Complete Intestinal Metaplasia Research Articles

Expression of cytokeratin 7/20 and Ki67 in Helicobacter pylori-associated gastritis and intestinal metaplasia.

Cytokeratins (CKs) have been associated with precancerous and cancerous gastric lesions in patients with Helicobacter pylori-associated chronic gastritis, making them useful for diagnosing epithelial tumors. A retrospective study was conducted utilizing 200 formalin-fixed paraffin-embedded gastric biopsy samples collected from the lesser curvature of the stomach. Samples from the control group, patients with H. pylori infection, and patients with H. pylori-associated gastritis, with complete and incomplete intestinal metaplasia (IM) were immunostained. Monoclonal antibodies were utilized to determine the expression of CK7, CK20, and Ki-67. Patients infected with H. pylori had strong CK20 expression on the surface, and weak CK7 expression on the surface and deep glands; while non-specific chronic gastritis patients had weak focal CK7 expression and strong CK20 expression. The normal gastric mucosa of patients in the control group had relatively weak CK7 expression, restricted to a few cells in the neck and deep glands. CK20 showed diffuse strong reactivity on the surface. On the other hand, patients with complete IM showed a CK7 staining pattern that was either negative or weakly focal on the surface and crypts associated with diffuse surface CK20 and focal crypt staining corresponding to gastric type IM. The Ki67 proliferating index was low (≤ 15%) in H. pylori infected patients, high (> 30%) in patients with incomplete IM, and intermediate (16-30%) in patients with complete IM. These results indicate a significant link between the expressions of CK7/CK20 and Ki67 in patients afflicted with H. pylori and IM.

OLFM4 promotes the progression of intestinal metaplasia through activation of the MYH9/GSK3β/β-catenin pathway

BackgroundIntestinal metaplasia (IM) is classified into complete intestinal metaplasia (CIM) and incomplete intestinal metaplasia (IIM). Patients diagnosed with IIM face an elevated susceptibility to the development of gastric cancer, underscoring the critical need for early screening measures. In addition to the complexities associated with diagnosis, the exact mechanisms driving the progression of gastric cancer in IIM patients remain poorly understood. OLFM4 is overexpressed in several types of tumors, including colorectal, gastric, pancreatic, and ovarian cancers, and its expression has been associated with tumor progression.MethodsIn this study, we used pathological sections from two clinical centers, biopsies of IM tissues, precancerous lesions of gastric cancer (PLGC) cell models, animal models, and organoids to explore the role of OLFM4 in IIM.ResultsOur results show that OLFM4 expression is highly increased in IIM, with superior diagnostic accuracy of IIM when compared to CDX2 and MUC2. OLFM4, along with MYH9, was overexpressed in IM organoids and PLGC animal models. Furthermore, OLFM4, in combination with Myosin heavy chain 9 (MYH9), accelerated the ubiquitination of GSK3β and resulted in increased β-catenin levels through the Wnt signaling pathway, promoting the proliferation and invasion abilities of PLGC cells.ConclusionsOLFM4 represents a novel biomarker for IIM and could be utilized as an important auxiliary means to delimit the key population for early gastric cancer screening. Finally, our study identifies cell signaling pathways involved in the progression of IM.

Epithelial cell proliferation index in patients with atrophic gastritis depending on the presence of complete or incomplete intestinal metaplasia in the gastric antrum

Introduction. There is a debate about the significance of intestinal metaplasia (IM) subtypes for the development of gastric cancer. Therefore, determining the indicators of cellular renewal in individuals with complete and incomplete IM is certainly a topical issue.Aim. To study the proliferative activity of epithelial cells of the gastric antrum in patients with Helicobacter pylori-positive antral atrophic gastritis depending on the subtype of IM.Materials and methods. The study included 20 people with chronic antral non-atrophic gastritis (CNG; group A), 20 patients with chronic antral atrophic gastritis (CAG) without IM (group B), 20 patients with CAG with complete IM (group C) and 20 people with CAG with incomplete IM (group D). The stage of chronic gastritis was assessed by the morphological method in accordance with the modified Sydney classification. Typing of IM foci in the gastric mucosa was performed using the PAS reaction. Proliferation activity was studied by the expression of nuclear protein Ki67 using immunohistochemistry.Results. The proliferation index in the foci of complete BM in group C was 5%, and in group D in the foci of incomplete BM the Ki67 expression index was significantly higher and was 39% (p < 0.001). Outside the foci of metaplasia, the proliferation index was 23.5% in group C and 19% in group D (p = 0.06).Conclusion. We have registered significantly higher proliferation indicators of gastric epithelial cells in foci with incomplete IM compared to foci with complete IM. Determination of proliferation indicators in foci of incomplete intestinal metaplasia may be a marker of an increased risk of developing gastric cancer.

Gastric Carcinoma in Autoimmune Gastritis: A Histopathologic and Molecular Study

Patients with autoimmune gastritis (AIG) have a 13-fold risk of developing type-1 neuroendocrine tumors, whereas the risk for gastric adenocarcinoma is still uncertain. Here we describe the clinicopathologic and molecular features of a series of gastric carcinomas (GC) arising in the context of AIG. A total of 26 AIG-associated GC specimens were collected from 4 Italian Institutions. Immunohistochemistry for MUC1, MUC2, MUC5AC, MUC6, CDX2, HER2, PD-L1, CLDN18, mismatch repair (MMR) proteins, and p53 and EBV-encoded RNA (EBER) in situ hybridization were performed. Histologic and immunohistochemical features were jointly reviewed by 5 expert gastrointestinal pathologists. Next-generation sequencing analysis (TrueSight Oncology 500, Illumina) of 523 cancer-related genes was performed on 19 cases. Most tumors were diagnosed as pT1 (52%) and they were located in the corpus/fundus (58%) and associated with operative link for gastritis assessment stage II gastritis (80.8%), absence of parietal cells, complete intestinal metaplasia, and enterochromaffin-like-cell micronodular hyperplasia. Only 4 (15.4%) GCs were diagnosed during follow-up for AIG. The following histotypes were identified: 20 (77%) adenocarcinomas; 3 (11%) mixed neuroendocrine–non-neuroendocrine neoplasms, and 2 (8%) high-grade solid adenocarcinomas with focal neuroendocrine component, 1 (4%) adenocarcinoma with an amphicrine component. Overall, 7 cases (27%) showed MMR deficiency, 3 (12%) were positive (score 3+) for HER2, 6 (23%) were CLDN18 positive, and 11 (42%) had PD-L1 combined positive score ≥ 10. EBER was negative in all cases. Molecular analysis revealed 5/19 (26%) microsatellite instability (MSI) cases and 7 (37%) tumor mutational burden (TMB) high. The most frequently altered genes were TP53 (8/19, 42%), RNF43 (7/19, 37%), ERBB2 (7/19, 37% [2 amplified and 5 mutated cases]), ARID1A (6/19, 32%), and PIK3CA (4/19, 21%). In summary, AIG-associated GCs are often diagnosed at low stage in patients with longstanding misrecognized severe AIG; they often display a neuroendocrine component or differentiation, have relatively higher rates of MMR deficiency, and TMB high.

Histopathologic evaluation of gastric intestinal metaplasia in non-neoplastic biopsy specimens: Accuracy and interobserver reliability among general pathologists and pathology residents

ObjectivesThis study aimed to evaluate the accuracy and interobserver reliability of diagnosing and subtyping gastric intestinal metaplasia (IM) among general pathologists and pathology residents at a university hospital in Thailand, focusing on the challenges in the histopathologic evaluation of gastric IM for less experienced practitioners. MethodsThe study analyzed 44 non-neoplastic gastric biopsies, using a consensus diagnosis of gastrointestinal pathologists as the reference standard. Participants included 6 general pathologists and 9 pathology residents who assessed gastric IM and categorized its subtype (complete, incomplete, or mixed) on digital slides. After initial evaluations and receiving feedback, participants reviewed specific images of gastric IM, as agreed by experts. Following a one-month washout period, a reevaluation of the slides was conducted. ResultsDiagnostic accuracy, interobserver reliability, and time taken for diagnosis improved following training, with general pathologists showing higher accuracies than residents (median accuracy of gastric IM detection: 100 % vs. 97.7 %). Increased years of experience were associated with more IM detection accuracy (p-value<0.05). However, the overall median accuracy for diagnosing incomplete IM remained lower than for complete IM (86.4 % vs. 97.7 %). After training, diagnostic errors occurred in 6 out of 44 specimens (13.6 %), reported by over 40 % of participants. Errors involved omitting 5 slides with incomplete IM and 1 with complete IM, all showing a subtle presence of IM. ConclusionsThe study highlights the diagnostic challenges in identifying incomplete gastric IM, showing notable discrepancies in accuracy and interobserver agreement. It underscores the need for better diagnostic protocols and training to enhance detection and management outcomes.

Clinical and morphological characteristics of patients with chronic gastritis and high risk of gastric cancer

The purpose of this study is to conduct a clinical and morphological analysis of cases of chronic gastritis with a high risk of gastric cancer (GC). Materials and methods. The study included 26 cases of chronic atrophic gastritis of stages 3 and 4 with a high risk of developing GC according to the assessment using the OLGA system (Operative Link for Gastritis Assessment). The cases were diagnosed on material of gastric tissue biopsy in 2022. In total, 678 histological studies were performed during the year. Cases of chronic gastritis with a high risk of developing GC accounted for 3.8% of all chronic gastritis. Results. Cases of chronic gastritis with a high risk of developing GC were more often observed in older men (average age 67±12 years, ratio 2.25:1). Multifocal atrophic gastritis was in the first place in frequency of occurrence (61.5%), the connection with helicobacter infection was confirmed only in a third of cases (34.6%). Morphological changes were characterized by a predominant lesion of the antrum of the stomach and mixed complete and incomplete intestinal metaplasia. With the exception of one case in which pseudopancreatic metaplasia was detected in the antrum of the stomach, all cases of autoimmune gastritis (n=26) were assigned to stage 2 with a low risk of developing GC, which seems controversial to us. Conclusion. The results of our study showed a high percentage of pre-existing tumor lesions of the stomach in the group of chronic gastritis with a high risk of developing GC. Dysplasia was diagnosed in 5 out of 26 cases, GC with previously performed mucosectomy in 3 out of 26 cases. In addition, the patients had other tumor and precancerous lesions of the gastrointestinal tract. These data show the validity and practical value of using the OLGA system to identify high-risk groups for the development of tumors not only of the stomach, but also of gastrointestinal tumors of other localizations.

CEACAM5 and TROP2 define metaplastic and dysplastic transitions in human antral gastric precancerous lesions and tumors.

Mucosal gastric atrophy and intestinal metaplasia (IM) increase the risk for the development of gastric cancer (GC) as they represent a field for development of dysplasia and intestinal-type gastric adenocarcinoma. We have investigated the expression of two dysplasia markers, CEACAM5 and TROP2, in human antral IM and gastric tumors to assess their potential as molecular markers. In the normal antral mucosa, weak CEACAM5 and TROP2 expression was only observed in the foveolar epithelium, while inflamed antrum exhibited increased expression of both markers. Complete IM exhibited weak CEACAM5 expression at the apical surface, but no basolateral TROP2 expression. On the other hand, incomplete IM demonstrated high levels of both CEACAM5 and TROP2 expression. Notably, incomplete IM with dysplastic morphology (dysplastic incomplete IM) exhibited higher levels of CEACAM5 and TROP2 expression compared to incomplete IM without dysplastic features (simple incomplete IM). In addition, dysplastic incomplete IM showed diminished SOX2 and elevated CDX2 expression compared to simple incomplete IM. CEACAM5 and TROP2 positivity in incomplete IM was similar to that of gastric adenomas and GC. Significant association was found between CEACAM5 and TROP2 positivity and histology of GC. These findings support the concept that incomplete IM is more likely associated with GC development. Overall, our study provides evidence of the heterogeneity of gastric IM and the distinct expression profiles of CEACAM5 and TROP2 in dysplastic incomplete IM. Our findings support the potential use of CEACAM5 and TROP2 as molecular markers for identifying individuals with a higher risk of GC development in the context of incomplete IM.

Clinicopathological significance of intestinal metaplasia in endoscopically resected early gastric carcinoma.

To investigate the clinicopathological and prognostic significance of intestinal metaplasia (IM) in endoscopically resected early gastric carcinoma (EGC). Altogether 136 consecutive cases with EGC resected by endoscopic submucosal dissection over 5 years were included and divided into theearly gastric cardiac (EGCC; n = 60) and non-cardiac carcinoma (EGNCC; n = 76) groups. Goblet cell IM and subtypes were determined with histology and immunostaining. Recurrence-free survival (RFS) was compared among various IM groups. IM was identified in 128 (94.1%) EGC cases, including complete IM (n = 39), incomplete IM (n = 27), and mixed IM (n = 62). Incomplete IM was significantly more common in EGCC and exhibited a lower frequency of en bloc resection than the complete subtype. The frequency of synchronous or metachronous gastric tumor was significantly more common in EGCC with complete IM than in those with incomplete IM. Compared to EGC without IM, EGC with IM showed a significantly higher frequency of non-poorly cohesive carcinoma, en bloc resection, and non-eCuraC-1 grade. EGNCC with IM was significantly associated with negative resection margins and en bloc resection. The 5-year RFS was significantly lower in EGNCC patients with incomplete IM compared with those with mixed IM. The independent risk factors for RFS included tumor size >2 cm and eCuraC-1 grade. Subtyping IM in EGC helped predict endoscopic resectability, prognosis, and risk of synchronous or metachronous gastric tumor. The significance of IM differed between EGCC and EGNCC. Large studies with longer follow-up are warranted to validate our findings.

Assessment of morphological changes in the gastroduodenal area of patients with chronic pancreatitis in comorbidity with chronic viral hepatitis C

Background. Viral hepatitis C (HCV) is not only as a liver disease but also as a systemic (generalized) infection that affects ot­her organs, in particular, the pancreas and gastroduodenal zone. The state of the gastrointestinal mucosa in combined course of chronic pancreatitis (CP) and chronic HCV is little studied, but extremely relevant, as it is important for the clinical course, the quality of life of patients, as well as for assessing the safety of the performed (etiotropic, etc.) and planned restorative comprehensive treatment of such patients. The purpose is to evaluate the morphological changes of the gastroduodenal mucosa of patients with chronic pancreatitis associated with chronic viral hepatitis C who were treated etiotropically. Materials and methods. Thirty patients with CP and 65 patients with CP in comorbidity with chronic HCV after etiotropic treatment of HCV were examined. Regardless of the HCV genotype, they received a course of treatment with sofosbuvir at a dose of 400 mg and velpatasvir 100 mg in the morning after meals for 3 months (some patients took daclatasvir at a dose of 60 mg also in the morning after meals for 3 months instead of velpatasvir). The period after diagnosed and treated HCV before the examination was on average (2.35 ± 0.61) years. All patients underwent a morphological study of gastric and duodenal biopsy samples obtained by esophagogastroscopy. The prepared samples were evaluated according to the international OLGA and OLGIM systems based on the evaluation of 5 gastric biopsies (1 from the corner of the stomach, 2 from the body, and 2 from the antrum) with a description of the main pathomorphological changes evaluated on a visual analog scale. Alcian yellow and toluidine blue were used to detect H.pylori. An own system for assessing the morphological state of the gastroduodenal mucosa was also proposed. Results. The detected structural changes indicate the presence of chronic atrophic gastritis with moderate dysplasia of the glandular epithelium. Stage of chronic gastritis according to the OLGA system was III. Stage of chronic gastritis according to the OLGIM system was III. Thus, the practically asymptomatic course of quite significant gastroduodenal changes in CP combined with chronic HCV requires additional therapeutic influence, as well as an assessment of comprehensive treatment based on the effect on the gastroduodenal mucosa. In case of changes in gastroduodenal mucosa in CP on the background of chronic HCV, in contrast to those with isolated CP, a significantly higher level of inflammatory infiltrate density (moderate (2+) vs. mild (1+)) is determined, which is accompanied by moderate neutrophilic infiltration (2+) vs. mild (1+) and mild lymphohistiocytic infiltration (1+) versus no such infiltration (0), the appearance of intestinal metaplasia (2+) and moderate non-metaplastic glandular atrophy (2+) versus the absence of metaplasia (0) and mild non-metaplastic glandular atrophy (1+), as well as zones of metaplastic atrophy (1+), which was manifested by the appearance of Paneth cells and goblet cells. In CP with chronic HCV, mucosa has atrophic changes. Metaplasia is manifested by a change in cellular phenotype: complete intestinal metaplasia type I–II is manifested by the appearance of Paneth cells and goblet cells; incomplete — by the presence of columnar epithelium and goblet cells; colonic metaplasia — by enlargement of the glands and the absence of Paneth cells. Conclusions. It was proved that the state of the gastric and duodenal mucosa in the group of patients with CP and chronic HCV was significantly severe than that in isolated CP: lymphohistiocytic infiltration of the mucous membrane was detected 2.68 times more often, non-metaplastic infiltration glandular atrophy (there was practically no glandular atrophy in the group of isolated CP) — 12.65 times more often, metaplastic atrophy (it was not detected in the group of CP) — 10.64 times more often, acute leukocyte infiltration — 2.31 times more often, dysplasia of the mucosal epithelium (with isolated CP, mild dysplasia was detected) — 7.30 times more often, erosion of the mucosal epithelium — 3.07 times more often, focal hyperplasia of the glands — 3.88 times more often, intestinal metaplasia — 12.89 times more often, which was practically absent in CP. In general, the total number of pathological signs of the mucous membrane in the group of CP with comorbid chronic HCV was found to be 2.76 times higher than that in isolated CP.

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.

The Morphologic Spectrum of Gastric Type 1 Enterochromaffin–Like Cell Neuroendocrine Tumors

Although most well-differentiated gastric neuroendocrine tumors (gNETs) arise from enterochromaffin-like (ECL) cells in patients with autoimmune metaplastic atrophic gastritis (AMAG), the morphologic spectrum of these type 1 ECL-cell gNETs is not well defined. The extent of metaplastic progression in the background mucosa of AMAG patients with gNETs is likewise unclear. Here we report the histomorphology of 226 gNETs, including 214 type 1 gNETs (78 cases from 50 AMAG patients) pooled from a population with high AMAG prevalence. Most type 1 gNETs were ≤1.0 cm, of low grade, and multifocal, consistent with the results of previous reports. However, a high proportion (70/214, 33%) displayed unusual gNET morphologies not previously appreciated in AMAG patients. Unlike other type 1 gNETs with conventional neuroendocrine tumor morphologies, unconventional type 1 gNETs displayed cribriform networks of atrophic cells embedded within myxoid matrix (secretory-cribriform variant, 59%), sheets of deceptively bland discohesive cells resembling inflammatory infiltrates (lymphoplasmacytoid variant, 31%), or wreath-like arrangements of columnar cells wrapped around collagenous cores (pseudopapillary variant, 14%). Another unusual feature was that unconventional gNETs grew laterally within the mucosa (50/70, 71%) and were only rarely sampled from the submucosa (3/70, 4%). These features also differed from the conspicuous radial nodules (99/135, 73%) and frequent submucosal involvement (57/135, 42%) observed for conventional gNETs (P < .0001). Irrespective of morphology, type 1 gNETs were nearly always detected at first AMAG diagnosis (45/50, 90%) and tended to persist thereafter (34/43, 79%), despite similar clinical symptoms and laboratory values between AMAG patients with gNETs and those without. However, unlike AMAG patients without gNETs (n = 50), the background mucosa in patients with gNETs (n = 50) had already progressed to the morphologic equivalent of end-stage metaplasia (P < .0001). This included diffuse loss of parietal cells (92% vs 52%), complete intestinal metaplasia (82% vs 40%), and pancreatic metaplasia (56% vs 6%). Thus, type 1 ECL-cell gNETs are morphologically heterogeneous with a high prevalence of unconventional gNET morphologies. They tend to present silently at first AMAG diagnosis as multifocal lesions that persist within fields of mature metaplasia.

Ntestinal Metaplasia in Barrett’s Oesophagus: A Clinicopathological Study

Introduction: The incidence of Oesophageal Adenocarcinoma (EAC) has increased at a faster rate than any other cancer in the developed nations. Despite advances in treatment, five year survival rate for EAC is &lt;15%. Till date, Barrett’s Oesophagus (BE) is the only known precursor of EAC increasing its risk by greater than 30 to 60 fold. Most important risk factor for development of dysplasia and EAC is specialised Intestinal Metaplasia (IM) in BE. Aim: To find the association between clinical, endoscopic and histopathological features and presence of IM in patients with endoscopically suspected BE. Materials and Methods: This was an institution based descriptive study with a cross-sectional design conducted in the Departments of Pathology and Surgery, in a tertiary care centre of North Bengal for four years (2017-2021), among patients attending surgery and medicine Outpatient Department (OPDs) or Inpatient Department (IPDs), suspected on clinical basis and subsequent endoscopic detection of BE utilising Prague criteria. Periodic Acid-Schiff (PAS) and Alcian Blue (pH 2.5) stains were used to detect complete or incomplete IM and results were analysed using appropriate statistical software. Results: Among 120 cases included in the study, 72 (60%) had Short Segment Barrett’s Oesophagus (SSBE) and 48 (40%) Long Segment Barrett’s Oesophagus (LSBE). Hiatal hernia was significantly more frequent in LSBE patients (32 out of 48) compared to patients with SSBE (24 out of 72). The associations of tobacco and alcohol abuse with microscopically proven BE were statistically significant with p-values of 0.005 and 0.004, respectively. The association of IM with the increasing length of Columnar Lined Oesophagus (CLE) was statistically significant (p-value=0.004). Conclusion: Tobacco and alcohol abuse, presence of hiatal hernia (particularly in LSBE patients) were significantly associated with BE. Increasing length of CLE is more commonly associated with IM. Incomplete IM was observed more commonly in LSBE cases whereas complete IM was detected more frequently in cases diagnosed as SSBE by endoscopy

A rare case of heterotopic gastric mucosa of the rectum with complete intestinal metaplasia highlighting the utility of molecular microsatellite testing in diagnostic corroboration

Heterotopic gastric mucosa (HGM) is common in the esophagus but exceedingly rare in other sites. Only 73 cases of HGM of the rectum

Narrow-band imaging Dual focus endoscopy capabilities in diff erential diagnosis of intestinal metaplasia types

Stomach cancer has an important place in medicine. Unfortunately, diagnosis of gastric cancer is being established in majority of cases at the IV stage. So, yt is necessary to detect tumors at the earliest stages of carcinogenesis and to evaluate and treat precancerous diseases, such as gastric atrophy and intestinal metaplasia. Aims : To estimate the value of Narrow-band imaging Dual focus (NBI Dual Focus) endoscopy capabilities in differential diagnosis of intestinal metaplasia types. We evaluated the data of Russian and foreign articles on this topic from 2011 to 2021. In our study 46 patients with suspected intestinal metaplasia admitted to Nizhny Novgorod Oncology Dispensary. We have performed multimodal endoscopy, including White light endoscopy (WLI), narrow-band imaging (NBI, WLI, BLI — 28) and Dual focus endoscopy (18). Sydney system based multifocal biopsy and targeted biopsy of IM foci were performed in all cases. Results : Verification of intestinal metaplasia, visualized with WLI, was confirmed in only 59% cases. However, intestinal metaplasia, observed with NBI, was confirmed by pathology in 100% cases. NBI Dual Focus endoscopy made possible to differentiate complete and incomplete intestinal metaplasia also in all patients. Conclusions : Intestinal metaplasia can be successfully diagnosed with NBI endoscopy. Differential diagnosis of types of intestinal metaplasia and other variants of gastric mucosa metaplasia is possible using narrow-spectrum endoscopy with dual focus (NBI Dual Focus).

S2265 A Rare Case of Esophageal Carcinoma After Tracheoesophageal Fistula Repair

Introduction: Tracheoesophageal fistula (TEF) constitutes one of the commonest congenital anomalies with an incidence of roughly 1 in 3500 births with treatment consisting of surgical correction in very early life. Chronic complications can include esophageal stricture, dysphagia, gastroesophageal reflux disease (GERD), Barrett’s esophagus, and esophageal cancer. While rare, these patients do have an increased risk of esophageal carcinoma attributable to chronic GERD leading to ongoing mucosal disruption. Sparce data on esophageal cancer after TEF repair appears to show an increased risk of this event occurring after 40 years of age. Case Description/Methods: The patient is a 32-year-old man with a past medical history of Cystic Fibrosis, GERD, osteoporosis, and tobacco use, and a past surgical history significant for Tracheoesophageal fistula repair. The patient presented to a primary care physician with complaints of dysphagia. He reported dysphagia only to liquids that started 2 months before presentation. The dysphagia was gradually progressed to solids. He was referred to gastroenterology, and an EGD was performed showing a single traversable mass measuring 5 cm in the esophagus (20 cms. from incisors) covering one-quarter of the circumference, and cold forceps biopsy was performed. The EGD also revealed signs of the previous tracheoesophageal fistula repair and mild generalized atrophic mucosa. Biopsies taken from the esophagus and stomach were sent for pathology. Pathology from the esophageal biopsy came back positive for moderately differentiated Squamous cell carcinoma and gastric biopsy revealed chronic gastritis with complete intestinal metaplasia. The patient was referred to oncology and underwent a PET scan which revealed the esophageal malignancy and bilateral pulmonary nodules. The patient was started on chemoradiation therapy and follows up with oncology regularly (Figure). Discussion: This case describes the importance of continuity of care during the transition from pediatrics to adult care in the field of gastroenterology in patients with a history of TEF repair, given the patient’s young age. While it appears esophageal cancer after TEF repair is rare, there should be an investigation into guidelines for adequate screening in this disease process.Figure 1.: Histopathology and endoscopic images.

Gastric intestinal metaplasia: Long-term follow-up results.

Precancerous lesions are the most commonly cited factor in gastric cancer etiology. The sequence of events in intestinal-type gastric carcinogenesis is considered to be chronic gastritis, atrophy, intestinal metaplasia (IM), dysplasia, and carcinoma, respectively. Early diagnosis and treatment of advanced precursor lesions and gastric cancer is possible by identifying and monitoring patients with such premalignant lesions. In our study, we aimed to evaluate the long-term follow-up results of intestinal metaplasia in our hospital and the rate of progression to malignancy by comparing these patients with patients who have undergone gastroscopy without a diagnosis of intestinal metaplasia. One hundred and fifty-six followed-up patients out of 700 between the ages of 18 and 85 who were admitted to our hospital between 2009 and 2019, who were diagnosed with IM by pathological examination from biopsy material, and 150 patients who were not diagnosed with IM between 2009 and 2011 were included. The results of the cases were evaluated first retrospectively; then, the patients who were invited for control and underwent endoscopy were evaluated prospectively. IM and control groups were compared in terms of dysplasia and gastric cancer development. In addition, the IM group was compared in terms of 5 and 10 years of follow-up, extensive or local involvement, and complete and incomplete involvement in terms of dysplasia and cancer development. The follow-up period of the patients ranged from 1 to 10 years, and the mean follow-up interval was 4.2 ± 2.8 (min: 1; max: 10) years. Age, gender, and pathology results of the patients were examined in terms of IM type, localization of IM, pathology accompanying IM, and presence of Helicobacter pylori (Hp) infection and compared with the control group. While gastric carcinoma was detected in three of 156 patients in the IM group, gastric carcinoma was not detected in the follow-up of 150 patients in the control group. IM was most common in the antrum. Incomplete IM was detected in 89 patients, and complete IM in 69 patients. While two of the three patients with gastric carcinoma were localized to the antrum, one patient had incomplete-type IM and two patients had complete-type IM, and Hp was positive in two patients. While dysplasia was detected in nine of the patients diagnosed with IM, it was detected in two patients in the control group. A statistically significant difference was found between the IM and control groups in terms of dysplasia positivity (p = 0.037). On the other hand, no statistically significant difference was found between the IM and control groups in terms of age-group, gender, follow-up time group, and Hp positivity (p > 0.05). There was no significant difference between those who were followed up for 5 and 10 years in the IM group in terms of dysplasia and cancer development. Therefore, it is considered that patients with intestinal metaplasia may be followed up at longer intervals, except for patients with race, ethnicity, incomplete type, extensive involvement, and a family history of gastric cancer.

Is intestinal metaplasia the point of no return in the progression of gastric carcinogenesis?

Is intestinal metaplasia the point of no return in the progression of gastric carcinogenesis?

Differences in Regression Patterns of Complete and Incomplete Intestinal Metaplasia at Ten Years after Helicobacter pylori Eradication.

This study was conducted to reveal the reversibility of subtype of intestinal metaplasia (IM) and Paneth cells after H. pylori eradication (HPE). Among 75 patients, we retrospectively examined the proportions of patients with complete type of IM (CIM), incomplete type of IM (IIM) and Paneth cells in their biopsy specimens obtained from the greater curvature of the antrum (A2) and the greater curvature of the middle corpus (B2) before and during a follow-up period of 10 years after HPE. Immunohistochemistry was used to determine IM type. Compared to before HPE, the proportion of patients with CIM did not decrease significantly during the 10-year follow-up after HPE both in A2 (32% vs. 21.3%, P = 0.13) and in B2 (6.7% vs. 2.7%, P = 0.60). IIM rates in A2 was significantly lower during this time (26.7% vs. 10.7%, P = 0.04), whereas no patients showed IIM in B2 before HPE. The proportion of patients with Paneth cells decreased significantly in A2 after 3, 8, and 9 years of HPE and in B2 after 4, 6 and 9 years of HPE (P < 0.05 for all). Thus, IIM and Paneth cells regressed during a period of 10 years after HPE.

Comparative outcomes of radiofrequency ablation and cryoballoon ablation in dysplastic Barrett’s esophagus: a propensity score−matched cohort study

Strong evidence supports the use of radiofrequency ablation (RFA) in the management of dysplastic/neoplastic Barrett's esophagus (BE). Recently, the efficacy of the cryoballoon ablation (CBA) system was demonstrated in multicenter cohort studies. We aimed to assess the comparative effectiveness and safety of these 2 ablation modalities for endoscopic eradication therapy (EET) in a cohort study. Data were abstracted on patients with dysplastic BE or intramucosal carcinoma undergoing EET using RFA or CBA as the primary ablation modality at 2 referral centers. The primary outcome was the rate of complete remission intestinal metaplasia (CRIM). Secondary outcomes were rates of complete remission of dysplasia (CRD) and adverse events. Cox proportional hazards models and propensity scored-matched analyses were conducted to compare outcomes. Three hundred eleven patients (CBA, 85 patients; RFA, 226 patients) with a median follow-up of 1.5 years (interquartile range, .8, 2.5) in the RFA group and 2.0 years (interquartile range, 1.3, 2.5) in the CBA group were studied. On multivariable analyses, the chances of reaching CRD and CRIM were not influenced by ablation modality. Propensity score-matched analysis revealed a comparable chance of achieving CRIM (CBA vs RFA: hazard ratio, 1.24; 95% confidence interval, .79-1.96; P= .35) and CRD (CBA vs RFA: hazard ratio, 1.19; 95% confidence interval, .82-1.73; P= .36). The CBA group had a higher stricture rate compared with the RFA group (10.4% vs 4.4%, P= .04). Histologic outcomes of EET using CBA and RFA for dysplastic BE appear to be comparable. A randomized trial is needed to definitively compare outcomes between these 2 modalities.

Gastric Cancer Risk of Intestinal Metaplasia Subtypes: A Systematic Review and Meta-Analysis of Cohort Studies.

INTRODUCTION:Intestinal metaplasia (IM) is an independent risk factor for gastric cancer (GC). However, the subtypes of IM as a risk factor for GC remain controversial. We performed a systematic review and meta-analysis to evaluate the relationship between IM subtypes and GC risk.METHODS:Systematic searches were conducted in PubMed, EMBASE, and the Cochrane Library for published cohort studies of patients with complete IM (type I) or incomplete IM (type II or type III) from inception to May 15, 2021. We extracted relevant data and calculated pooled risk ratios (RRs) and 95% confidence intervals (CIs) comparing the GC risk with IM subtypes.RESULTS:Twelve cohort studies comprising 6,498 individuals were included in the study. Compared with complete IM, the pooled relative risk of GC risk of patients with incomplete IM was 5.16 (95% CI, 3.28–8.12), and the GC risk of type III IM was the highest, with a pooled relative risk of 2.88 (95% CI, 1.37–6.04) compared with that of type II. Compared with complete IM, the pooled relative risk of dysplasia risk in patients with incomplete IM was 3.72 (95% CI, 1.42–9.72), and the dysplasia risk of type III IM was 11.73 (95% CI, 2.08–66.08) compared with that of type I.DISCUSSION:Patients with incomplete IM, especially type III, were at a higher risk of GC and dysplasia than those with complete IM. The current evidence indicates a potential correlation between IM subtypes and GC risk, which may support the use of IM subtypes in GC surveillance.