Esophageal Metaplasia Research Articles

S3270 Scoping the Uncommon: Esophageal Epidermoid Metaplasia as a Premalignant Phenomenon

S3270 Scoping the Uncommon: Esophageal Epidermoid Metaplasia as a Premalignant Phenomenon

361. PHOTODYNAMIC THERAPY IN THE TREATMENT OF ESOPHAGEAL MUCOSAL METAPLASIA IN CHILDREN

Abstract Background The urgency of the problem of gastroesophageal reflux disease (GERD) in pediatrics is due to the high prevalence of this pathology in children. The problem of GERD in childhood has become especially important, when a direct correlation between the duration of esophagitis and the development of Barrett's esophagus (BE) and, later, esophageal adenocarcinoma has been revealed. Photodynamic therapy (PDT) is used as one of the elements of complex treatment after antireflux surgeries for direct impact on metaplastic mucosa and restoration of normal esophageal lumen. Due to the increased detection of esophageal malignancies in adult patients, we aimed to investigate this method in the treatment of Barrett's esophagus in children. Methods There were 3 patients diagnosed with esophageal mucosal metaplasia in the thoracic surgery department. Intestinal esophageal metaplasia was detected and histologically confirmed in 1 patient, in 2 patients - gastric metaplasia of cardiac type. All patients were female. The average age of the patients was 15 years. Children underwent multiple sessions of balloon dilatation of esophageal stenosis with temporary positive effect. Taking into account persistent restenosis, presence of metaplasia areas we applied PDT. Intravenous injection of photosensitizer (PS) of chlorine series for 30 minutes was carried out 5 hours before the beginning of PDT. For PDT we used a laser unit with a wavelength of 662 nm, power of 1 W with exposure of 25-30 minutes (at the rate of 300 J/cm2), optical power meter, video gastroscope, spectroanalyzer. Results To achieve the result: complete destruction of metaplasia sites and recanalization of the esophageal lumen, 1 patient with intestinal metaplasia needed 3 sessions, 2 patients with gastric metaplasia of cardiac type - 4 sessions of PDT. In children with gastric metaplasia, an "initiation" method was developed and applied at first PDT session to induce inflammation in the esophageal mucosa. During PDT macroscopic changes of mucosa in the metaplasia area were registered: ischemia, edema and hyperemia, hemorrhagic manifestations, "parchment" mucosa. We were also focused on the amount of PS in tissues according to the graphic images of the spectroanalyzer. During control examinations we noted healing of the metaplasia zone with subsequent regeneration of the epithelium, which was confirmed histologically, and preservation of the normal esophageal lumen. Conclusion Thus, there is a possibility of effective use of photodynamic therapy for esophageal mucosal metaplasia in children and adolescents. Taking into account the minimally invasive technique, comparative cheapness of photosensitizers, equipment for generation of laser radiation, registration of photosensitizer concentration in tissues, it is possible to create the basis for conducting studies in the treatment of this pathology in children. The method of photodynamic therapy in Barrett's esophagus demonstrates high efficiency in its eradication. Increasing the number of observations will allow to make more meaningful conclusions in the future. Eradication of Barrett's esophagus in children meets the requirements of cancer vigilance.

352. A RARE CASE OF ESOPHAGEAL EPIDERMOID METAPLASIA: A POTENTIAL PRECURSOR TO ESOPHAGEAL MALIGNANCY

Abstract A 62-year-old woman with medical history of fibromyalgia and depression was referred to the gastroenterology consultation due to dysphagia for solids for the past 3 months. She had previously performed an upper endoscopy which revealed an esophageal lesion, interpreted as a papillomatous lesion. Upper endoscopy was repeated, showing a whitish, irregular, semi-elevated and hemi-circumferential lesion between 16 and 19cm from the incisors (Figure A and B). Biopsies were performed. Histology revealed a stratified squamous epithelium with mild inflammation, with spongiosis, hyperorthokeratosis and a prominent granular cell layer. This was consistent with esophageal epidermoid metaplasia (Figures C and D). No dysplasia or carcinoma was noted. Esophageal epidermoid metaplasia is a rare condition described only in case reports and small series. It is thought that may be sporadically associated with esophageal squamous cell carcinoma. Endoscopically, this entity might have different appearances such as white plaques, altered texture, keratotic patches, sloughing, granularity, nodularity, furrows, decreased vascularity, and lacy appearance. We report this case to raise awareness for this entity and its association with dysplasia and esophageal cancer. Therefore, in the case of esophageal epidermoid metaplasia lesions a close follow-up or endoscopic treatment may be warranted. Patient is currently on endoscopic surveillance every one year to screen for early dysplasia.

Clinical and Biological Perspectives on Noncanonical Esophageal Squamous Cell Carcinoma in Rare Subtypes.

Esophageal squamous cell carcinoma (ESCC) remains the most common malignancy of the esophagus worldwide. Environmental and lifestyle exposures such as alcohol and tobacco have been well defined in the pathogenesis of ESCC, acting in concert with cell intrinsic epigenomic, genomic and transcriptomic changes. However, a variety of nonenvironmental etiologies including Fanconi anemia, lichen planus, chronic mucocutaneous candidiasis, esophageal epidermoid metaplasia, epidermolysis bullosa, tylosis, esophageal atresia, and achalasia receive minimal attention despite a high risk of ESCC in these diseases. The goal of this review was to promote clinical recognition and suggest a diagnostic framework for earlier detection of ESCC in patients with these rare diseases. In all the discussed conditions, a change in symptoms should trigger a prompt endoscopic evaluation, and endoscopic surveillance programs with advanced imaging techniques and chromoendoscopy should be considered. Moreover, we leverage the convergence of these diseases on ESCC to identify common mechanisms underlying malignant transformation including aberrant proliferation, mucosal barrier dysfunction, increased inflammation, and genome instability. In this study, we summarize the clinical presentation, pathologic findings, potential screening strategies, and common mechanisms of malignant transformation associated with these rare diseases that drive ESCC.

The Tissue Systems Pathology Test Objectively Risk-Stratifies Patients With Barrett's Esophagus: Results From a Multicenter US Clinical Experience Study.

Barrett's esophagus (BE) is a diagnosis of esophageal intestinal metaplasia, which can progress to esophageal adenocarcinoma (EAC), and guidelines recommend endoscopic surveillance for early detection and treatment of EAC. However, current practices have limited effectiveness in risk-stratifying patients with BE. This study aimed to evaluate use of the TSP-9 test in risk-stratifying clinically relevant subsets of patients with BE in clinical practice. TSP-9 results for tests ordered by 891 physicians for 8080 patients with BE with clinicopathologic data were evaluated. Orders were from nonacademic (94.3%) and academic (5.7%) settings for nondysplastic BE (NDBE; n=7586; 93.9%), indefinite for dysplasia (IND, n=312, 3.9%), and low-grade dysplasia (LGD, n=182, 2.3%). The TSP-9 test scored 83.2% of patients with low risk, 10.6% intermediate risk, and 6.2% high risk, respectively, for progression to HGD/EAC within 5 years. TSP-9 provided significant risk-stratification independently of clinicopathologic features, within NDBE, IND, and LGD subsets, male and female, and short- and long-segment subsets of patients. TSP-9 identified 15.3% of patients with NDBE as intermediate/high-risk for progression, which was 6.4 times more than patients with a pathology diagnosis of LGD. Patients with NDBE who scored intermediate or high risk had a predicted 5-year progression risk of 8.1% and 15.3%, respectively, which are similar to and higher than published progression rates in patients with BE with confirmed LGD. The TSP-9 test identified a high-risk subset of patients with NDBE who were predicted to progress at a higher rate than confirmed LGD, enabling early detection of patients requiring management escalation to reduce the incidence of EAC. TSP-9 scored the majority of patients with NDBE as low risk, providing support to adhere to 3- to 5-year surveillance per guidelines.

The Goblet Cell: Is It Needed for a Diagnosis of Barrett’s Esophagus and Does It Impact Surveillance and Treatment?—CON

Esophageal intestinal metaplasia generally is required for a diagnosis of Barrett’s esophagus (BE) and, in clinical practice, that intestinal metaplasia is identified by the presence of goblet cells. However, if BE is defined conceptually as an esophageal metaplasia that predisposes to adenocarcinoma, then the goblet cell becomes a very imperfect marker for that condition. False-positive diagnoses of BE can result from failure to distinguish true goblet cells from pseudogoblet cells, and false-negative diagnoses can result from inadequate biopsy sampling that misses goblet cells, which often are patchy in distribution. Furthermore, evidence is accumulating that there is a gastric foveolar pathway to esophageal adenocarcinoma that can occur in the absence of goblet cells, and that might be even more common and more aggressive than the familiar intestinal dysplasia pathway.

Multicenter, Prospective Trial of Nonendoscopic Biomarker-Driven Detection of Barrett's Esophagus and Esophageal Adenocarcinoma.

Preliminary data suggest that an encapsulated balloon (EsoCheck), coupled with a 2 methylated DNA biomarker panel (EsoGuard), detects Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC) with high accuracy. The initial assay requires sample freezing upon collection. The purpose of this study was to assess a next-generation EsoCheck sampling device and EsoGuard assay in a much-enlarged multicenter study clinically enhanced by using a Clinical Laboratory Improvement Amendments of 1988-compliant assay and samples maintained at room temperature. Cases with nondysplastic BE (NDBE), dysplastic BE (indefinite for dysplasia, low-grade dysplasia, high-grade dysplasia), EAC, junctional adenocarcinoma, plus endoscopy controls without esophageal intestinal metaplasia, were prospectively enrolled. Medical assistants at 6 institutions delivered the encapsulated balloon per orally with inflation in the stomach. The inflated balloon sampled the distal 5 cm of the esophagus and then was deflated and retracted into the capsule, preventing sample contamination. EsoGuard bisulfite sequencing assayed levels of methylated vimentin and methylated cyclin A1. A total of 243 evaluable patients-88 cases (median age 68 years, 78% men, 92% White) and 155 controls (median age 57 years, 41% men, 88% White)-underwent adequate EsoCheck sampling. The mean procedural time was approximately 3 minutes. Cases included 31 with NDBE, 16 with indefinite for dysplasia/low-grade dysplasia, 23 with high-grade dysplasia, and 18 with EAC/junctional adenocarcinoma. Thirty-seven NDBE and dysplastic BE cases (53%) were short-segment BE (<3 cm). Overall sensitivity was 85% (95% confidence interval 0.78-0.93) and specificity was 85% (95% confidence interval 0.79-0.90). Sensitivity for NDBE was 84%. EsoCheck/EsoGuard detected 100% of cancers (n = 18). EsoCheck/EsoGuard demonstrated high sensitivity and specificity in detecting BE and BE-related neoplasia.

Abstract 6099: Identification of intrinsic precursors of Barrett's and gastric intestinal metaplasia

Abstract The origin of Barrett's esophagus (BE) and gastric intestinal metaplasia (GIM), obligate precursors of esophageal adenocarcinoma (EAC) and intestinal gastric cancer (iGC), has intrigued investigators for decades and would likely guide preemptive strategies. From endoscopic biopsies of clinically confirmed BE and GIM, we have cloned stem cells committed to intestinal metaplasia in vitro. Remarkably, the gene expression profiles of BE and GIM stem cells are highly related down to broad arrays of transcription factors compared with stem cells of the normal gastric mucosa. Using cell surface markers in common between BE and GIM stem cells, we have identified clusters of cells at the squamocolumnar junction and the distal stomach in mice and have used Fluorescence-activated cell sorting (FACS) to clone these cells from both sites. These murine clones can be differentiated in air-liquid interface cultures, and both are committed to intestinal metaplasia marked by goblet cells and Alcian blue staining. To ask whether similar cells exist in humans, we generated stem cell libraries from endoscopic biopsies taken from the gastroesophageal junction (GEJ) and the antrum-body junction (ABJ) in patients without BE or GIM. FACS sorting of these stem cell libraries using the same cell surface markers common to BE and GIM stem cells and the murine precursors, we have identified stem cells from the GEJ and ABJ that show similar gene expression profiles and share a commitment to intestinal metaplasia upon in vitro differentiation. Using identical transformation protocols involving retrovirally transduced protooncogenes, we find that these transformed intrinsic cells give rise to tumors with expression profiles similar to EAC and iGC in TCGA datasets, whereas transformed gastric mucosal stem cells yield tumors marked by signet ring cells typical of diffuse gastric cancer. Lastly, we find that drugs we have developed that target the stem cells of BE and GIM also eliminate the putative precursor cells of BE and GIM, suggesting the potential of therapeutics that might eliminate the emergence of intestinal metaplasia and the cancers derived from them. Citation Format: Wa Xian, Frank McKeon, Yusuke Yamamoto, Melika Khorrami, Melina Khorrami, Zaal Mory, Jeremy Siegelman, Amber Su, Raul Caballero Montes, Ashley Hoffman, Jaffer Ajani, Christopher Crum, William Bachovchin, Shan Wang, Matthew Vincent, Crystal Nguyen. Identification of intrinsic precursors of Barrett's and gastric intestinal metaplasia [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 6099.

Algorithm Training and Testing for a Nonendoscopic Barrett’s Esophagus Detection Test in Prospective Multicenter Cohorts

Endoscopic Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC) detection is invasive and expensive. Nonendoscopic BE/EAC detection tools are guideline-endorsed alternatives. We previously described a 5-methylated DNA marker (MDM) panel assayed on encapsulated sponge cell collection device (CCD) specimens. We aimed to train a new algorithm using a 3-MDM panel and test its performance in an independent cohort. Algorithm training and test samples were from 2 prospective multicenter cohorts. All BE cases had esophageal intestinal metaplasia (with or without dysplasia/EAC); control subjects had no endoscopic evidence of BE. The CCD procedure was followed by endoscopy. From CCD cell lysates, DNA was extracted, bisulfite treated, and MDMs were blindly assayed. The algorithm was set and locked using cross-validated logistic regression (training set) and its performance was assessed in an independent test set. Training (N= 352) and test (N= 125) set clinical characteristics were comparable. The final panel included 3 MDMs (NDRG4, VAV3, ZNF682). Overall sensitivity was 82% (95% CI, 68%-94%) at 90% (79%-98%) specificity and 88% (78%-94%) sensitivity at 84% (70%-93%) specificity in training and test sets, respectively. Sensitivity was 90% and 68% for all long- and short-segment BE, respectively. Sensitivity for BE with high-grade dysplasia and EAC was 100% in training and test sets. Overall sensitivity for nondysplastic BE was 82%. Areas under the receiver operating characteristic curves for BE detection were 0.92 and 0.94 in the training and test sets, respectively. A locked 3-MDM panel algorithm for BE/EAC detection using a nonendoscopic CCD demonstrated excellent sensitivity for high-risk BE cases in independent validation samples. (Clinical trials.gov: NCT02560623, NCT03060642.).

Endoscopic Follow-Up Between 3 and 7 Years After Sleeve Gastrectomy Reveals Antral Reactive Gastropathy but no Barrett's Esophagus.

The main concerns following sleeve gastrectomy (SG) include the risk of gastroesophageal reflux disease (GERD) and its complications, such as Barrett's esophagus (BE). However, there is conflicting data on esophageal conditions, and studies on alterations of gastric mucosa after SG are lacking, despite reported cases of gastric cancer. Our aim was to assess esophageal and gastric lesions after SG. From November 2017, an upper gastrointestinal endoscopy (UGE) was proposed at least 3 years after SG to all patients operated on in our institution. Endoscopic results and gastric histological findings were analyzed. BE was defined as endoscopically suspected esophageal metaplasia with histological intestinal metaplasia. Between September 2008 and August 2018, 375 patients underwent SG at our institution, of which 162 (43%) underwent at least one UGE 3 years or more after SG (91% women, mean preoperative age: 43.3±10.3 years). Despite a significant increase in the prevalence of symptomatic GERD, hiatal hernia, and esophagitis after SG (p<0.001 vs. preoperatively), no cases of BE were detected. Gastric dysplasia was not found and the prevalence of gastric atrophy tended to decrease after SG. However, 27% of patients with gastric biopsies developed antral reactive gastropathy. At a mean follow-up of 54 months after SG, no BE or gastric dysplasia was identified. However, reactive gastric lesions appeared, and their long-term consequences need to be further clarified. Thus, the timing of endoscopic follow-up, starting as early as 3 years after SG should be reevaluated to improve patient adherence with long-term endoscopies.

Signaling Pathways in the Pathogenesis of Barrett's Esophagus and Esophageal Adenocarcinoma.

Barrett's esophagus (BE) is a premalignant lesion that can develop into esophageal adenocarcinoma (EAC). The development of Barrett's esophagus is caused by biliary reflux, which causes extensive mutagenesis in the stem cells of the epithelium in the distal esophagus and gastro-esophageal junction. Other possible cellular origins of BE include the stem cells of the mucosal esophageal glands and their ducts, the stem cells of the stomach, residual embryonic cells and circulating bone marrow stem cells. The classical concept of healing a caustic lesion has been replaced by the concept of a cytokine storm, which forms an inflammatory microenvironment eliciting a phenotypic shift toward intestinal metaplasia of the distal esophagus. This review describes the roles of the NOTCH, hedgehog, NF-κB and IL6/STAT3 molecular pathways in the pathogenesis of BE and EAC.

Abstract 3496: p53 mutation biases SCJ progenitor cells towards dysplasia rather than metaplasia in Barrett's esophagus

Abstract Objectives: Barrett's esophagus (BE) is a form of metaplasia that involves the aberrant differentiation of stem or progenitor cells at the squamocolumnar junction (SCJ). p53 mutation occurs early in BE cases that do progress to dysplasia or esophageal adenocarcinoma. Here, we aimed to elucidate the mechanisms by which p53 mutation promotes the early neoplastic progression of cardia progenitor cells in a mouse model of BE (L2-IL1β). Methods: We generated the transgenic mice L2-IL1β; Cck2r-CreERT2; tdTomato; p53R172H/+ to determine the effect of p53 mutation on Cck2r+ cardia progenitor cell activity. Lineage tracing and pathological assessment were performed in combination at different time points to explore the effects of p53 mutation on development of precancerous lesions in the cardia glands. Organoids were derived from sorted Cck2r+ cardia cells with or without p53 mutation. Organoid forming capacity and growth assessment were tested to assess stemmness potential. Organoids were treated with the DNA damaging agent N-methyl-N-nitrosourea (MNU) to test the resistance of p53 mutant organoids to carcinogenic injury. Orthotopic transplantation of organoids into immunodeficient (NSG) mice was performed to study the influence of p53 mutation on growth in vivo. Single-cell RNA sequencing (scRNA-seq) analysis of precancerous lesions and bulk RNA-seq analysis of cardia organoids from BE mice were carried out to investigate the effects of p53 mutation on key regulatory pathways. Results: Characterization of pathological progression combined with lineage tracing showed that over time, most p53 mutant cells did not undergo metaplasia but progressed to dysplasia in the cardia glands of IL1β mice. This suggests that the dysplastic cells likely arose directly from stem or progenitor cells rather than progressing first through metaplasia, a finding consistent with the scRNA-seq analysis. In vitro, p53 mutation increased the number and size of organoids derived from Cck2r+ progenitor cells from IL1β mice, suggesting an expansion of stem or progenitor cells. Furthermore, p53 mutation led to increased resistance of these organoids to MNU. Orthotopic transplantation experiments demonstrated that p53 mutation increased survival and proliferation of organoids in the stroma of immunodeficient murine stomach. Moreover, p53 mutant transplanted organoids retained dysplastic features with little to no metaplastic events relative to their WT counterparts. Computational analyses suggested that these heterotypic gains function in vivo and in vitro are relate to their inhibitory effect of stem cell differentiation through Notch signaling activation. Conclusion: These findings suggest that p53R172H/+ mutation in SCJ progenitor cells directly promotes their progression toward dysplasia, rather than differentiating into metaplasia, due in part through activation of Notch signaling to maintain stemness. Citation Format: Guodong Lian, Ermanno Malagola, Junfei Zhao, Richard A. Friedman, Leah B. Zamechek, Timothy C. Wang. p53 mutation biases SCJ progenitor cells towards dysplasia rather than metaplasia in Barrett's esophagus [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3496.

Single-cell RNA sequencing unifies developmental programs of Esophageal and Gastric Intestinal Metaplasia.

Intestinal metaplasia in the esophagus (Barrett's Esophagus BE-IM) and stomach (GIM) are considered precursors for esophageal and gastric adenocarcinoma, respectively. We hypothesize that BE-IM and GIM follow parallel developmental trajectories in response to differing inflammatory insults. Here, we construct a single-cell RNA-seq atlas, supported by protein expression studies, of the entire gastrointestinal tract spanning physiologically normal and pathological states including gastric metaplasia in the esophagus (E-GM), BE-IM, atrophic gastritis, and GIM. We demonstrate that BE-IM and GIM share molecular features, and individual cells simultaneously possess transcriptional properties of gastric and intestinal epithelia, suggesting phenotypic mosaicism. Transcriptionally E-GM resembles atrophic gastritis; genetically, it is clonal and has a lower mutational burden than BE-IM. Finally, we show that GIM and BE-IM acquire a pro-tumorigenic, activated fibroblast microenvironment. These findings suggest that BE-IM and GIM can be considered molecularly similar entities in adjacent organs, opening the path for shared detection and treatment strategies.

Endoscopic Assessment Prior to Bariatric Surgery in Saudi Arabia.

There are marked local inconsistencies in the Arabian Peninsula about the role of preoperative esophagogastroduodenoscopy (EGD) in bariatric surgery. Thus, this study was conducted to determine the frequency of endoscopic and histological findings in the Saudi population presenting for pre-bariatric surgery evaluation. This was a retrospective study that included all the patients who were evaluated by EGD at Dammam Medical Complex, Dammam, Saudi Arabia, between 2018 and 2021 as a part of their pre-bariatric-surgery evaluation. A total of 684 patients were included. They consisted of 250 male and 434 female patients (36.5% and 63.5%, respectively). The mean ± standard deviation for the patients' age and body mass index (BMI) were 36.4±10.6 years and 44.6±5.1 kg/m2, respectively. Significant endoscopic or histopathological findings as defined by the presence of large (≥ 2 cm) hiatus hernia, esophagitis, gastroesophageal reflux disease (GERD), Barrett esophagus, gastric ulcer, duodenal ulcer, or intestinal metaplasia were found in 143 patients (20.9%); 364 patients (53.2%) were diagnosed to have Helicobacter pylori infection. The high number of significant endoscopic and histopathological findings in our study supports the routine use of preoperative EGD in all bariatric surgery patients. However, omitting EGD before Roux-en-Y gastric bypass (RYGB) in asymptomatic patients is still reasonable as the most frequently found significant findings, esophagitis, and hiatus hernia, are less likely to impact the operative plans in RYGB. Similarly, active surveillance and treatment of H. pylori infections in obese patients are important but it is not clear whether H. pylori eradication should be done before bariatric surgery.

Shared features of metaplasia and the development of adenocarcinoma in the stomach and esophagus.

Introduction: Plasticity is an inherent property of the normal gastrointestinal tract allowing for appropriate response to injury and healing. However, the aberrancy of adaptable responses is also beginning to be recognized as a driver during cancer development and progression. Gastric and esophageal malignancies remain leading causes of cancer-related death globally as there are limited early disease diagnostic tools and paucity of new effective treatments. Gastric and esophageal adenocarcinomas share intestinal metaplasia as a key precancerous precursor lesion. Methods: Here, we utilize an upper GI tract patient-derived tissue microarray that encompasses the sequential development of cancer from normal tissues to illustrate the expression of a set of metaplastic markers. Results: We report that in contrast to gastric intestinal metaplasia, which has traits of both incomplete and complete intestinal metaplasia, Barrett's esophagus (i.e., esophageal intestinal metaplasia) demonstrates hallmarks of incomplete intestinal metaplasia. Specifically, this prevalent incomplete intestinal metaplasia seen in Barrett's esophagus manifests as concurrent development and expression of both gastric and intestinal traits. Additionally, many gastric and esophageal cancers display a loss of or a decrease in these characteristic differentiated cell properties, demonstrating the plasticity of molecular pathways associated with the development of these cancers. Discussion: Further understanding of the commonalities and differences governing the development of upper GI tract intestinal metaplasias and their progression to cancer will lead to improved diagnostic and therapeutic avenues.

Surveillance Endoscopy After Foregut Surgery: Is It Necessary?

Patients undergoing foregut surgeries can have de novo findings or worsening of underlying upper gastrointestinal pathologies including Barrett’s esophagus and gastric intestinal metaplasia. These changes carry a potentially increased risk for malignancy development in the future raising the question of the utility of post-operative surveillance endoscopy after esophagectomy, bariatric and metabolic surgeries (Sleeve gastrectomy and Roux-en-Y Gastric Bypass), achalasia treatment, and anti-reflux surgery. In this narrative review, we conduct a literature exploration of available data on post-operative endoscopic surveillance findings following the procedures summarizing the prevalence of upper gastrointestinal pathologies and recommendations on the utility of postoperative endoscopy from established medical societies.

The optical-morphological diagnosis ratio in esophageal metaplasia

Objective. To analyze the esophageal metaplasia types in accordance to data of videoesophagogastroduodenoscopy and morphological investigations, to determine the ratio of optical and morphological diagnosis in esophageal metaplasia.&#x0D; Materials and methods. Retrospective investigation was conducted, concerning the results of 237 videoesophagogastroduodenoscopy with high resolution capacity in presence of suspicion for BE diagnosis, using gastroscopes Olympus GIF HQ-190, -180, Olympus EVIS EXERA II, Olympus EVIS EXERA III, EVIS X1 in conjunction with digital chromoscopy and epithelial biopsy of the esophageal mucosa affected with further morphological investigation on base of Shalimov National Institute of Surgery and Transplantology during 2014 - 2022 yrs, using modern protocols (biopsies taken from 4 quadrants along the metaplasia esophageal coverage every 2 sm and on the apex of the mostly proximally located fragment) with further histological investigation.&#x0D; Results. In accordance to videoesophagogastroduodenoscopy data there was diagnosed BE in 237 patients. Endoscopic picture of metaplasia in regime of digital chromoscopy looks like tongues of flame of reddish color on background of gray esophageal epithelium. In total a complete coincidence of optical and morphological diagnosis was noted in 192 (81.0%) of 237 patients.&#x0D; Conclusion. For today practice morphological verification of BE remains an objective criterion. But optical diagnosis, established, using videoesophagogastroduodenoscopy of high resolution capacity and digital chromoscopy, was confirmed in 81.0% of observations. It is possible to prognosticate, that in near future, taking into account technical progress in possibilities of endoscopes, for establishment of the BE diagnosis application of videoesophagogastroduodenoscopy with high resolution capacity and narrow-band chromoscopy would appear sufficient. Further retrospective investigations in this direction, using modernized gastroscopes with high resolution capacity may constitute a good perspective.

The Role of Artificial Intelligence in Surveillance in Barrett’s Esophagus and Gastric Intestinal Metaplasia

Artificial Intelligence (AI) has been increasingly applied in medical imaging for improved accuracy and efficiency. One area that has seen significant advances is the use of AI in the detection of Barrett’s esophagus (BE) and gastric intestinal metaplasia (GIM). BE is a pre-cancerous condition that occurs in the esophagus and can lead to esophageal adenocarcinoma, while GIM is a precancerous lesion that occurs in the stomach. In this review article, we will provide an overview of current AI techniques used in the detection and diagnosis of BE and GIM, including computer-aided diagnosis (CAD) systems, deep learning algorithms, and image analysis techniques. The performance of AI in detecting these conditions will be evaluated and compared to traditional methods. The challenges and limitations of using AI in the diagnosis of BE and GIM will also be discussed. The article aims to provide a comprehensive understanding of the use of AI in BE and GIM detection and to guide future research in this field.

ENDOSCOPIC TREATMENT OF BARRETT’S ESOPHAGUS IN KAZAKHSTAN

Relevance: Barrett’s esophagus (BE) is a special disease characterized by metaplasia of the flat epithelium of the esophagus.&#x0D; The main danger of esophageal epithelial metaplasia is the high probability of develop-ing a malignant neoplasm at the site of the lesion – esophageal adenocarcinoma or can-cer of the cardioesophageal zone.&#x0D; The study aimed to evaluate the clinical effectiveness of new BE endoscopic treat-ment methods for their subsequent implementation in wide practice throughout the Re-public of Kazakhstan.&#x0D; Methods: This article presents cases of clinical use of argon plasma coagulation of dysplasia lesions less than 2.0 cm in two patients with Barrett’s esophagus and the use of loop resection of dysplasia lesions more than 2.0 cm in three patients with Barrett’s esophagus.&#x0D; Results: All the presented cases have shown the effectiveness of applied treatment. Control morphological examination showed no signs of BE in the epithelium.&#x0D; Conclusion: The presented article describes the results of the introduction of endo-scopic BE treatment methods in our clinic and is available for wide implementation throughout Kazakhstan. A widespread introduction of endoscopic treatment of precan-cerous pathology will reduce the incidence of esophageal cancer in the Kazakhstani population.

ENDOSCOPIC TREATMENT OF BARRETT’S ESOPHAGUS&#x0D; IN KAZAKHSTAN

Relevance: Barrett’s esophagus (BE) is a special disease characterized by metaplasia of the flat epithelium of the esophagus.&#x0D; The main danger of esophageal epithelial metaplasia is the high probability of develop-ing a malignant neoplasm at the site of the&#x0D; lesion – esophageal adenocarcinoma or can-cer of the cardioesophageal zone.&#x0D; The study aimed to evaluate the clinical effectiveness of new BE endoscopic treat-ment methods for their subsequent implementation&#x0D; in wide practice throughout the Re-public of Kazakhstan.&#x0D; Methods: This article presents cases of clinical use of argon plasma coagulation of dysplasia lesions less than 2.0 cm in two patients&#x0D; with Barrett’s esophagus and the use of loop resection of dysplasia lesions more than 2.0 cm in three patients with Barrett’s esophagus.&#x0D; Results: All the presented cases have shown the effectiveness of applied treatment. Control morphological examination showed no&#x0D; signs of BE in the epithelium.&#x0D; Conclusion: The presented article describes the results of the introduction of endo-scopic BE treatment methods in our clinic and is&#x0D; available for wide implementation throughout Kazakhstan. A widespread introduction of endoscopic treatment of precan-cerous pathology&#x0D; will reduce the incidence of esophageal cancer in the Kazakhstani population