Incomplete 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.

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.

Endoscopic Kyoto and Kimura-Takemoto Classifications Are Comparable in Predicting High-Risk Gastric Precancerous Lesions

Introduction: Severe and extensive gastric atrophy, extensive or incomplete gastric intestinal metaplasia, and gastric dysplasia are considered high-risk gastric precancerous lesions (HGPLs). Endoscopic findings based on the endoscopic Kyoto classification (EKC) and the Kimura-Takemoto classification (KTC) have been reported to be significantly associated with HGPLs. This study aimed to compare these two classifications in predicting active Helicobacter pylori (H. pylori) infection and HGPLs. Methods: This is a cross-sectional study conducted on naïve dyspeptic patients who underwent upper gastrointestinal endoscopy at a tertiary hospital. Endoscopic findings were scored according to the EKC and KTC. Mapping biopsies were taken, and H. pylori infection was determined using a locally validated rapid urease test and histology. The performance of EKC was compared with that of KTC using the area under the receiver operating characteristic curve (AUC) in predicting active H. pylori infection and HGPLs. Results: There were 292 patients with a median age of 46 and a male-to-female ratio of 1:1. The rates of active H. pylori infection and HGPLs were 61.3% and 14.0%, respectively. The EKC was better than the KTC in predicting active H. pylori infection (AUC: 0.771 vs. 0.658, respectively; p < 0.001). However, these two classifications had comparable performance in predicting HGPLs (AUC: 0.792 vs. 0.791, respectively; p = 0.956). Conclusion: Compared to EKC, KTC is inferior in predicting active H. pylori infection but has comparable performance in predicting HGPLs.

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.

Spasmolytic polypeptide-expressing metaplasia (SPEM) cell lineages can be an origin of gastric cancer.

Intestinal-type gastric cancer arises in a field of precancerous metaplastic lineages. Two types of metaplastic glands are found in the stomachs of humans with the characteristics of pyloric metaplasia or intestinal metaplasia. While spasmolytic polypeptide-expressing metaplasia (SPEM) cell lineages have been identified in both pyloric metaplasia and incomplete intestinal metaplasia, it has been unclear whether SPEM lineages or intestinal lineages can give rise to dysplasia and cancer. A recent article published in The Journal of Pathology describes a patient with evidence of an activating Kras(G12D) mutation in SPEM that is propagated into adenomatous and cancerous lesions which manifest further oncogenic mutations. This case therefore supports the concept that SPEM lineages can serve as a direct precursor for dysplasia and intestinal-type gastric cancer. © 2023 The Pathological Society of Great Britain and Ireland.

Role of pre-existing incomplete intestinal metaplasia in gastric adenocarcinoma: A retrospective case series analysis.

Risk stratification for patients with gastric precancerous lesions for endoscopic surveillance remains controversial. To analysis of patients having developed gastric adenocarcinoma during the period of follow-up. We conducted a retrospective study on patients having undergone upper endoscopy prior to the development of gastric adenocarcinoma. The presence and stage of precancerous lesions as well as subtype of intestinal metaplasia at the baseline endoscopy got evaluated. Literature mini-review was performed. Out of 1681 subjects in the Biobank, gastric adenocarcinoma was detected in five cases in whom previous endoscopy data with biopsies either from the corpus or antral part were available. All of the patients had incomplete intestinal metaplasia during the baseline endoscopy; all three subjects in whom intestinal metaplasia subtyping was performed according to Filipe et al, had Type III intestinal metaplasia. Two of the five cases had low Operative Link on Gastritis Assessment (OLGA) and Operative Link on Gastritis Intestinal Metaplasia Assessment (OLGIM) stages (I-II) at the baseline. The presence of incomplete intestinal metaplasia, in particular, that of Type III is a better predictor for gastric adenocarcinoma development than OLGA/OLGIM staging system. Subtyping of intestinal metaplasia have an important role in the risk stratification for surveillance decisions.

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.

Incomplete Intestinal Metaplasia Is Rare in Autoimmune Gastritis

Background: Incomplete intestinal metaplasia (IM) is reportedly associated with higher gastric cancer (GC) risk than its complete variant. AGA Guidelines recommend including IM subtyping in routine pathology reports. This study assesses the prevalence of complete versus incomplete IM in gastric conditions with different GC risks. Methods: IM subtyping (complete vs. incomplete) and grading (IM extension: G1: ≤30%; G2: >30%) were assessed in 386 patients with IM + ve gastric biopsy sets that included both antral and oxyntic samples. Cases were categorized as: (a) IM foci in otherwise normal mucosa (n = 59); (b) Helicobacter pylori gastritis (n = 138); (c) reactive gastropathy (141); and (d) autoimmune atrophic gastritis (AIG, n = 48). Odds ratios (OR) and their 95% CI were used in comparing the prevalence of incomplete IM and the correlation between subtype and IM extension. Results: Incomplete IM was present in 37.7% of patients with H. pylori gastritis, 8.3% of those with AIG 5.0% of those with reactive gastropathy, and none of those with otherwise normal mucosa. Incomplete IM was strongly associated with more extensive (G2-IM) mucosal intestinalization (OR = 6.69; 95% CI = 2.77–9.40). Conclusion: Incomplete IM is significantly more prevalent in conditions (H. pylori gastritis) known to carry a higher risk of GC and is strongly associated with its extension. The low prevalence of incomplete IM in AIG (8.3%) and reactive gastropathy (5.2%) is in keeping with the low GC risk associated with these conditions.

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

Magnifying endoscopy with narrow-band imaging for diagnosis of subtype of gastric intestinal metaplasia.

Patients with incomplete gastric intestinal metaplasia (GIM) have a higher risk of gastric cancer (GC) than those with complete GIM. We aimed to clarify whether micromucosal patterns of GIM in magnifying endoscopy with narrow-band imaging (M-NBI) were useful for diagnosis of incomplete GIM. We enrolled patients with a history of endoscopic resection of GC or detailed inspection for suspicious or definite GC. The antrum greater curvature and corpus lesser curvature were regions of interest. Areas with endoscopic findings of light blue crest and/or white opaque substance (WOS) were defined as endoscopic GIM, and subsequent M-NBI was applied. Micromucosal patterns were classified into Foveola and Groove types, and targeted biopsies were performed on GIM with each pattern. GIM was classified into complete and incomplete types using mucin (MUC)2, MUC5AC, MUC6, and CD10 immunohistochemical staining. The primary endpoint was the association between micromucosal pattern and histological subtype. The secondary endpoint was endoscopic findings associated with incomplete GIM. We analyzed 98 patients with 156 GIMs. Univariate analysis (odds ratio [OR] 3.4, P=0.004), but not multivariate analysis (OR 0.87, P=0.822), demonstrated a significant association between micromucosal pattern and subtype. The antrum (OR 3.7, P=0.006) and WOS (OR 43, P=0.002) were independent predictors for incomplete GIM. The WOS had 69% sensitivity and 93% specificity. The M-NBI micromucosal pattern is not useful for diagnosis of GIM subtype. WOS is a promising endoscopic indicator for diagnosis of incomplete GIM. (UMIN-CTR000041119).

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).

S1617 Incomplete Intestinal Metaplasia Is Rare in Autoimmune Gastritis

Introduction: Incomplete intestinal metaplasia (IM) is reportedly associated with greater risk for gastric cancer (GC). AGA Guidelines recommend including IM type in pathology reports. In a long-term follow-up of a large cohort of patients with Helicobacter-naïve autoimmune atrophic gastritis (AIG), we did not detect any excess risk for CG (Rugge et al. Gut, In press). We hypothesized that if incomplete IM is a reliable harbinger of GC, it should be uncommon in patients with AIG. Methods: We assessed the IM type in biopsies from 377 subjects with IM and one of the following gastric phenotypes: 1) minimal-change gastritis (MCG – 58 subjects); 2) reactive gastropathy (RG – 135 subjects); 3) H. pylori chronic active gastritis (Hp-CAG, 136 subjects); 4) AIG (48 subjects). To minimize inclusion of patients with previous H. pylori infection we used strict criteria for the diagnosis of AIG, (uninflamed antrum without IM; corpus-restricted atrophy; and ECL-cell hyperplasia). All biopsies were reviewed to confirm diagnosis and location and to categorize the type of IM (complete or incomplete). The prevalence of incomplete IM was compared across gastritis groups. Differences were evaluated using odds ratios (OR) and their 95% confidence intervals (95% CI). Results: Table 1 summarizes the prevalence of incomplete IM in the 4 different groups. Compared to subjects with H. pylori-CAG, those with AIG were >4 times less likely to have the incomplete type of IM (OR 0.23; 0.08 – 0.70; P < .01) Conclusion: Compared to subjects with H. pylori gastritis – a condition known to carry a high risk of GC – patients with AIG had a low prevalence of incomplete IM, providing further support to the concept that AIG, in the absence of previous or concurrent Helicobacter infection, is not associated with a high GC risk. Most studies suggesting a GC risk associated with AIG likely included patients from the pre-Helicobacter era, and the cancer risk may have been induced by unrecognized H. pylori infection. Table 1. - Prevalence of incomplete IM in 4 gastric phenotypes Phenotype of the gastric mucosa Total cases Median Age (range) Female (%) Incomplete IM (%) Atrophic autoimmune gastritis 48 68 (40 – 82) 33 (68.8) 4 (8.3) H. pylori gastritis 136 66 (30 – 90) 78 (57.4) 53 (38.2) Reactive gastropathy 135 61 (14 – 96) 86 (63.7) 7 (5.2) Normal 58 59 (7 – 91) 37 (63.8) 0

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.

Subtyping intestinal metaplasia in patients with chronic atrophic gastritis: an interobserver variability study

Incomplete gastric intestinal metaplasia (GIM) is associated with an increased risk of gastric cancer. We aimed to examine the interobserver variability of GIM subtyping (incomplete vs complete) in histological diagnosis of patients with chronic atrophic gastritis and to identify factors with potential impact on agreement. Nine international gastrointestinal expert pathologists assessed 46 cases with complete, incomplete or mixed-type GIM on scanned haematoxylin and eosin (H&E)-stained slides. Results were compared with the consensus diagnosis driven by two experts. Interobserver variability was evaluated by kappa statistics. Focusing on the predominant pattern, the agreement between each observer and the consensus diagnosis ranged from 78% to 98%. The level of agreement was moderate to almost perfect (weighted kappa=0.464-0.984). The participating pathologists reached substantial overall agreement (Fleiss' kappa=0.716, 95% confidence interval 0.677-0.755). Misclassification with potential impact on clinical decision making occurred in 5.7% of case ratings. The pattern of GIM (pure GIM versus mixed-type GIM) differed significantly between cases with high and low agreement (p=0.010), while the number of biopsy pieces per sample and the portion of mucosal surface involved by GIM did not. Pathologists who apply subtyping in daily routine performed better than those who do not (p=0.040). In conclusion, subtyping GIM on H&E-stained slides can be achieved satisfactorily with high interobserver agreement. The implementation of GIM subtyping as a risk stratifying tool in current practice guidelines by the European Society of Gastrointestinal Endoscopy (ESGE) and the American Gastroenterological Association (AGA) carries a low rate of misclassification, at least among gastrointestinal expert pathologists.

Comparison of the diagnostic accuracy of the updated Sydney system and single biopsy.

Updated Sydney system (USS) recommends taking biopsies from certain areas of the stomach for the diagnosis of precancerous lesions associated with Helicobacter pylori. Our aim was to evaluate the contribution of each of the biopsy sites to the diagnosis. This prospective study included 97 patients aged 40 and over with dyspeptic complaints. Biopsies were taken from five regions: the lesser curvature of the antrum (LCA), the lesser curvature of the corpus (LCC), incisura angularis (IA), the greater curvature of the antrum (GCA), and the greater curvature of the corpus (GCC). Biopsy specimens were stained with hematoxylin-eosin stain, periodic acid Schiff-alcian blue, and Giemsa histochemical stain and evaluated according to the Sydney classification. Thirty-seven (38%) patients were positive for H. pylori in at least one biopsy site. Atrophic gastritis without intestinal metaplasia (IM) was found in 17 (17.5%) of the patients (6.2% in IA, 5.2% in each of LCA, GCA, and LCC, and 2% in GCC). The prevalence of atrophic gastritis with IM was 42.3% (21.6% in LCA, 20.6% in GCA, 20.6% in IA, 14.4% in LCC, and 5.2% in GCC). Endoscopic follow-up was planned in 21 (22%) patients due to the presence of extensive atrophy or incomplete IM. If a single biopsy of the LCA or a biopsy of both LCA and GCA was taken, endoscopic follow-up would have been missed in 12 (57%) or 6 (29%) patients, respectively. Taking biopsies in accordance with the USS had higher sensitivity in detecting atrophic gastritis with or without IM compared to single biopsy. One or two biopsies is not sufficient to identify patients for whom endoscopic follow-up is recommended.

Clinical Recommendations of Russian Gastroenterological Association and RENDO Endoscopic Society on Diagnosis and Treatment of Gastritis and Duodenitis

Aim.The clinical guidelines are intended to supplement specialty decision-making for improved aid quality in patients with gastritis and duodenitis though acknowledging the latest clinical evidence and principles of evidencebased medicine.Key points.Gastritis is an inflammatory disease of stomach mucosa, with a separate definition of acute and chronic gastritis. Chronic gastritis is a cohort of chronic diseases uniting a typical morphology of persistent inflammatory infiltration, impaired cellular renewal with emergent intestinal metaplasia, atrophy and epithelial dysplasia of gastric mucosa. Oesophagogastroduodenoscopy (OGDS) or high-resolution OGDS with magnified or non-magnified virtual chromoendoscopy, including targeted biopsy for atrophy and intestinal metaplasia grading and neoplasia detection, are recommended to verify gastritis and duodenitis, precancer states and/or gastric mucosal changes. All chronic gastritis patients positive for H. рylori should undergo eradication therapy as aetiological and subsidiary for gastric cancer prevention. Chronic gastritis patients with symptoms of dyspepsia (epigastric pain, burning and congestion, early satiety), also combined with functional dyspepsia, are recommended proton pump inhibitors, prokinetics, rebamipide and bismuth tripotassium dicitrate in symptomatic treatment. With focal restricted intestinal metaplasia, follow-up is not required in most cases, mainly when advanced atrophic gastritis is ruled out in high-quality endoscopy with biopsy. However, a familial history of gastric cancer, incomplete intestinal metaplasia and persistent H. pylori infection render endoscopy monitoring with chromoendoscopy and targeted biopsy desirable once in three years. Patients with advanced atrophic gastritis should have high-quality endoscopy every 3 years, and once in 1–2 years if complicated with a familial history of gastric cancer.Conclusion.The recommendations condense current knowledge on the aetiology and pathogenesis of gastritis and duodenitis, as well as laboratory and instrumental diagnostic techniques, main approaches to aetiological H. pylori eradication and treatment of dyspeptic states.