Despite the rising global incidence of inflammatory bowel disease (IBD), curative therapies remain unavailable. While our previous work implicated the intestinal proteoglycan Syndecan-1 (SDC1) in IBD-associated barrier dysfunction and inflammation, the underlying mechanism was unclear. This study aimed to elucidate how SDC1 maintains intestinal barrier integrity through interactions with the gut microbiome. In DSS-induced colitis, global knockout of Sdc1 (Sdc1-/-) exhibited exacerbated inflammatory infiltration and greater impairment of barrier structure and function than wild-type (WT). Formation of intestinal organoids was independent of genotype, indicating that Sdc1-/- does not impair barrier function via disrupting epithelial development. The heightened colitis susceptibility in Sdc1-/- mice was abolished in the antibiotic-treated pseudo-germ-free models, and transmissible to WT mice via fecal microbiota transplantation. Similar results were reproduced in a germ-free mouse model. Metagenomic sequencing identified Faecalibacterium prausnitzii as the most significantly depleted species upon Sdc1 knockout. In vitro, SDC1-attached glycosaminoglycans (heparan sulfate (HS) and chondroitin sulfate (CS)) but not the SDC1 core protein promoted F. prausnitzii growth. Prokaryotic transcriptome profiling indicated that HS/CS induces cobalamin biosynthesis in F. prausnitzii. The critical role of cobalamin as a mediator was confirmed, as its synthetic inhibition significantly diminished the growth-promoting effect of HS/CS. Mechanism studies showed that HS/CS enhanced biofilm formation in F. prausnitzii, thereby facilitating cobalamin biosynthesis. Oral administration of HS ameliorated DSS-induced colitis and promoted mucosal colonization of F. prausnitzii, independent of the host genotype. Finally, human IBD biopsies revealed a positive correlation between epithelial SDC1 and mucosal F. prausnitzii, as well as an inverse correlation with bacterial translocation and the number of LPS‑positive cells. Our study elucidates a novel mechanism in which the glycosaminoglycan chains of SDC1 promote F. prausnitzii colonization and growth through enhanced biofilm formation and cobalamin synthesis, thereby highlighting the therapeutic potential of HS for IBD and offering a new basis for host-directed microbiota regulation.

BackgroundEndoscopic resection is the standard treatment for colorectal adenoma (CRA), a key precursor to colorectal cancer (CRC). However, a high rate of recurrence post-procedure poses a significant challenge for long-term CRC prevention. Growing evidence suggests gut microbial dysbiosis contributes to adenoma development and recurrence. This trial will test the hypothesis that restoring a healthy gut microbiome with fecal microbiota transplantation (FMT) can reduce the recurrence of CRA after endoscopic resection.MethodsThis protocol describes a multicenter, open-label, randomized, no-treatment-controlled trial that will enroll 466 participants with CRA following endoscopic resection. Participants will be randomly assigned in a 1:1 ratio to receive either FMT or no treatment (control). The FMT intervention consists of an initial colonoscopic infusion and oral capsules, followed by oral maintenance capsules at months 3, 6, and 9. The primary outcome is the rate of CRA recurrence at the 12-month follow-up colonoscopy. Key secondary outcomes include the incidence of all polypoid lesions, changes in the gut and mucosal microbiota composition, the incidence of CRC, and a comprehensive assessment of adverse events to evaluate safety.DiscussionThis trial is designed to provide high-quality evidence on the efficacy and safety of FMT for preventing CRA recurrence. The findings may support a novel, microbiome-based strategy for the secondary prevention of CRC and provide mechanistic insights into the role of the gut microbiota in colorectal carcinogenesis.Trial registrationClinicalTrials.gov NCT06205862. Registered on 16 January, 2024. https://clinicaltrials.gov/study/NCT06205862.

Accumulating studies have highlighted the biological significance of immunogenic cell death (ICD) in cancer immunity. However, the influence of ICD on tumor microenvironment (TME) formation and immune response in Hepatocellular carcinoma (HCC) remains largely unexplored. In this study, we systematically analyzed the mRNA profiles of ICD-related genes in 1847 HCC patients and identified three molecular subtypes with significantly different immune features and prognostic stratification. A reliable risk model named ICD score was constructed via machine learning algorithms to assess the immunological status, therapeutic responses, and clinical outcomes of individual HCC patients. High ICD score indicated an immune-excluded TME phenotype, with lower anticancer immunity and shorter survival time. In contrast, low ICD score corresponded to abundant immune cell infiltration, high sensitivity to immunotherapy and a positive prognosis, indicating an “immune-hot” phenotype. Pan-cancer analysis further validated a negative association between ICD score and the immune cell infiltration levels. In conclusion, our findings revealed that the ICD score could serve as a robust prognostic biomarker to predict the benefits of immunotherapy and optimize the clinical decision-making of HCC patients.

BACKGROUND AND AIMS:Hepatic steatosis is characterised by hepatic lipid accumulation, inflammation and fibrosis, with macrophage polarisation playing a central role in disease progression. This study investigates the role of interleukin-25 (IL-25) in modulating macrophage polarisation and Notch signalling in a methionine-choline-deficient (MCD) diet-induced metabolic dysfunction-associated fatty liver disease (MAFLD) model. METHODS:C57BL/6 mice were fed a MCD diet to induce MAFLD. Human hepatocytes and primary hepatic macrophages were treated with palmitic acid and/or IL-25. Methods included RT-qPCR, ELISA, Western blot and immunofluorescence for gene/protein expression. ChIP and luciferase assays were used to analyse STAT3/Notch-1 signalling. RESULTS:We found that IL-25 expression was significantly downregulated in the livers of MCD-fed mice and in palmitic acid-treated hepatocytes. IL-25 treatment promoted M2 macrophage polarisation, evidenced by increased expression of Arg1, Chi3l3 and anti-inflammatory cytokines (IL-10, TGF-β), while suppressing pro-inflammatory cytokines (TNF-α, IL-6). Mechanistically, IL-25 inhibited the STAT3/Notch-1 pathway and induced IL-33, which negatively regulated the NF-κB/Jagged-1 axis, preventing M1 macrophage polarisation. Adoptive transfer of IL-25-induced M2a macrophages ameliorated hepatic steatosis and reduced ductular reaction in MCD-fed mice. CONCLUSIONS:These findings suggest a role for IL-25 in modulating macrophage polarisation and inflammation in metabolic dysfunction-associated fatty liver disease, supporting its further exploration as a potential therapeutic strategy for inflammatory liver diseases.

To explore the short-term efficacy and safety of endoscopic low dose injection of sclerotherapy and cyanoacrylate for gastric varices (GVs) combined with endoscopic variceal ligation (EVL) for esophageal varices (EVs) in cirrhosis with type GOV1 varices. A total of 521 patients with cirrhosis and GOV1 varices, who were divided into emergence endoscopy treatment layer and secondary prophylaxis for rebleeding layer, were selected. All patients underwent combined therapy or EVL alone (ligation therapy) for the treatment of type GOV1 varices. The baseline between the two groups with significant differences were used as covariates for 1:1 propensity score matching. The early rebleeding rate was compared and the risk factors for rebleeding were identified in each layer. After propensity score matching, a total of 122 patients were included in the emergence endoscopy treatment layer, and 234 patients were included in the secondary prophylaxis layer. The early rebleeding rates in the combined therapy group vs. ligation therapy group was 4.92

Abstract Purpose Metastasis is crucial for the prognosis of hepatocellular carcinoma (HCC). Distinguishing the potential risk factors for distant metastasis in small HCC (diameter ≤ 5 cm) is of great significance for improving the prognosis. Patients and methods: HCC patients in the Surveillance, Epidemiology and End Results (SEER) registry with tumors ≤ 5 cm in diameter between January 2010 and December 2015 were retrieved. Demographic and clinicopathological metrics were extracted, including age, sex, race, marital status, tumor size, histological grade, T stage, N stage, M stage, alpha-fetoprotein (AFP), and liver fibrosis score. Univariate and multivariate logistic regression analyses were used to identify independent risk factors correlated with extrahepatic metastasis in small HCC. Propensity score matching (PSM) analysis was performed to balance the confounding factors in baseline characteristics. Results A total of 4,176 eligible patients were divided into a non-metastasis group (n = 4,033) and a metastasis group (n = 143) based on metastasis status. In multivariate analysis, larger tumor size, poor histological differentiation, regional lymph node metastasis, and elevated serum AFP levels were identified as independent risk factors for distant metastasis (P < 0.05), while age, sex, race, marital status, and liver fibrosis score were not associated with extrahepatic metastasis. After propensity score analysis, the AFP level was no longer associated with metastatic risk. Conclusion AFP may not be a metastatic risk for patients with small hepatocellular carcinoma.

BACKGROUND Acute kidney injury (AKI) is a common and severe complication in patients with cirrhosis, and is associated with poor prognosis. Therefore, identifying cirrhotic patients with AKI who are at high risk of mortality is very important and may be helpful for providing timely medical interventions to improve the prognosis of these patients. However, studies focused on investigating the risk factors for the mortality of cirrhotic patients with AKI were scarce. AIM To identify risk factors for mortality and establish a nomogram for predicting the prognosis of these patients. METHODS Two hundred fifty consecutive patients with cirrhosis and AKI were recruited and randomly divided into training cohort (n = 173) and validation cohort (n = 77). In the training cohort, potential risk factors for death were identified by performing a Cox regression analysis, and a nomogram was established. The predictive performance of the nomogram was internally and externally validated by calculating the area under the receiver operating characteristic curve (AUROC), constructing a calibration curve and performing decision curve analysis. RESULTS The serum sodium level, international normalized ratio, peak serum creatinine level > 1.5 mg/dL, the presence of hepatic encephalopathy and diabetes were potential risk factors for mortality of cirrhotic patients with AKI in the training dataset. A prognostic nomogram incorporating these variables was established for predicting the overall survival of these patients. Compared with Child-Turcotte-Pugh, the model for end-stage liver disease (MELD) and the MELD-Na scores, the nomogram in predicting 90- and 180-d mortality exhibited better discriminatory power with AUROCs of 0.792 and 0.801 for the training dataset and 0.817 and 0.862 for the validation dataset, respectively. With a nomogram score of 98, patients were divided into low- and high-risk groups, and high-risk patients had a higher mortality rate. CONCLUSION A prognostic nomogram displayed good performance for predicting the overall survival of cirrhotic patients with AKI, and will assist clinicians in evaluating the prognosis of these patients.

Background Hepatocellular carcinoma (HCC) is the third-most deadly cancer worldwide. More breakthroughs are needed in the clinical practice for liver cancer are needed, and new treatment strategies are required. This study aims to determine the significant differences in genes associated with LIHC and further analyze its prognostic value further. Methods Here, we used the TCGA-LIHC database and the profiles of GSE25097 from GEO to explore the differentially co-expressed genes in HCC tissues compared with paratumor (or healthy) tissues. Then, we utilized WGCNA to screen differentially co-expressed genes. Finally, we explored the function of FYN in HCC cells and xenograft tumor models. Results We identified ten hub genes in the protein-protein interaction (PPI) network, but only three (COLEC10, TGFBR3, and FYN) appeared closely related to the prognosis. The expression of FYN was positively correlated with the prognosis of HCC patients. The xenograft model showed that overexpression of FYN could significantly inhibit malignant tumor behaviors and promote tumor cell apoptosis. Conclusion Thus, FYN may be central to the development of LIHC and maybe a novel biomarker for clinical diagnosis and treatment.

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.

Metastasis is crucial for the prognosis of hepatocellular carcinoma (HCC). Distinguishing the potential risk factors for distant metastasis in small HCC (diameter ≤ 5 cm) is of great significance for improving the prognosis. HCC patients in the Surveillance, Epidemiology and End Results (SEER) registry with tumors ≤ 5 cm in diameter between January 2010 and December 2015 were retrieved. Demographic and clinicopathological metrics were extracted, including age, sex, race, marital status, tumor size, histological grade, T stage, N stage, M stage, alpha-fetoprotein (AFP), and liver fibrosis score. Univariate and multivariate logistic regression analyses were used to identify independent risk factors correlated with extrahepatic metastasis in small HCC. Propensity score matching (PSM) analysis was performed to balance the confounding factors in baseline characteristics. A total of 4176 eligible patients were divided into a non-metastasis group (n = 4033) and a metastasis group (n = 143) based on metastasis status. In multivariate analysis, larger tumor size, poor histological differentiation, regional lymph node metastasis, and elevated serum AFP levels were identified as independent risk factors for distant metastasis ( P < 0.05), while age, sex, race, marital status, and liver fibrosis score were not associated with extrahepatic metastasis. After propensity score analysis, the AFP level was no longer associated with metastatic risk. The present study provided no evidence for a correlation between the clinical threshold of AFP and metastasis in small hepatocellular carcinoma.

INTRODUCTION: Compared with endoscopic variceal ligation (EVL), cap-assisted endoscopic sclerotherapy (CAES) improves efficacy in the treatment of small esophageal varices (EVs) but has not been evaluated in the management of medium EVs. The aim of this study was to compare CAES with EVL in the long-term management of patients exhibiting cirrhosis with medium EVs and a history of esophageal variceal bleeding (EVB), with respect to variceal eradication and recurrence, adverse events, rebleeding, and survival. METHODS: Cirrhotic patients with medium EVs and a history of EVB were divided randomly into EVL and CAES groups. EVL or CAES was repeated each month until variceal eradication. Lauromacrogol was used as a sclerosant. Patients were followed up until 1 year after eradication. RESULTS: In total, 240 patients (age: 51.1 ± 10.0 years; men: 70.8%) were included and randomized to the EVL and CAES groups. The recurrence rate of EVs was much lower in the CAES group than in the EVL group (13.0% vs 30.7%, P = 0.001). The predictors for variceal recurrence were eradication by EVL (hazard ratio [HR]: 2.37, P = 0.04), achievement of complete eradication (HR: 0.27, P < 0.001), and nonselective β-blocker response (HR: 0.32, P = 0.003). There was no significant difference in the rates of eradication, rebleeding, requirement for alternative therapy, and mortality or the incidence of complications between groups. DISCUSSION: CAES reduces the recurrence rate of EVs with comparable safety to that of EVL in the long-term management of patients presenting cirrhosis with medium EVs and a history of EVB.

The goal of this study was to compare the efficacy and safety of needle-knife fistulotomy (NKF) to that of conventional cannulation methods (CCMs) when used for primary biliary access in patients with duodenal papillary tumors. Consecutive patients who had duodenal papillary tumors and who underwent endoscopic retrograde cholangiopancreatography (ERCP) were retrospectively enrolled. Successful cannulation rates, cannulation and procedure times, and the prevalence of adverse events were compared between the NKF and CCM groups. A total of 404 patients (NKF, n = 124; CCM, n = 280) with duodenal papillary tumors were included. The primary and overall cannulation rates were 92.1% (372/404) and 96.0% (388/404), respectively. Compared to CCMs, NKF was associated with a significantly higher successful cannulation rate (99.2% versus 88.9%, P < 0.001) and significantly lower cannulation times (2.1 ± 2.0 min versus 4.7 ± 5.2 min), procedure times (8.8 ± 3.8 min versus 12.9 ± 7.6 min), and unintentional pancreatic duct cannulation rates (1.6% versus 20%), with P < 0.001 for all. Overall adverse events occurred less frequently in the NKF group (3.2% versus 10.7%, P = 0.011). Of these adverse events, post-ERCP pancreatitis (PEP) was significantly lower in the NKF group than in the CCM group (1.6% versus 6.8%, P = 0.03). Bleeding and cholangitis rarely occurred with either cannulation method (0.8% versus 2.1%, P = 0.681, and 0.8% versus 1.7%, P = 0.671, respectively). NKF is a more effective and safer procedure than CCMs for patients with duodenal papillary tumors.

Objective To investigate the expression levels of interleukin 25 (IL-25) and its related factors in the serum and liver of patients with non-alcoholic fatty liver disease (NAFLD) and explore the significance. Methods Between September 2017 and February 2019, NAFLD patients (n=50) who met the criteria of the disease and control patients (n=20) who undergoing partial hepatectomy due to hepatic hemangioma or hepatic cyst in the First Affiliated Hospital of Nanchang University were enrolled in this study. Serum levels of IL-25 and other cytokines were detected by ELISA. Then 6 patients in control group and 12 patients in NAFLD group were chosen to analyze hepatic mRNA expression levels of IL-25 and other cytokines by real-time fluorescent quantitative PCR, and protein levels of IL-25, CD68 (macrophage marker), CD206 (M2 macrophage marker) and glutaminase transaminase 2 (TGM2) by immunohistochemistry or immunofluorescence assay. Results ① Compared with the patients in control group, those of the NAFLD group had significantly reduced serum levels of IL-25 (P=0.003), IL-13 (P=0.007) and IL-4 (P=0.001). ② The mRNA levels of IL-13 (P=0.007) and IL-4 (P=0.003) in the liver of NAFLD patients were also obviously lower while that of CD68 (P < 0.001) was higher than those in the control group. ③ The NAFLD patients had more Küpffer cells (P < 0.001), fewer M2 macrophages (P < 0.001) and lower level of IL-25 (P < 0.001) in the liver than the patietns of the control group. With the aggravation of hepatic steatosis, the number of Küpffer cells was increased gradually (P < 0.001), while that of M2 macrophages (P < 0.001) and the level of IL-25 (P < 0.001) was decreased gradually. Conclusion The serum levels and liver contents of IL-25, Th2 type cytokine and intrahepatic M2 type macrophages are significantly reduced in the NAFLD patients, and these indicators are negatively correlated with the severity of liver steatosis.

Objective To observe and analyze the relationships among the level of interleukin 25 (IL-25), the stage of liver fibrosis and the polarization of hepatic M2 macrophages in patients with non-alcoholic fatty liver disease (NAFLD). Methods A total of 36 patients with NAFLD and 20 control patients were enrolled. Fibrotouch, HE staining, and immunohistochemistry were used to evaluate the stage of liver fibrosis. Patients with NAFLD were classified into groups of mild liver fibrosis (F1) (20 cases) and significant liver fibrosis (≥ F2) (16 cases). The level of serum IL-25 in each group was detected by ELISA. Real-time fluorescent quantitative PCR was used to detect the hepatic mRNA expression levels of IL-25, collagen1 (Col1), α mooth muscle actin (α-SMA), macrophage mannose receptor 1 (CD206/MR1) and transglutaminase 2 (TGM2). Immunohistochemistry was used to detect the protein levels of IL-25, α-SMA, CD206 and TGM2. Results There was no significant difference in the level of serum IL-25 among groups. Compared with patients in the control group and the mild liver fibrosis group, patients with significant liver fibrosis showed reduced mRNA expression levels of IL-25, CD206, and TGM2 in addition to lower levels of hepatic IL-25 protein and less polarization of M2 macrophages. Conclusion Down-regulation of IL-25 is accompanied by a decrease in the number of the M2 macrophages with the progression of liver fibrosis in NAFLD patients.

Background: Ectopic varices (EcVs) may cause massive bleeding, which can be difficult to control, with a high rate of mortality. The purpose of this study was to analyze the clinical characteristics of EcVs and the efficacy of endoscopic treatment. Methods: From January 2008 to July 2017, the clinical data of 150 patients with EcVs in our center were retrospectively collected and analyzed. Results: One hundred and fifty patients with EcVs (male 74.7%), with a mean age of: 54.1 ± 14.6 years were included. The prevalence of EcVs was 0.92% in gastrointestinal varices. Cirrhosis was the most common cause of EcVs (67.0%). The rates of bleeding were 57.14%, 4.34%, 30.0%, 33.3%, and 100% in the duodenal varices rectal varices, colonic varices, anastomotic varices, and small bowel varices, respectively. An age under 55 years, varices in the duodenum, and erythema were considered risk factors for EcV bleeding. Endoscopic treatments were performed in 15 patients with EcV bleeding. The follow-up period of the patients who underwent endoscopic treatment ranged from 0.5 to 24 months. The overall rate of treatment success was 73.33% for endoscopic treatment of EcV bleeding. The overall rates of rebleeding and mortality during 2 years were as high as 53.3% and 26.7%, respectively. Conclusion: Age, erythema, and the location of EcVs are considered risk factors for EcV bleeding, and the rate of bleeding is higher in patients with duodenal varices than in those with other EcVs. Endoscopic treatment is safe, effective, and feasible for controlling EcV bleeding.

Background: Hepatocellular Carcinoma (HCC) is the third deadly cancer worldwide. More breakthroughs are needed in the clinical practice of liver cancer, and new treatment strategies are required to carry out to benefit patients. This study aims to screen out other significant differences in genes associated with LIHC and analyze its prognostic value further. Methods: Here, we use the TCGA-LIHC database and the profiles of GSE25097 from GEO to explore the differential co-expression genes in HCC tissues compared with para-tumor (or healthy) tissues. Then, we utilized WGCNA to screen out differential co-expression genes. Finally, we explored the function of FYN in HCC cells and xenograft tumor models.Results: We identified ten hub genes in the protein-protein interaction (PPI) network, but only three ( COLEC10, TGFBR3 , and FYN ) of them seem to have a close-related to the prognosis. The expression of FYN was negatively correlated with the prognosis of HCC patients. The xenograft model showed that overexpression of FYN could significantly inhibit malignant tumor behaviors and promote tumor cell apoptosis.Conclusion: Thus, FYN may be central to the development of LIHC and maybe a novel biomarker for clinical diagnosis and treatment.

Background: Clinical trials examining the therapeutic benefits of glucagon-like peptide-1 receptor agonists (GLP-1RA) on patients with metabolic associated fatty liver disease (MAFLD) have reported inconsistent results. The aim of this meta-analysis was to verify the role of GLP-1RA in the treatment of MAFLD patients. Materials and Methods: We searched PubMed, Embase, Medline, and the Cochrane Library for randomized controlled trials published that compared GLP-1RA with the control treatment in patients with MAFLD till to July 30, 2020. The effects of GLP-1RA on liver histology, body mass index, waist circumference (WC), aspartate aminotransferase, total cholesterol, triglycerides (TG), low-density lipoprotein and high-density lipoprotein were evaluated. Results: Thirteen trials involving 704 patients were included in the meta-analysis. Compared with the control treatment, GLP-1RA treatment induced a greater resolution of steatohepatitis [RR=2.87; 95% confidence interval (CI): 0.89 to 9.23], delayed the progression of liver fibrosis (RR=3.83, 95% CI: 0.91 to 16.07) and reduced liver fat deposition (MD: -1.40; 95% CI: -2.75 to -0.05). In addition, it reduced the body mass index (MD: -1.15; 95% CI: -2.26 to -0.04), WC (MD: -3.33; 95% CI: -6.31 to -0.35) and improved serum aspartate aminotransferase (MD: -3.04; 95% CI: -5.93 to -0.16) and total cholesterol (MD: -0.20; 95% CI: -0.28 to -0.13). Conclusion: GLP-1RA improves liver steatosis and fibrosis. It is also beneficial to metabolic syndrome as it reduces BMI, WC, and hyperlipidemia.

Background Bedside biliary drainage by endoscopic retrograde cholangiopancreatography (ERCP) without fluoroscopy for critically ill patients in the intensive care unit (ICU) remains challenging for endoscopists. The present study was to evaluate the efficacy and safety of radiation-free ERCP for these patients. Methods Consecutive ICU patients with severe pancreaticobiliary disorders who underwent bedside radiation-free ERCP were retrospectively analyzed. Results Radiation-free ERCP was performed in 80 patients with acute physiology and chronic health evaluation (APACHE II) score of 24.1 ± 6.2. Cannulation was achieved in 75 (93.75%) patients. Biliary drainage was successfully conducted in 74 (92.5%) patients, including 54 (67.5%) and 20 (25.0%) cases of endoscopic retrograde biliary drainage (ERBD) and endoscopic nasobiliary drainage (ENBD), respectively. Adverse event (mild post-ERCP pancreatitis (PEP)) occurred only in 1 case. The 30-day mortality rate of these patients was 36.25% (29/80) and was much more higher in patients with ERBD in contrast to that of patients with ENBD, 40.7% (22/54) vs. 20% (4/20), OR = 2.750, 95%CI = 0.810 − 9.3405, P = 0.110. The APACHE II score in nonsurvivors was significantly higher than survivors, 27.6 ± 4.3 versus 22.2 ± 6.3, P = 0.009. The APACHE II score > 22 was an independent risk factor for mortality, 50% versus 10.7%, 95%CI = 2.148 − 31.569, P = 0.002. Conclusions Radiation-free ERCP guided bedside biliary drainage is effective and safe for critically ill patients, and ENBD may be an optimal procedure due to a low mortality in these patients.

To investigate whether second-look endoscopy (SLE)-guided therapy could be used to prevent post-endoscopic variceal ligation (EVL) early bleeding. Consecutive cirrhotic patients with large esophageal varices (EV) receiving successful EVL for acute variceal bleeding (AVB) or secondary prophylaxis were enrolled. The patients were randomized into a SLE group and a non-SLE group (NSLE) 10 days after EVL. Additional endoscopic interventions as well as proton pump inhibitors and octreotide administration were applied based on the SLE findings. The post-EVL early rebleeding and mortality rates were compared between the two groups. A total of 252 patients were included in the final analysis. Post-EVL early rebleeding (13.5% vs 4.8%, P = 0.016) and bleeding-caused mortality (4.8% vs 0%, P = 0.013) were more frequently observed in the NSLE group than in the SLE group. However, post-EVL early rebleeding and mortality rates were reduced by SLE in patients receiving EVL for AVB only but not in those receiving secondary prophylaxis. Patients with Child-Pugh classification B to C at randomization (hazard ratio [HR] 8.77, P = 0.034), AVB at index EVL (HR 3.62, P = 0.003), discontinuation of non-selective β-blocker after randomization (HR 4.68, P = 0.001) and non-SLE (HR 2.63, P = 0.046) were more likely to have post-EVL early rebleeding. No serious adverse events occurred during SLE. SLE-guided therapy reduces post-EVL early rebleeding and mortality rates in cirrhotic patients with large EV receiving EVL for AVB.

It remains challenging for endoscopists to manage pancreaticobiliary diseases in patients with ectopic papilla of Vater by endoscopic retrograde cholangiopancreatography (ERCP). The present study sought to evaluate the efficacy and safety of ERCP for this issue. Consecutive patients with ectopic papilla of Vater who underwent initial ERCP due to pancreaticobiliary diseases were retrospectively analyzed. One hundred seven patients with ectopic papilla of Vater were included. The success rate of cannulation was 83.2%. Endoscopic sphincterotomy, endoscopic papillary balloon dilation, and mechanical lithotripsy were performed in 12 (11.2%), 25 (23.4%), and 1 (0.9%) patients, respectively. The technical success rate was 83.2%; of these, endoscopic nasobiliary drainage, endoscopic retrograde biliary drainage, endoscopic retrograde pancreatic drainage, and stone extraction was conducted in 61 (57.0%), 17 (15.9%), 5 (4.7%), and 45 (42.1%) patients, respectively. Bile duct stone size >= 1 cm, number >= 2, and duodenum stenosis were risk factors for stone extraction inability. Adverse events occurred in 20 (18.7%) patients, including post-ERCP pancreatitis (3.7%), hyperamylasemia (12.1%), and infection of biliary tract (2.8%); all of the adverse events were mild and alleviated by conventional therapies. ERCP is an appropriate choice for pancreaticobiliary diseases in patients with ectopic papilla of Vater due to its high efficacy and safety. Bile duct stone size >= 1 cm, number >= 2, and duodenum stenosis increase difficulties for stone extraction.