Evaluation of ERCP-related perforation: a single-center retrospective study.

Background: Endoscopic retrograde cholangiopancreatography (ERCP)-related perforation is a rare and serious adverse event. The aim of our study was to evaluate the risk factors and management of ERCP-related perforation, and to further determine the predictive factors associated with perforation outcome. Methods: A total of 27,018 ERCP procedures performed at the First Affiliated Hospital of Nanchang University (Nanchang, China) between January 2007 and March 2022 were included in the investigation of ERCP-related perforation. Medical records and endoscopic data were extracted to analyse the risk factors, management, and clinical outcome of ERCP-related perforation. Results: Seventy-six patients (0.28%) were identified as having experienced perforation following ERCP. Advanced age, Billroth II anatomy, precut sphincterotomy, and papillary balloon dilatation were significantly associated with ERCP-related perforation. Most patients with perforation (n = 65) were recognized immediately during ERCP whereas 11 were recognized later on. The delay in recognition primarily resulted from stent migration (n = 9). In addition, 12 patients experienced poor clinical outcome including death or hospice discharge (n = 3), ICU admission for >3 days (n = 6), and prolonged hospital stay for >1 month due to perforation (n = 3). Cancer and systemic inflammatory response syndrome (SIRS) are associated with a higher risk of poor outcome. Conclusions: Advanced age, Billroth II anatomy, precut sphincterotomy, and balloon dilation increase the risk of ERCP-related perforation whereas cancer and SIRS independently predicted poor clinical outcome.

Nomogram for predicting electrocoagulation syndrome after endoscopic submucosal dissection of esophageal tumors.

BACKGROUND: Endoscopic submucosal dissection (ESD) was widely used for the removal of esophageal tumors, and post-endoscopic submucosal dissection electrocoagulation syndrome (PEECS) was one of the postoperative adverse events. The aim of this research was to develop and validate a model to predict electrocoagulation syndrome after endoscopic submucosal dissection of esophageal tumors. MATERIALS AND METHODS: Patients who underwent esophageal ESD in our hospital were retrospectively included. A predictive nomogram was established based on the results of multivariate logistic regression analysis, and bootstrapping resampling was used for internal validation. Besides, the clinical usefulness of the nomogram was evaluated using decision curve analysis (DCA) and clinical impact curve. RESULTS: A total of 552 patients who underwent esophageal ESD were included in the study, and the incidence of PPECS was 12.5% (69/552). Risk factors associated with PEECS (p < 0.1) were analyzed by multivariate logistic regression analysis, and the final model included four variables, namely gender, diabetes, tumor size and operation time. The predictive nomogram was constructed based on the above four variables, and the area under the ROC curve (AUC) was 0.811 (95% CI 0.767-0.855). The calibration curve of the nomogram presented good agreement between the predicted and actual probabilities. DCA showed that the model improved patient outcomes by helping to assess the risk of PEECS in patients compared to an all-or-no treatment strategy. In addition, the clinical impact curve of the model also indicates that the nomogram has a high clinical net benefit. CONCLUSION: In conclusion, we have developed a predictive nomogram for PEECS after ESD for esophageal tumors with good predictive accuracy and discrimination. This predictive nomogram can be effectively used to identify high-risk patients with PEECS, which will help clinicians in clinical decision-making and early intervention.

Macrophage Tim-3 maintains intestinal homeostasis in DSS-induced colitis by suppressing neutrophil necroptosis.

T-cell immunoglobulin domain and mucin domain-3 (Tim-3) is a versatile immunomodulator that protects against intestinal inflammation. Necroptosis is a type of cell death that regulates intestinal homeostasis and inflammation. The mechanism(s) underlying the protective role of macrophage Tim-3 in intestinal inflammation is unclear; thus, we investigated whether specific Tim-3 knockdown in macrophages drives intestinal inflammation via necroptosis. Tim-3 protein and mRNA expression were assessed via double immunofluorescence staining and single-cell RNA sequencing (sc-RNA seq), respectively, in the colonic tissues of patients with inflammatory bowel disease (IBD) and healthy controls. Macrophage-specific Tim3-knockout (Tim-3M-KO) mice were generated to explore the function and mechanism of Tim-3 in dextran sodium sulfate (DSS)-induced colitis. Necroptosis was blocked by pharmacological inhibitors of receptor-interacting protein kinase (RIP)1, RIP3, and reactive oxygen species (ROS). Additionally, in vitro experiments were performed to assess the mechanisms of neutrophil necroptosis induced by Tim-3 knockdown macrophages. Although Tim-3 is relatively inactive in macrophages during colon homeostasis, it is highly active during colitis. Compared to those in controls, Tim-3M-KO mice showed increased susceptibility to colitis, higher colitis scores, and increased pro-inflammatory mediator expression. Following the administration of RIP1/RIP3 or ROS inhibitors, a significant reduction in intestinal inflammation symptoms was observed in DSS-treated Tim-3M-KO mice. Further analysis indicated the TLR4/NF-κB pathway in Tim-3 knockdown macrophages mediates the TNF-α-induced necroptosis pathway in neutrophils. Macrophage Tim-3 regulates neutrophil necroptosis via intracellular ROS signaling. Tim-3 knockdown macrophages can recruit neutrophils and induce neutrophil necroptosis, thereby damaging the intestinal mucosal barrier and triggering a vicious cycle in the development of colitis. Our results demonstrate a protective role of macrophage Tim-3 in maintaining gut homeostasis by inhibiting neutrophil necroptosis and provide novel insights into the pathogenesis of IBD.

Identification of basement membrane-related signatures for estimating prognosis, immune infiltration landscape and drug candidates in pancreatic adenocarcinoma.

Background: Pancreatic adenocarcinoma (PAAD) is a frequent digestive system cancer, which has high mortality and bad outcome. However, the role of basement membrane (BM)-related gene in assessing patient's outcome, microenvironment and treatment response remain unclear. Methods: Basement membrane (BM)-associated genes were detected by univariate and least absolute shrinkage and selection operator (LASSO) Cox regression analyses using data from the TCGA databases. A risk score system was constructed to distinguish patients in the high- and low-risk groups. Prognostic gene distribution in various immune cell forms was explored through scRNA-seq. Immune cell infiltration was assessed using CIBERSORT and ESTIMATE. The IC50 of common chemotherapeutic drugs and useful molecule compounds were evaluated. The mRNA and protein expression of important signatures were validated utilizing GEPIA and HPA databases. Results: Compared to low risk PAAD patients, PAAD patients with high risk showed a significant much worse overall survival (OS). Risk score of BM-associated genes could estimate patient outcome well, and areas under the curve (AUC) of receiver operating characteristic (ROC) survival curve were 0.76, 0.85, and 0.85 at 1-, 3-, and 5-year. Clinical impact curve (CIC) curve demonstrated the clinical importance of risk score. scRNA-seq revealed that BM-related genes were mainly distributed in malignant cells. Significant variations existed in the immune microenvironment, immune checkpoint expression and chemotherapy response between the studied groups. Furthermore, the mRNA expression levels of FAM83A, LY6D, MET, MUC16, MYEOV, and WNT7A were elevated in PAAD tissues, while the protein expression patterns of LY6D, MET, MUC16, and WNT7A were higher in tumor sample. RO-90-7501, Scriptaid, TG-101348, XMD-892, and XMD-1150 may be valuable small molecule drugs to treat PAAD. Conclusions: In conclusion, we develop a novel BM-related gene signature provide new insights and targets for the diagnosis, outcome estimation, candidate drugs and therapy management of PAAD patients.

NSUN6 Regulates NM23-H1 Expression in an m5C Manner to Affect Epithelial-Mesenchymal Transition in Lung Cancer.

PURPOSE: The expression and regulatory mechanism of NSUN6 in lung cancer are still unclear. Our study explored whether NSUN6 mediates progression of lung cancer by affecting NM23-H1 expression in an m5C-dependent manner. METHODS: qRT-PCR, CCK-8, colony formation, transwell, and Western blot analysis were employed to probe the impact of NSUN6 on lung cancer cell proliferation, migration, and epithelial-mesenchymal transition (EMT). RMVar database was utilized to forecast the downstream genes of NSUN6. The mode of interaction between NSUN6 and NM23-H1 was determined by dot blot, luciferase assay, m5C RIP, and cell function assays. The effect of NSUN6 expression on tumor growth was verified in vivo. RESULTS: Expression of NSUN6 was reduced in lung cancer cells, and over-expression of NSUN6 restricted the proliferation of lung cancer cells, migration, and EMT. NSUN6 regulated NM23-H1 expression by modifying the 3'-UTR of NM23-H1 mRNA through m5C and inhibited lung cancer cell proliferation, migration, and EMT. In vivo experiments also showed that over-expression of NSUN6 inhibited the occurrence of lung cancer. CONCLUSION: NSUN6 regulates NM23-H1 expression in an m5C-dependent manner to affect EMT in lung cancer. Thus, NSUN6 may be considered as a potential therapeutic target for lung cancer.

Intestinal barrier in inflammatory bowel disease: A bibliometric and knowledge-map analysis.

BACKGROUND: Barrier surfaces composed of specialized epithelial cells separate the host body from the external environment, and are essential for maintaining proper intestinal physiologic and immune homeostasis. AIM: To explore the development trends and research hotspots of intestinal barrier research in inflammatory bowel disease (IBD). METHODS: The publications related to the intestinal barrier in IBD were obtained from the Web of Science Core Collection database. Bibliometric analysis and visualization were conducted using VOSviewer, CiteSpace and R software. RESULTS: A total of 4482 articles published between 2002 and 2022 were identified. The United States is dominant in intestinal barrier research, whereas the University of Chicago is the most active institution. Jerrold from Harvard Medical School was the most productive authors with the most citations. The journals Inflammatory Bowel Disease and Gastroenterology have made significant contributions in this field. The keywords appearing at high frequency related to the intestinal barrier in IBD were detected, including nuclear factor kappa B, tumor necrosis factor-α, apoptosis, oxidative stress and probiotics. Among them, antioxidants, Akkermansia muciniphila, nanoparticles, short-chain fatty acids and extracellular vesicles have received growing interest in recent research. CONCLUSION: The intestinal barrier field is developing rapidly with extensive cooperation. Targeting the gut microbiota and dietary metabolism to regulate the intestinal barrier has shown promising prospective applications and has generated broad interest. The importance of the intestinal barrier in IBD is gradually being fully recognized, providing a new therapeutic perspective for improving inflammation and prognosis.

Mammalian cleavage factor 25 targets KLF14 to inhibit hepatic stellate cell activation and liver fibrosis.

Liver fibrosis is primarily caused by the activation of hepatic stellate cells (HSCs), which results from chronic liver damage. Understanding the pathogenesis of HSC activation could identify new therapeutic targets to treat liver fibrosis. In this study, we examined the protective role of the mammalian cleavage factor I 25 kD subunit (CFIm25, NUDT21) in inhibiting hepatic stellate cell activation. CFIm25 expression was measured in liver cirrhosis patients and a CCl4-induced mouse model. Adeno-associated viruses and adenoviruses were used to alter hepatic CFIm25 expression in vivo and in vitro to investigate how CFIm25 functions in liver fibrosis. The underlying mechanisms were explored using RNA-seq and co-IP assays. Here, we found that CFIm25 expression was drastically decreased in activated murine HSCs and fibrotic liver tissues. CFIm25 overexpression downregulated the expression of genes involved in liver fibrosis, inhibiting the progression of HSC activation, migration and proliferation. These effects resulted from direct activation of the KLF14/PPARγ signaling axis. KLF14 inhibition abrogated the CFIm25 overexpression-mediated reduction in antifibrotic effects. These data reveal that hepatic CFIm25 regulates HSC activation through the KLF14/PPARγ pathway as liver fibrosis progresses. CFIm25 may be a novel therapeutic target for liver fibrosis.

Dissecting the alternation landscape of mitochondrial metabolism-related genes in lung adenocarcinoma and their latent mechanisms.

Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer with high incidence and unsatisfactory prognosis. The majority of LUAD patients eventually succumb to local and/or distinct metastatic recurrence. Genomic research of LUAD has broadened our understanding of this disease's biology and improved target therapies. However, the alternation landscape and characteristics of mitochondrial metabolism-related genes (MMRGs) in LUAD progression remain poorly understood. We performed a comprehensive analysis to identify the function and mechanism of MMRGs in LUAD based on the TCGA and GEO databases, which might offer therapeutic values for clinical researchers. Then, we figured out three hub prognosis-associated MMRGs (also termed as PMMRGs: ACOT11, ALDH2, and TXNRD1) that were engaged in the evolution of LUAD. To investigate the correlation between clinicopathological characteristics and MMRGs, we divided LUAD samples into two clusters (C1 and C2) based on key MMRGs. In addition, important pathways and the immune infiltration landscape affected by LUAD clusters were also delineated. Further, we nominated potential regulatory mechanisms underlying the MMRGs in LUAD development and progression. In conclusion, our integrative analysis enables a more comprehensive understanding of the mutation landscape of MMRGs in LUAD and provides an opportunity for more precise treatment.

Hepatic Krüppel-like factor 14 regulates lipid metabolism in nonalcoholic steatohepatitis mice.

Excessive lipid accumulation is a critical characteristic in the development of nonalcoholic steatohepatitis (NASH). The underlying molecular mechanism, however, is unclear. In this study, we explored whether and how Krüppel-like factor 14 (KLF14) affects hepatic lipid metabolism in NASH. KLF14 expression was detected in NASH patients and mice fed a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD). Adeno-associated viruses and adenoviruses were used to alter hepatic KLF14 expression in vivo or in vitro to investigate how KLF14 functions in lipid regulation. The molecular mechanisms were explored using RNA-seq, luciferase reporter, and ChIP assays. The fatty liver phenotype was analyzed histopathologically, and serum and hepatocyte biochemical parameters were measured. The NASH mouse model developed quickly in C57BL/6J mice fed a CDAHFD for 8 weeks. We found that KLF14 expression was decreased in NASH patients and CDAHFD mice. Oleic acid and palmitic acid treatment also reduced KLF14 levels in hepatocytes. KLF14 knockdown downregulated the genes involved in fatty acid oxidation, promoting the progression of hepatic steatosis. In contrast, hepatic KLF14 overexpression alleviated lipid accumulation and oxidative stress in CDAHFD mice. These effects resulted from direct activation of the PPARα signaling pathway. PPARα inhibition diminished the KLF14 overexpression-reduced protective effects against steatosis in OA&PA-treated MPHs and AAV-KLF14-infected CDAHFD mice. These data reveal that hepatic KLF14 regulates lipid accumulation and oxidative stress through the KLF14-PPARα pathway as NASH progresses. KLF14 may be a novel therapeutic target for hepatic steatosis.

Autotaxin promotes the degradation of the mucus layer by inhibiting autophagy in mouse colitis.

Autotaxin (ATX or ENPP2) is an autocrine enzyme associated with the metabolism of various phospholipids. ATX has recently been identified as a regulatory factor in immune-related and inflammation-associated diseases, such as inflammatory bowel disease, but the exact mechanism is unclear. Here, we treated mice with recombinant ATX protein or an ATX inhibitor to investigate the effect of ATX on colitis in mice and the underlying mechanism. In a mouse model of colitis, ATX expression was increased, autophagy was impaired, and the mucus barrier was disrupted. Recombinant ATX protein promoted intestinal inflammation, inhibited autophagy, and disrupted the mucus barrier, while an ATX inhibitor had the opposite effect. Next, we treated mice that received ATX with an autophagy activator and an adenosine 5'-monophosphate-activated protein kinase (AMPK) agonist. We observed that autophagy activator and AMPK agonist could repair the mucus barrier and alleviate intestinal inflammation in ATX-treated mice. In vitro, we obtained consistent results. Thus, we concluded that ATX could inhibit autophagy through the AMPK pathway, which consequently disordered the mucus barrier and aggravated intestinal inflammation.

Knowledge landscape of tumor-associated macrophage research: A bibliometric and visual analysis.

Background and aims: Tumor-associated macrophage (TAM) is a highly abundant immune population in tumor microenvironment, which plays an important role in tumor growth and progression. The aim of our study was to explore the development trends and research hotspots of TAM by bibliometric method. Methods: The publications related to TAM were obtained from the Web of Science Core Collection database. Bibliometric analysis and visualization were conducted using VOSviewer, CiteSpace and R software. Results: A total of 6,405 articles published between 2001 and 2021 were included. The United States and China received the most citations, whereas the University of Milan, the university of California San Francisco and Sun Yat-sen University were the main research institutions. Mantovani, Alberto from Humanitas University was the most productive authors with the most citations. Cancer Research published the most articles and received the most co-citations. Activation, angiogenesis, breast cancer, NF-κB and endothelial growth factor were important keywords in TAM research. Among them, PD-1/L1, nanoparticle, PI3Kγ, resistance and immune microenvironment have become the focus of attention in more recent research. Conclusions: The research on TAM is rapidly evolving with active cooperation worldwide. Anticancer therapy targeting TAM is emerging and promising area of future research, especially in translational application. This may provide guidance and new insights for further research in the field of TAM.

Routine nasogastric tube placement after gastric endoscopic full-thickness resection of tumor size ≤ 2 cm may be unnecessary: a propensity score-matching analysis.

BACKGROUND: Endoscopic full-thickness resection is a common endoscopic procedure for treating gastrointestinal submucosal tumors. Nasogastric tube placement is frequently performed after abdominal surgery, but the routine use of this approach remains controversial. The aim of this research was to explore whether nasogastric tube placement after gastric endoscopic full-thickness resection is necessary. METHODS: A retrospective study enrolled patients who underwent gastric endoscopic full-thickness resection in our hospital between January 2014 and January 2019, and all the patients had a tumor size ≤ 2 cm. The patients were divided into two groups according to whether a nasogastric tube was placed. Postprocedural adverse events and hospital stay duration were compared between the two groups using 1:1 propensity score matching. RESULTS: A total of 461 patients were enrolled in this study, including 385 patients in the nasogastric tube group (NGT group) and 76 patients in the non-nasogastric tube group (non-NGT group). After matching, the baseline characteristics of 73 patients in the NGT group and 73 patients in the non-NGT group were balanced (p > 0.05). The postprocedural fever rate in the NGT group was significantly higher than that in the non-NGT group (23.3% vs. 9.6%, p = 0.044). 6.9% (5/73) of patients experienced severe nasogastric tube-related throat discomfort. However, the duration of hospitalization stay was not different between the two groups. CONCLUSIONS: For patients with tumor size ≤ 2 cm, routine nasogastric tube placement after gastric endoscopic full-thickness resection may be unnecessary.

Clinical analysis of 45 cases of perforation were identified during endoscopic retrograde cholangiopancreatography procedure.

Background: Endoscopic retrograde cholangiopancreatography (ERCP) has become an important method to diagnose and treat biliary-pancreatic diseases. Perforations are infrequent but serious complications can occur during ERCPs. However, it is unclear which patients are suitable for surgery and when these patients should receive surgery. Aim: To analyze the outcome of 45 patients with endoscopic retrograde cholangiopancreatography (ERCP) related perforation. Materials and methods: We retrospectively reviewed all 45 patients with ERCP-related perforation between January 2003 and December 2017, and observed the location and causes of perforation, treatment strategies, and mortality. Results: Twenty thousand four hundred and seventy-nine patients received ERCP procedures from January 2003 to December 2017 in our digestive endoscopy center. Forty-five patients suffered from ERCP-related perforations. The incidence rate of ERCP-related perforations was 0.22%. Twenty-six patients suffered from periampullary perforations, 15 patients suffered from duodenal wall perforations, 1 patient suffered from a fundus perforation, 1 patient suffered from a residual gallbladder duct perforation, 1 patient suffered from a papillary diverticulum perforation, and 1 patient suffered from an intrahepatic bile duct perforation. Six patients with duodenal perforations underwent surgery, and the other patients received conservative treatment. One patient with a duodenal perforation and ERCP-related pancreatitis died of heart failure, and all the other patients recovered. The mortality rate was 2.2%. Conclusion: Endoscopic closure is seen as the first method for treating Stapfer type I perforations in the early phase, and surgery is seen as a remedial method when local treatment was failed. The Stapfer type II to type IV perforations can recover by conservative treatment.

Bibliometric analysis of publications on necroptosis from 2001 to 2021.

Background: Necroptosis plays an important role in inflammation, cancer, and neurodegenerative diseases. In recent years, the number of studies related to necroptosis has increased and research has become increasingly in-depth. This study aimed to summarize the research conducted since 2001 to discover hotspots and trends in the field of necroptosis. Methods: The Web of Science Core database was used to identify global publications on necroptosis from 2001 to 2021. Bibliometric analysis was performed using Rstudio, VOSviewer, and CiteSpace. Results: The number of publications related to necroptosis gradually increased from 2001 to 2021. Vandenabeele P had the most publications at 45. Yuan JY had the most citations at 5,901. Necroptosis research has been dominated by China and Chinese institutions. Cell Death and Disease had the highest number of related publications among the examined journals. Seven of the top 10 most cited papers had more than 500 citations. Necroptosis, cell death, autophagy, injury, cancer, activated B cell nuclear factor kappa-light chain enhancer, and oxidative stress were important keywords in keyword analysis. Recent research has increasingly focused on breast cancer, receptor-interacting serine/threonine protein kinase 1, modulation, pseudokinase mixed lineage kinase domain-like protein, membrane, protection, and cycle. Conclusion: Interest in necroptosis-related research continues to increase steadily, and there is close cooperation between countries and institutions in the field of necroptosis. The study of necroptosis-related molecules and mechanisms, and the relationship between necroptosis and cancer, may be hotspots and directions in future research.

Efficacy and safety of indocyanine green tracer-guided lymph node dissection in minimally invasive radical gastrectomy for gastric cancer: A systematic review and meta-analysis.

Background: The implementation of indocyanine green (ICG) tracer-guided lymph node dissection is still in the preliminary stages of laparoscopic surgery, and its safety and efficacy for gastric cancer remain unclear. Methods: A systematic review was conducted in PubMed, Embase, Web of Science, the Cochrane Library, and Scopus to identify relevant subjects from inception to June 2022. The core indicators were the total number of harvested lymph nodes and the safety of the laparoscopic gastrectomy with ICG. A meta-analysis was performed to estimate the pooled weighted mean difference (WMD) and 95% confidence interval (CI). Results: Thirteen studies and 2,027 participants were included (642 for the ICG-group and 1,385 for the non-ICG group). The mean number of lymph nodes dissected in the ICG group was significantly greater than that in the non-ICG group (WMD = 6.24, 95% CI: 4.26 to 8.22, P <0.001). However, there was no significant difference in the mean number of positive lymph nodes dissected between the ICG and the non-ICG groups (WMD = 0.18, 95% CI: -0.70 to 1.07, P = 0.879). Additionally, ICG gastrectomy did not increase the risk in terms of the operative time, estimated blood loss, and postoperative complications. Conclusion: ICG tracer with favorable safety increases the number of harvested lymph nodes but not the number of positive lymph nodes in laparoscopic gastrectomy. More high-quality, large-sample-size randomized controlled trials are still needed to enhance this evidence.

miR-1273h-5p suppresses CXCL12 expression and inhibits gastric cancer cell invasion and metastasis.

The aim of this study was to verify the biological function of miR-1273h-5p in gastric cancer (GC) and its underlying mechanisms. The differential expression of microRNAs between GC and tumor-adjacent normal tissues was detected using microarrays, miR-1273h-5p, and chemokine (C-X-C motif) ligand 12 (CXCL12) mRNA, and protein levels were evaluated using polymerase chain reaction and Western blotting methods, cell proliferation, apoptosis, migration, and invasion were determined by CCK-8, flow cytometry, and transwell assay. Compared to tumor-adjacent normal tissue and gastric epithelial mucosa cell line cells, miR-1273h-5p was significantly downregulated in tissues and cells of GC. The overexpression of miR-1273h-5p could inhibit cell proliferation, migration, invasion, and promote cell apoptosis; in contrast, inhibition of miR-1273h-5p expression could reverse this process. Moreover, a significant upregulation of CXCL12 was observed when the miR-1273h-5p was downregulated in GC cells. Additionally, miR-1273h-5p significantly reduces tumor volume and weight. Thus, this study suggests that miR-1273h-5p regulates cell proliferation, migration, invasion, and apoptosis during GC progression by directly binding to CXCL12 mRNA 3'-untranslational regions, which may be a novel diagnostic and therapeutic target in GC.

Potential Factors Predicting Histopathologically Upgrade Discrepancies between Endoscopic Forceps Biopsy of the Colorectal Low-Grade Intraepithelial Neoplasia and Endoscopic Resection Specimens.

Background: It was gradually accepted that endoscopic fragment biopsy (EFB) diagnosis cannot accurately guarantee the absence of higher-grade neoplasms within the lesion of the digestive tract. There are no well-established predictors for histopathologically upgrade discrepancies between EFB diagnosing colorectal low-grade intraepithelial neoplasia (LGIN) and endoscopic resection (ER) specimens. Methods: A total of 918 colorectal LGINs was histopathologically diagnosed by EFB, including 162 cases with upgrade discrepancy and 756 concordant cases. We compared clinicopathological data of EFB and ER specimens between these two groups. Multivariate analysis was performed to identify predictors for this upgrade histopathology. Results: The predominant upgrade discrepancy of LGINs diagnosed by EFB was upgrades to high-grade dysplasia (114/918, 12.4%), followed by upgrades to intramucosal carcinoma (33/918, 3.6%), submucosal adenocarcinoma (10/918, 1.1%), and advanced adenocarcinoma (5/918, 0.5%). NSAID history (OR 4.83; 95% CI, 2.27-10.27; p < 0.001), insufficient EFB number (OR 2.99; 95% CI, 1.91-4.68; p < 0.001), maximum diameter ≥ 1.0 cm (OR 6.18; 95% CI, 1.32-28.99; p = 0.021), lobulated shape (OR 2.68; 95% CI, 1.65-4.36; p < 0.001), erythema (OR 2.42; 95% CI, 1.50-3.91; p < 0.001), erosion (OR 7.12; 95% CI, 3.91-12.94; p < 0.001), surface unevenness (OR 2.31; 95% CI, 1.33-4.01; p = 0.003), and distal location of the target adenoma (OR 3.29; 95% CI, 1.68-6.41; p < 0.001) were associated with the histologically upgrade discrepancies. Conclusion: NSAID history, insufficient EFB number, adenoma size and location, and abnormal macroscopic patterns are potential predictors for upgrade histopathology of LGINs diagnosed by EFBs. The standardization of EFB number and advanced imaging techniques could minimize the risk of neglecting the potential of this upgrade histopathology.

The assessment of the ASGE-grading system of ERCP: a large-sample retrospective study.

BACKGROUND AND AIMS: The American Society for Gastrointestinal Endoscopy (ASGE) has developed a complexity-grading system for endoscopic retrograde cholangiopancreatography (ERCP) to predict technical success and adverse events. This study aimed to assess the association between the degree of difficulty for ERCP and the rates of success and adverse event, in turn demonstrating the validity and practicality of this system. METHODS: ERCP procedures performed in the First Affiliated Hospital of Nanchang University from January 2011 to December 2020 were retrospectively reviewed. Procedural success and adverse events were recorded based on difficulty level according to the ASGE-grading system. RESULTS: A total of 20,652 ERCP procedures performed during the study period were analyzed, including 1908 procedures considered grade 1(9.2%), 10,170 procedures considered grade 2 (49.2%), 7764 procedures considered grade 3 (37.6%), 810 procedures considered grade 4 (3.9%). The overall success rate increased from 92.8% in 2011-2015 to 94.0% in 2016-2020, while the distribution of procedures and the incidence of complications showed little variation. The success rate revealed a significantly decreasing trend with increasing difficulty (ranging from 55.6 to 98.6%), mainly for biliary diseases. In addition, the difficulty scale was not associated with any differences in the rate of adverse event, except for the pancreatitis for grade 1 procedures, which had a low incidence. CONCLUSIONS: The ASGE-grading system can help predict the success rate of ERCP procedures but showed poor performance in predicting adverse events. Further exploration may be required to improve the grading system by adjusting or including certain clinical parameters, and to validate the system for extrapolation to other endoscopy units.

The clinical effect of a strategy called transcystic gallbladder-preserving cholecystolithotomy based on endoscopic retrograde cholangiopancreatography for cholecystolithiasis: A retrospective study from a single center.

Background: Choledocholithiasis complicated with cholecystolithiasis is a common disease. This study explores a novel strategy, called ERCP-based transcystic gallbladder-preserving cholecystolithotomy, for the simultaneous removal of common bile duct stones and gallbladder stones. Methods: From December 2018 to June 2021, all patients with cholecystolithiasis and common bile duct stones who met the criteria for gallbladder preservation in our hospital were included in the study and prospectively followed up. Results: We included 48 patients, including 20 patients with acute biliary pancreatitis. All patients successfully underwent ERCP to remove common bile duct stones. One patient had gallbladder perforation during gallbladder-preserving cholecystolithotomy. The guide wire successfully entered the gallbladder, and the transpapillary gallbladder metal-covered stent was successfully placed in 44 patients. The technical success rate was 91.67% (44/48). All stones were removed in 34 patients, for a clinical success rate of 77.27% (34/44). The total postoperative complication rate was 6.25% (3/48), with 2 cases of pancreatitis (4.17%) and 1 case of cholangitis (2.08%). Three patients were lost to follow-up. Among the 31 patients who were followed up for a mean of 27 months (6-40), 5 patients (16.13%) experienced gallstone recurrence. The recurrence rates at 12 months, 18 months, 24 months, 30 months and 36 months were 0%, 3.23%, 6.45%, 12.9%, and 16.13%, respectively. Conclusion: For patients with cholecystolithiasis and common bile duct stones, ERCP-based transcystic gallbladder-preserving cholecystolithotomy without gallbladder incision can preserve gallbladder structure, and this procedure is safe and feasible for the protection of gallbladder function.Clinical trial registration: The study was registered in the Chinese Clinical Trial Registry, and the registry number is ChiCTR1900028006.

The role of periampullary diverticulum on the incidence of pancreaticobiliary diseases and the outcome of endoscopic retrograde cholangiopancreatography.

INTRODUCTION: Periampullary diverticulum (PAD), although commonly discovered in patients undergoing endoscopic retrograde cholangiopancreatography (ERCP), remains controversial regarding its role in pancreaticobiliary diseases and the failure rate of cannulation. The aim of this study was to evaluate the association of PAD with pancreaticobiliary diseases and its impact on the outcome of ERCP. MATERIAL AND METHODS: A retrospective analysis was carried out on 1455 patients who underwent an ERCP. Patients were divided into a PAD group and a control group without PAD, and propensity score matching was performed to adjust for clinical differences. The comparison was focused on pancreaticobiliary diseases, technical success, and complications of ERCP. RESULTS: The occurrence of PAD is associated significantly with increasing age (p < 0.001). Incidences of acute pancreatitis (AP), suppurative cholangitis, and pancreatic head cancer were significantly higher in the PAD group (p < 0.05). After propensity score matching, the PAD group exhibited a higher rate of post-ERCP complications including haemorrhage, post-ERCP pancreatitis (PEP), and hyperamylasaemia (p < 0.05). However, the prevalence of perforation and the success rate of ERCP did not differ between groups (p > 0.05). CONCLUSIONS: Periampullary diverticulum develops with aging and seems to be associated with an increase in pancreaticobiliary diseases and post-ERCP complications except for perforation. Additionally, the presence of PAD does not affect the technical success of ERCP.