Background: Endoscopic submucosal dissection (ESD) is commonly used to treat early gastric cancer (EGC). The effects of Helicobacter pylori (HP) infection on ESD and the potential benefits of preoperative eradication of HP remain unclear. The study aims to evaluate the impact of HP infection on bleeding and lesion detection during ESD in patients with EGC.
Methods: We retrospectively analyzed 634 consecutive patients who underwent ESD for EGC at our center between January 2018 and January 2023. Logistic regression was used to assess the impact of HP infection status on intraoperative bleeding and lesion detection rates. We developed a predictive model based on selected indicators and evaluated its performance using the ROC curve.
Results: HP-positive patients experienced a higher rate of intraoperative bleeding (28.8%) compared with HP-negative patients (8.9%) (P < 0.001). HP-positive patients also had longer procedure time (median: 58.5 vs. 50.0 min, P < 0.001) and postoperative hospital stays (median: 4.35 vs. 4.07 days, P = 0.036). Multivariate analysis identified HP-positive (OR = 4.84), multiple lesions (OR = 1.81), specimen size > 40 mm (OR = 3.67), and submucosal invasion (OR = 2.27) as independent risk factors for intraoperative bleeding. The predictive model achieved an AUC of 0.807 (95%CI 0.761-0.852), with a sensitivity of 72.1% and specificity of 75.9%. Preoperative HP eradication was associated with an increased rate of lesion detection (OR = 2.82).
Conclusions: Eradicating HP before ESD in patients with EGC reduces intraoperative bleeding and improves lesion detection. Preoperative HP eradication is therefore recommended in patients with EGC.
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http://dx.doi.org/10.1007/s00464-024-11332-6 | DOI Listing |
Int J Biol Macromol
January 2025
Supplementary General Sciences Department, Faculty of Oral and Dental Medicine, Future University in Egypt, Cairo 11835, Egypt.
Helicobacter pylori (H. pylori) is an extremely prevalent human pathogen globally that leads to severe illnesses. Sadly, the worldwide issue of H.
View Article and Find Full Text PDFBMJ Open Gastroenterol
December 2024
Division of Gastroenterology & Hepatology, Weill Cornell Medicine, New York, New York, USA
Objective: Globally, over 50% of the population is affected by , yet research on its prevalence and impact in patients with obesity undergoing laparoscopic sleeve gastrectomy (LSG) is inconclusive. This study aimed to assess the prevalence of infection in individuals with obesity undergoing LSG, evaluate the percentage of postoperative staple-line leaks, and explore the potential link between infection and staple-line leaks.
Methods: This retrospective analysis assessed adult patients with class III obesity who underwent LSG between 2015 and 2020 at a tertiary care hospital in Riyadh, Saudi Arabia.
J Clin Med
December 2024
Department of Oncological, Transplant and General Surgery, Faculty of Medicine, Medical University of Gdansk, 80-214 Gdansk, Poland.
: (HP) is under investigation for its potential role in postoperative complications. While some studies indicate no impact, they often cite short or incomplete follow-up. This study aims to compare 1-year outcomes in groups with and without active HP infection after bariatric surgery, also assessing HP prevalence in postoperative specimens of sleeve gastrectomy (SG) patients.
View Article and Find Full Text PDFCancers (Basel)
January 2025
Faculty of Medicine, University of Ljubljana, Vrazov trg 2, 1000 Ljubljana, Slovenia.
Background/objectives: Gastric intestinal metaplasia (GIM) is considered an irreversible preneoplastic precursor for gastric adenocarcinoma in adults. However, its significance in children and the long-term outcome remain poorly understood.
Methods: All children diagnosed with GIM between 2000 and 2020 were identified at a large tertiary referral centre.
Cancers (Basel)
December 2024
Division of Hematology and Oncology, School of Medicine, University of Alabama at Birmingham, Birmingham, AL 35233, USA.
Dysbiosis in the gut microbiota plays a significant role in GI cancer development by influencing immune function and disrupting metabolic functions. Dysbiosis can drive carcinogenesis through pathways like immune dysregulation and the release of carcinogenic metabolites, and altered metabolism, genetic instability, and pro-inflammatory signalling, contributing to GI cancer initiation and progression. infection and genotoxins released from dysbiosis, lifestyle and dietary habits are other factors that contribute to GI cancer development.
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