World Journal of Gastroenterology最新文献

Background: Type II diabetes mellitus (T2DM) has been associated with increased risk of colon cancer (CC) and worse prognosis in patients with metastases. The effects of T2DM on postoperative chemoresistance rate (CRR) and long-term disease-free survival (DFS) and overall survival (OS) in patients with stage III CC who receive curative resection remain controversial.

Aim: To investigate whether T2DM or glycemic control is associated with worse postoperative survival outcomes in stage III CC.

Methods: This retrospective cohort study included 278 patients aged 40-75 years who underwent surgery for stage III CC from 2018 to 2021. Based on preoperative T2DM history, the patients were categorized into non-DM (n = 160) and DM groups (n = 118). The latter was further divided into well-controlled (n = 73) and poorly controlled (n = 45) groups depending on the status of glycemic control. DFS, OS, and CRR were compared between the groups and Cox regression analysis was used to identify risk factors.

Results: Patients in the DM and non-DM groups demonstrated similar DFS, OS, and CRR (DFS: 72.03% vs 78.75%, P = 0.178; OS: 81.36% vs 83.12%, P = 0.638; CRR: 14.41% vs 7.5%, P = 0.063). Poorly controlled DM was associated with a significantly worse prognosis and higher CRR than well-controlled DM (DFS: 62.22% vs 78.07%, P = 0.021; OS: 71.11% vs 87.67%, P = 0.011; CRR: 24.40% vs 8.22%, P = 0.015). High preoperative fasting plasma glucose [DFS: Hazard ratio (HR) = 2.684, P < 0.001; OS: HR = 2.105, P = 0.019; CRR: HR = 2.214, P = 0.005] and glycosylated hemoglobin levels (DFS: HR = 2.344, P = 0.006; OS: HR = 2.119, P = 0.021; CRR: HR = 2.449, P = 0.009) indicated significantly poor prognosis and high CRR, while T2DM history did not (DFS: HR = 1.178, P = 0.327; OS: HR = 0.933, P = 0.739; CRR: HR = 0.997, P = 0.581).

Conclusion: Increased preoperative fasting plasma glucose and glycosylated hemoglobin levels, but not T2DM history, were identified as risk factors associated with poor postoperative outcomes and high CRR in patients with stage III CC.

Background: Focal nodular hyperplasia (FNH)-like lesions are hyperplastic formations in patients with micronodular cirrhosis and a history of alcohol abuse. Although pathologically similar to hepatocellular carcinoma (HCC) lesions, they are benign. As such, it is important to develop methods to distinguish between FNH-like lesions and HCC.

Aim: To evaluate diagnostically differential radiological findings between FNH-like lesions and HCC.

Methods: We studied pathologically confirmed FNH-like lesions in 13 patients with alcoholic cirrhosis [10 men and 3 women; mean age: 54.5 ± 12.5 (33-72) years] who were negative for hepatitis-B surface antigen and hepatitis-C virus antibody and underwent dynamic computed tomography (CT) and magnetic resonance imaging (MRI), including superparamagnetic iron oxide (SPIO) and/or gadoxetic acid-enhanced MRI. Seven patients also underwent angiography-assisted CT.

Results: The evaluated lesion features included arterial enhancement pattern, washout appearance (low density compared with that of surrounding liver parenchyma), signal intensity on T1-weighted image (T1WI) and T2-weighted image (T2WI), central scar presence, chemical shift on in- and out-of-phase images, and uptake pattern on gadoxetic acid-enhanced MRI hepatobiliary phase and SPIO-enhanced MRI. Eleven patients had multiple small lesions (< 1.5 cm). Radiological features of FNH-like lesions included hypervascularity despite small lesions, lack of "corona-like" enhancement in the late phase on CT during hepatic angiography (CTHA), high-intensity on T1WI, slightly high- or iso-intensity on T2WI, no signal decrease in out-of-phase images, and complete SPIO uptake or incomplete/partial uptake of gadoxetic acid. Pathologically, similar to HCC, FNH-like lesions showed many unpaired arteries and sinusoidal capillarization.

Conclusion: Overall, the present study showed that FNH-like lesions have unique radiological findings useful for differential diagnosis. Specifically, SPIO- and/or gadoxetic acid-enhanced MRI and CTHA features might facilitate differential diagnosis of FNH-like lesions and HCC.

Alcohol-related liver disease (ALD), which is induced by excessive alcohol consumption, is a leading cause of liver-related morbidity and mortality. ALD patients exhibit a spectrum of liver injuries, including hepatic steatosis, inflammation, and fibrosis, similar to symptoms of nonalcohol-associated liver diseases such as primary biliary cholangitis, metabolic dysfunction-associated steatotic liver disease, and nonalcoholic steatohepatitis. Elafibranor has been approved for the treatment of primary biliary cholangitis and has been shown to improve symptoms in both animal models and in vitro cell models of metabolic dysfunction-associated steatotic liver disease and nonalcoholic steatohepatitis. However, the efficacy of elafibranor in treating ALD remains unclear. In this article, we comment on the recent publication by Koizumi et al that evaluated the effects of elafibranor on liver fibrosis and gut barrier function in an ALD mouse model. Their findings indicate the potential of elafibranor for ALD treatment, but further experimental investigations and clinical trials are warranted.

In this article, we comment on an article published in a recent issue of the World Journal of Gastroenterology. We specifically focus on the roles of human leukocyte antigen (HLA) and donor-specific antibodies (DSAs) in pediatric liver transplantation (LT), as well as the relationship between immune rejection after LT and DSA. Currently, LT remains the standard of care for pediatric patients with end-stage liver disease or severe acute liver failure. However, acute and chronic rejection continues to be a significant cause of graft dysfunction and loss. HLA mismatch significantly reduces graft survival and increases the risk of acute rejection. Among them, D→R one-way mismatch at three loci was significantly related to graft-versus-host disease incidence after LT. The adverse impact of HLA-DSAs on LT recipients is already established. Therefore, the evaluation of HLA and DSA is crucial in pediatric LT.

Inflammatory bowel disease, particularly Crohn's disease (CD), has been linked to modifications in mesenteric adipose tissue (MAT) and the phenomenon known as "creeping fat" (CrF). The presence of CrF is believed to serve as a predictor for early clinical recurrence following surgical intervention in patients with CD. Notably, the incorporation of the mesentery during ileocolic resection for CD has been correlated with a decrease in surgical recurrence, indicating the significant role of MAT in the pathogenesis of CD. While numerous studies have indicated that dysbiosis of the gut microbiota is a critical factor in the development of CD, the functional implications of translocated microbiota within the MAT of CD patients remain ambiguous. This manuscript commentary discusses a recent basic research conducted by Wu et al. In their study, intestinal bacteria from individuals were transplanted into CD model mice, revealing that fecal microbiota transplantation (FMT) from healthy donors alleviated CD symptoms, whereas FMT from CD patients exacerbated these symptoms. Importantly, FMT was found to affect intestinal permeability, barrier function, and the levels of proinflammatory factors and adipokines. Collectively, these findings suggest that targeting MAT and CrF may hold therapeutic potential for patients with CD. However, the study did not evaluate the composition of the intestinal microbiota of the donors or the subsequent alterations in the gut microbiota. Overall, the gut microbiota plays a crucial role in the histopathology of CD, and thus, targeting MAT and CrF may represent a promising avenue for treatment in this patient population.

Background: Rebleeding after recovery from esophagogastric variceal bleeding (EGVB) is a severe complication that is associated with high rates of both incidence and mortality. Despite its clinical importance, recognized prognostic models that can effectively predict esophagogastric variceal rebleeding in patients with liver cirrhosis are lacking.

Aim: To construct and externally validate a reliable prognostic model for predicting the occurrence of esophagogastric variceal rebleeding.

Methods: This study included 477 EGVB patients across 2 cohorts: The derivation cohort (n = 322) and the validation cohort (n = 155). The primary outcome was rebleeding events within 1 year. The least absolute shrinkage and selection operator was applied for predictor selection, and multivariate Cox regression analysis was used to construct the prognostic model. Internal validation was performed with bootstrap resampling. We assessed the discrimination, calibration and accuracy of the model, and performed patient risk stratification.

Results: Six predictors, including albumin and aspartate aminotransferase concentrations, white blood cell count, and the presence of ascites, portal vein thrombosis, and bleeding signs, were selected for the rebleeding event prediction following endoscopic treatment (REPET) model. In predicting rebleeding within 1 year, the REPET model exhibited a concordance index of 0.775 and a Brier score of 0.143 in the derivation cohort, alongside 0.862 and 0.127 in the validation cohort. Furthermore, the REPET model revealed a significant difference in rebleeding rates (P < 0.01) between low-risk patients and intermediate- to high-risk patients in both cohorts.

Conclusion: We constructed and validated a new prognostic model for variceal rebleeding with excellent predictive performance, which will improve the clinical management of rebleeding in EGVB patients.

In this editorial, we comment on the article by Meng et al. Chronic hepatitis B (CHB) is a significant global health problem, particularly in developing countries. Hepatitis B virus (HBV) infection is one of the most important risk factors for cirrhosis and hepatocellular carcinoma. Prevention and treatment of HBV are key measures to reduce complications. At present, drug therapy can effectively control virus replication and slow disease progression, but completely eliminating the virus remains a challenge. Anti-HBV treatment is a long-term process, and there are many kinds of antiviral drugs with different mechanisms of action, it is essential to evaluate the safety and efficacy of these drugs to reduce side effects and improve patients' compliance. We will summarize the current status of CHB drug treatment, hoping to provide a reference for the selection of clinical antiviral drugs.

Gastric polyps are commonly detected during upper gastrointestinal endoscopy. They are most often benign and rarely become malignant. Nevertheless, adequate knowledge, diagnostic modalities, and management strategies should be the endoscopist's readily available "weapons" to defeat the potentially malignant "enemies". This article sheds light on the valuable effort by Costa et al to generate a new classification system of gastric polyps as "good", "bad", and "ugly". This comprehensive overview provides clinicians with a simplified decision-making process.

Background: Regulator of G protein signaling (RGS) proteins participate in tumor formation and metastasis by acting on the α-subunit of heterotrimeric G proteins. The specific effect of RGS, particularly RGS4, on the progression of gastric cancer (GC) is not yet clear.

Aim: To explore the role and underlying mechanisms of action of RGS4 in GC development.

Methods: The prognostic significance of RGS4 in GC was analyzed using bioinformatics based public databases and verified by immunohistochemistry and quantitative polymerase chain reaction in 90 patients with GC. Function assays were employed to assess the carcinogenic impact of RGS4, and the mechanism of its possible influence was detected by western blot analysis. A nude mouse xenograft model was established to study the effects of RGS4 on GC growth in vitro.

Results: RGS4 was highly expressed in GC tissues compared with matched adjacent normal tissues. Elevated RGS4 expression was correlated with increased tumor-node-metastasis stage, increased tumor grade as well as poorer overall survival in patients with GC. Cell experiments demonstrated that RGS4 knockdown suppressed GC cell proliferation, migration and invasion. Similarly, xenograft experiments confirmed that RGS4 silencing significantly inhibited tumor growth. Moreover, RGS4 knockdown resulted in reduced phosphorylation levels of focal adhesion kinase, phosphatidyl-inositol-3-kinase, and protein kinase B, decreased vimentin and N-cadherin, and elevated E-cadherin.

Conclusion: High RGS4 expression in GC indicates a worse prognosis and RGS4 is a prognostic marker. RGS4 influences tumor progression via the focal adhesion kinase/phosphatidyl-inositol-3-kinase/protein kinase B pathway and epithelial-mesenchymal transition.

Background: Chronic hepatitis B often progresses silently toward hepatocellular carcinoma (HCC), a leading cause of mortality worldwide. Early detection of HCC is crucial, yet challenging.

Aim: To investigate the role of dynamic changes in alkaline phosphatase to prealbumin ratio (APR) in hepatitis B progression to HCC.

Methods: Data from 4843 patients with hepatitis B (January 2015 to January 2024) were analyzed. HCC incidence rates in males and females were compared using the log-rank test. Data were evaluated using Kaplan-Meier analysis. The Linear Mixed-Effects Model was applied to track the fluctuation of APR levels over time. Furthermore, Joint Modeling of Longitudinal and Survival data was employed to investigate the temporal relationship between APR and HCC risk.

Results: The incidence of HCC was higher in males. To ensure the model's normality assumption, this study applied a logarithmic transformation to APR, yielding ratio. Ratio levels were higher in females (t = 5.26, P < 0.01). A 1-unit increase in ratio correlated with a 2.005-fold higher risk of HCC in males (95%CI: 1.653-2.431) and a 2.273-fold higher risk in females (95%CI: 1.620-3.190).

Conclusion: Males are more prone to HCC, while females have higher APR levels. Despite no baseline APR link, rising APR indicates a higher HCC risk.