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DescriptionThe purpose of this best practice advice (BPA) article from the Clinical Practice Update Committee of the American Gastroenterological Association is to provide an update on advances and innovation regarding the screening and surveillance of Barrett's esophagus.MethodsThe BPA statements presented here were developed from expert review of existing literature combined with discussion and expert opinion to provide practical advice. Formal rating of the quality of evidence or strength of BPAs was not the intent of this clinical practice update. This expert review was commissioned and approved by the AGA Institute Clinical Practice Updates Committee (CPUC) and the AGA Governing Board to provide timely guidance on a topic of high clinical importance to the AGA membership, and underwent internal peer review by the CPUC and external peer review through standard procedures of Clinical Gastroenterology and Hepatology. BEST PRACTICE ADVICE 1: Screening with standard upper endoscopy may be considered in individuals with at least 3 established risk factors for Barrett's esophagus (BE) and esophageal adenocarcinoma, including individuals who are male, non-Hispanic white, age >50 years, have a history of smoking, chronic gastroesophageal reflux disease, obesity, or a family history of BE or esophageal adenocarcinoma. BEST PRACTICE ADVICE 2: Nonendoscopic cell-collection devices may be considered as an option to screen for BE. BEST PRACTICE ADVICE 3: Screening and surveillance endoscopic examination should be performed using high-definition white light endoscopy and virtual chromoendoscopy, with endoscopists spending adequate time inspecting the Barrett's segment. BEST PRACTICE ADVICE 4: Screening and surveillance exams should define the extent of BE using a standardized grading system documenting the circumferential and maximal extent of the columnar lined esophagus (Prague classification) with a clear description of landmarks and the location and characteristics of visible lesions (nodularity, ulceration), when present. BEST PRACTICE ADVICE 5: Advanced imaging technologies such as endomicroscopy may be used as adjunctive techniques to identify dysplasia. BEST PRACTICE ADVICE 6: Sampling during screening and surveillance exams should be performed using the Seattle biopsy protocol (4-quadrant biopsies every 1-2 cm and target biopsies from any visible lesion). BEST PRACTICE ADVICE 7: Wide-area transepithelial sampling may be used as an adjunctive technique to sample the suspected or established Barrett's segment (in addition to the Seattle biopsy protocol). BEST PRACTICE ADVICE 8: Patients with erosive esophagitis should be biopsied when concern of dysplasia or malignancy exists. A repeat endoscopy should be performed after 8 weeks of twice a day proton pump inhibitor therapy. BEST PRACTICE ADVICE 9: Tissue systems pathology-based prediction assay may be utilized for risk stratification of patients with nondysplastic BE. BEST PRACTICE ADVICE 10: Risk stratification models may be utilized to selectively identify individuals at risk for Barrett's associated neoplasia. BEST PRACTICE ADVICE 11: Given the significant interobserver variability among pathologists, the diagnosis of BE-related neoplasia should be confirmed by an expert pathology review. BEST PRACTICE ADVICE 12: Patients with BE-related neoplasia should be referred to endoscopists with expertise in advanced imaging, resection, and ablation. BEST PRACTICE ADVICE 13: All patients with BE should be placed on at least daily proton pump inhibitor therapy. BEST PRACTICE ADVICE 14: Patients with nondysplastic BE should undergo surveillance endoscopy in 3 to 5 years. BEST PRACTICE ADVICE 15: In patients undergoing surveillance after endoscopic eradication therapy, random biopsies should be taken of the esophagogastric junction, gastric cardia, and the distal 2 cm of the neosquamous epithelium as well as from all visible lesions, independent of the length of the original BE segment.

Background: Traditional endoscopic treatments have limited success in gastric sleeve stenosis (GSS). Gastric peroral endoscopic myotomy (G-POEM) could conceivably obliterate the twist/angulation that causes GSS through a tunneled stricturotomy. We report early outcomes of G-POEM for GSS treatment.Methods: We retrospectively reviewed all patients with GSS treated with G-POEM at our center. The primary end point was clinical success, defined as symptom improvement with resumption of adequate oral intake, without requiring further intervention.Results: 13 patients (mean age 43 ± 10.9 years; 12 female) underwent G-POEM for predominantly helical (11/13, 85 %) GSS. Three (23 %) had concurrent sleeve leak and 10 (77 %) had prior GSS treatment. Two intraoperative complications occurred, with no deviation to the procedure; no major complications occurred. At median follow-up of 175 (interquartile range [IQR] 119-260) days, clinical success was achieved in 10 patients (77 %). Median Gastroparesis Cardinal Symptom Index score in responders decreased from 2.06 (IQR 1.5-2.8) to 0.39 (IQR 0.2-0.5). Three patients (23 %) required surgical revision.Conclusions: G-POEM was feasible and safe, and may provide an alternative option for those averse to undergoing surgical revision for treatment of GSS. [ABSTRACT FROM AUTHOR]

Background: The use of peroral endoscopic myotomy (POEM) for achalasia has a high incidence of post-procedural gastroesophageal reflux (GER). Transoral incisionless fundoplication (TIF) may be an ideal endoscopic treatment. We report our experience with the use of post-POEM TIF.Methods: In this multicenter retrospective study, post-POEM patients with GER who underwent TIF were included. The study end points were: (i) technical success; (ii) safety; (iii) effectiveness (changes in symptoms, scores, proton pump inhibitor [PPI] use, pH studies).Results: 12 patients underwent TIF after POEM, nine of whom had daily symptoms, with 91.7% requiring twice daily (BID) PPIs. Technical success was achieved in all patients. Two adverse events occurred. There were significant decreases in the percentage of patients on BID PPIs (P = 0.03), frequency of daily symptoms (P = 0.03), Reflux Severity Index questionnaire, and GERD Health-related Quality of Life scores (P = 0.03 and P = 0.003; n = 6). pH studies performed in seven of the patients showed a significant reduction in the mean DeMeester score (P = 0.05) and mean percentage acid exposure time (P = 0.04).Conclusion: Our experience suggests that TIF may be effective and safe in treating GER after POEM. Larger prospective trials are needed. [ABSTRACT FROM AUTHOR]

Introduction: Early neoplastic progression of Barrett's esophagus (BE) is often treated with endoscopic therapy. Although effective, some patients are refractory to therapy or recur after apparent eradication of the BE. The goal of this study was to determine whether genomic alterations within the treated BE may be associated with persistent or recurrent disease., Methods: We performed DNA sequencing on pre-treatment esophageal samples from 45 patients who were successfully treated by endoscopic therapy and did not recur as well as pre-treatment and post-treatment samples from 40 patients who had persistent neoplasia and 21 patients who had recurrent neoplasia. The genomic alterations were compared between groups., Results: The genomic landscape was similar between all groups. Patients with persistent disease were more likely to have pre-treatment alterations involving the receptor tyrosine kinase pathway ( P = 0.01), amplifications of oncogenes ( P = 0.01), and deletions of tumor suppressor genes ( P = 0.02). These associations were no longer significant after adjusting for patient age and BE length. More than half of patients with persistent (52.5%) or recurrent (57.2%) disease showed pre-treatment and post-treatment samples that shared at least 50% of their driver mutations., Discussion: Pre-treatment samples were genomically similar between those who responded to endoscopic therapy and those who had persistent or recurrent disease, suggesting there is not a strong genomic component to treatment response. Although it was expected to find shared driver mutations in pre-treatment and post-treatment samples in patients with persistent disease, the finding that an equal number of patients with recurrent disease also showed this relation suggests that many recurrences represent undetected minimal residual disease., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.)

Background: A family history of pancreatic cancer is associated with increased pancreatic cancer risk. However, risk estimates for individuals in kindreds with an aggregation of pancreatic cancer (>1 relative) are imprecise because of small samples sizes or potentially impacted by biases inherent in retrospective data., Objective: The objective of this study is to determine the age-specific pancreatic cancer risk as a function of family history using prospective data., Methods: We compared pancreatic cancer incidence (n = 167) in 21 141 individuals from 4433 families enrolled in the National Familial Pancreatic Cancer Registry with that expected based on Surveillance Epidemiology and End Results data and estimated the cumulative probability of pancreatic cancer using competing risk regression., Results: Familial pancreatic kindred members (kindreds with pancreatic cancer in 2 first-degree relatives [FDRs] or a pathogenic variant) had a standardized incidence ratio of 4.86 (95% confidence interval [CI] = 4.01 to 5.90), and sporadic kindred members (kindreds not meeting familial criteria) had a standardized incidence ratio of 2.55 (95% CI = 1.95 to 3.34). Risk in familial pancreatic cancer kindreds increased with an increasing number of FDRs with pancreatic cancer, with a standardized incidence ratio of 3.46 (95% CI = 2.52 to 4.76), 5.44 (95% CI = 4.07 to 7.26), and 10.78 (95% CI = 6.87 to 16.89) for 1, 2, and 3 or more FDRs with pancreatic cancer, respectively. Risk was also higher among individuals with a family history of young-onset (aged younger than 50 years) pancreatic cancer., Conclusion: Pancreatic cancer risk is strongly dependent on family history, including both the degree of relationship(s) and age of onset of pancreatic cancer in relatives. These risk estimates will help inform the design of early detection studies and the risk and benefit analysis of screening trials., (© The Author(s) 2022. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)