorphisms (SNPs) were screened in 315 healthy controls, 471 chronic hepatitis B patients, 250 patients with HBV-related liver cirrhosis, and 251 patients with HCC using TaqMan real-time PCR. We conducted Hardy-Weinberg equilibrium and linkage disequilibrium tests on the genotype distributions of rs2856718, rs3077, and rs9277535 before hierarchical clustering analysis to build the complex interaction between the markers in each patient group.

Results: The physical distance separating these SNPs was 29816 kB with the disequilibrium (D') values ranging from 0.07 to 0.34. The close linkage between rs3077 and rs9277535 was attributed to a distance of 21 kB. The D' value decreased from moderate in the healthy control group (D' = 0.50, P < 0.05) to weak in the hepatic disease group (D' < 0.3, P < 0.05). In a combination of the three variants rs2856718, rs3077, and rs9277535, the A allele decreased hepatic disease risk [A-A-A haplotype, risk ratio (RR) = 0.44 (0.14; 1.37), P < 0.05]. The G allele had the opposite effect [G-A/G-G haplotype, RR = 1.12 (1.02; 1.23), P < 0.05]. In liver cancer cases, the A-A-A/G haplotype increased the risk of HCC by 1.58 (P < 0.05).

Conclusion: Rs9277535 affects liver fibrosis progression due to HBV infection, while rs3077 is associated with a risk of HBV-related HCC. The link between rs2856718, rs3077, and rs9277535 and disease risk was determined using a multi-clustering analysis.

We read with great interest the systematic review and meta-analysis by Cigrovski Berkovic et al published recently, which evaluated the association between type 2 diabetes mellitus (T2DM) and pancreatic neuroendocrine tumors (pNETs). The study identified T2DM as a risk factor for the development of pNETs and linked it to poor tumor-free survival. However, due to the limited number of studies and high heterogeneity, the role of metformin in the diagnosis and prognosis of pNETs remained inconclusive. We believe the study has some limitations regarding literature search, risk of bias assessment, and analysis of heterogeneity and publication bias. Expanding the search to more databases, applying more appropriate bias assessment tools, and using better statistical methods to evaluate heterogeneity and publication bias would strengthen the study's conclusions. Addressing these concerns could provide more robust evidence for understanding the diagnostic and prognostic impact of T2DM in pNETs.

Dysfunction of the intestinal barrier is a prevalent phenomenon observed across a spectrum of diseases, encompassing conditions such as mesenteric artery dissection, inflammatory bowel disease, cirrhosis, and sepsis. In these pathological states, the integrity of the intestinal barrier, which normally serves to regulate the selective passage of substances between the gut lumen and the bloodstream, becomes compromised. This compromised barrier function can lead to a range of adverse consequences, including increased permeability to harmful substances, the translocation of bacteria and their products into systemic circulation, and heightened inflammatory responses within the gut and beyond. Understanding the mechanisms underlying intestinal barrier dysfunction in these diverse disease contexts is crucial for the development of targeted therapeutic interventions aimed at restoring barrier integrity and ameliorating disease progression. Lipocalin-2 (LCN2) expression is significantly upregulated during episodes of intestinal inflammation, making it a pivotal indicator for gauging the extent of such inflammatory processes. Notably, however, LCN2 derived from distinct cellular sources, whether intestinal epithelial cells or immune cells, exhibits notably divergent functional characteristics. Furthermore, the multifaceted nature of LCN2 is underscored by its varying roles across different diseases, sometimes even demonstrating contradictory effects.