Incomplete Intestinal Metaplasia Research Articles

Tu1155 – Expression of Gcrg213, Line-1 Endonuclease Variant, Significantly Different in Gastric Complete and Incomplete Intestinal Metaplasia

Tu1155 – Expression of Gcrg213, Line-1 Endonuclease Variant, Significantly Different in Gastric Complete and Incomplete Intestinal Metaplasia

Using Machine Learning to Predict Progression in the Gastric Precancerous Process in a Population from a Developing Country Who Underwent a Gastroscopy for Dyspeptic Symptoms.

Background Gastric cancer is the fourth most common cancer and the third most common cause of cancer deaths worldwide. Morbidity and mortality from gastric cancer may be decreased by identification of those that are at high risk for progression in the gastric precancerous process so that they can be monitored over time for early detection and implementation of preventive strategies. Method Using machine learning, we developed prediction models for gastric precancerous progression in a population from a developing country with a high rate of gastric cancer who underwent gastroscopies for dyspeptic symptoms. In the data imputed for completeness, we divided the data into a training and a validation test set. Using the training set, we used the random forest method to rank potential predictors based on their predictive importance. Using predictors identified by the random forest method, we conducted best subset linear regressions with the leave-one-out cross-validation approach to select predictors for overall progression and progression to dysplasia or cancer. We validated the models in the test set using leave-one-out cross-validation. Results We observed for all models that complete intestinal metaplasia and incomplete intestinal metaplasia were the strongest predictors for further progression in the precancerous process. We also observed that a diagnosis of no gastritis, superficial gastritis, or antral diffuse gastritis at baseline was a predictor of no progression in the gastric precancerous process. The sensitivities and specificities were 86% and 79% for the general model and 100% and 82% for the location-specific model, respectively. Conclusion We developed prediction models to identify gastroscopy patients that are more likely to progress in the gastric precancerous process, among whom routine follow-up gastroscopies can be targeted to prevent gastric cancer. Future external validation is needed.

Management of epithelial precancerous conditions and lesions in the stomach (MAPS II): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG), European Society of Pathology (ESP), and Sociedade Portuguesa de Endoscopia Digestiva (SPED) guideline update 2019.

Patients with chronic atrophic gastritis or intestinal metaplasia (IM) are at risk for gastric adenocarcinoma. This underscores the importance of diagnosis and risk stratification for these patients. High definition endoscopy with chromoendoscopy (CE) is better than high definition white-light endoscopy alone for this purpose. Virtual CE can guide biopsies for staging atrophic and metaplastic changes and can target neoplastic lesions. Biopsies should be taken from at least two topographic sites (antrum and corpus) and labelled in two separate vials. For patients with mild to moderate atrophy restricted to the antrum there is no evidence to recommend surveillance. In patients with IM at a single location but with a family history of gastric cancer, incomplete IM, or persistent Helicobacter pylori gastritis, endoscopic surveillance with CE and guided biopsies may be considered in 3 years. Patients with advanced stages of atrophic gastritis should be followed up with a high quality endoscopy every 3 years. In patients with dysplasia, in the absence of an endoscopically defined lesion, immediate high quality endoscopic reassessment with CE is recommended. Patients with an endoscopically visible lesion harboring low or high grade dysplasia or carcinoma should undergo staging and treatment. H. pylori eradication heals nonatrophic chronic gastritis, may lead to regression of atrophic gastritis, and reduces the risk of gastric cancer in patients with these conditions, and it is recommended. H. pylori eradication is also recommended for patients with neoplasia after endoscopic therapy. In intermediate to high risk regions, identification and surveillance of patients with precancerous gastric conditions is cost-effective.

The Microbiota of Gastric Premalignant Lesions: 16S Sequencing Data in a Central American Population

Introduction: Gastric cancer develops through a cascade, from gastritis to atrophic gastritis and gastric intestinal metaplasia, to dysplasia and adenocarcinoma. Helicobacter pylori (Hp) plays a prominent role in this cascade, contributing to the high cancer incidence in regions such as Central America, but the role of other bacteria is less defined. We compared the gastric microbiota of patients with and without premalignant lesions (atrophic gastritis or intestinal metaplasia). Methods: We sequenced the V3—V4 region of the 16S ribosomal RNA gene extracted from gastric corpus biopsies obtained during routine clinical endoscopies at the national university hospital in Leon, Nicaragua. Using the Illumina MiSeq platform and QIIME processing pipeline, we obtained microbiota measures of alpha diversity, beta diversity, and individual taxa-both phyla and operational taxonomic units (OTUs). We compared these measures between groups using the Kruskal—Wallis test. Results: Of 81 subjects, 30 had premalignant lesions and 51 did not, with characteristics described in Table 1. Firmicutes was the dominant phylum in both groups, but only composed 43% of sequences in the premalignant group, compared to 68% of non—premalignant sequences (Figure 1). The difference was related to the Proteobacteria phylum (35% of OTUs in premalignant and 18% in non—premaligant), predominantly from Hp. No differences in alpha or beta diversity existed between groups however, whether calculated with Hp reads included or excluded (Figure 2). Alpha diversity was correlated with number of Hp counts (p<0.001). One OTU was found to be significantly less prevalent in premalignant than non—premalignant samples. The OTU belonged to the Bacillales order of the Firmicutes phylum (p=0.006).1216_A Figure 1 No Caption available.1216_B Figure 2. Summary of phyla detected in gastric biopsy specimens with gastric intestinal metaplasia (GIM), multifocal atrophic gastritis (MAG), non—atrophic gastritis (NAG), and “normal” histology, with H. pylori OTUs included.Conclusion: In this study of the gastric corpus microbiome, premalignant lesions were associated with increasing Hp density and a corresponding decrease in Firmicutes, but otherwise limited differences in microbiota compared to stomachs with minimal or non—atrophic gastritis on histology. Additional areas warranting study include the antrum microbiome and the microbiome in higher risk premalignant lesions (e.g., incomplete gastric intestinal metaplasia or dysplasia).1216_C Figure 3. Box plots of mean alpha diversity of corpus biopsies with and without premalignant lesions (gastric intestinal metaplasia or multifocal atrophic gastritis), according to A) Observed OTUs, B) chao1 index, C) phylogenetic diversity, D) Shannon index. Helicobacter pylori reads are excluded. No significant difference between—group difference was detected for any measure.

Risk of gastric cancer among patients with gastric intestinal metaplasia

Plenty of studies have assessed the association between intestinal metaplasia (IM) and gastric cancer risk, while the results were inconsistent. We aimed to assess the risk of gastric cancer among patients with IM. Systematic literature searches were conducted in PubMed, Embase and Cochrane databases. Baseline characteristics and outcomes from the included studies were extracted independently by two investigators. Either a fixed-effects or a random-effects model was used to composite the pooled OR for gastric cancer risk. Finally, a total of 21 studies, which comprised 402,636 participants and 4,535 gastric cancer patients, were finally included in the current meta-analysis. Compared with those participants without IM, IM patients were at a higher risk of gastric cancer (pooled OR = 3.58, 95% CI 2.71-4.73). We observed that incomplete IM (pooled OR = 9.48, 95% CI 4.33-20.78) but not complete IM (pooled OR = 1.55, 95% CI 0.91-2.65) was significantly associated with a higher gastric cancer risk. Besides, it appeared that gastric cancer risk was higher among patients with IM in the corpus (pooled OR = 7.39, 95% CI 4.94-11.06) than those with IM in the antrum only (pooled OR = 4.06, 95% CI 2.79-5.91). And the pooled ORs for gastric noncardia cancer and gastric cardia cancer were 4.98 (95% CI 3.12-7.95) and 1.93 (95% CI 1.15-3.24), respectively. In conclusion, patients with IM were at a higher risk of gastric cancer, especially for incomplete IM and IM in the corpus. The current evidence supports the use of IM subtypes in the surveillance of gastric cancer.

A Case-Control Study of the Association between Vitamin D Levels and Gastric Incomplete Intestinal Metaplasia.

Aim: Low circulating vitamin D levels are associated with gastric adenocarcinoma, but whether vitamin D levels are associated with premalignant gastric mucosal changes is unknown. Here, we determined associations between vitamin D levels and gastric incomplete intestinal metaplasia, a known gastric adenocarcinoma risk factor. Methods: This was a retrospective, unmatched, case-control study comparing serum 25-hydroxyvitamin D levels among subjects with gastric incomplete intestinal metaplasia (cases; n = 103) and those without gastric incomplete intestinal metaplasia (controls; n = 216). The 25-hydroxyvitamin D levels were categorized as normal (30–100 ng/dL), vitamin D insufficiency (VDi; 20–29 ng/dL), and vitamin D deficiency (VDd; <20 ng/dL). Using multivariable logistic regression, odds ratios (ORs) were calculated and adjusted to age, gender, ethnicity, body mass index, history of hypertension or diabetes mellitus, and timing of vitamin D collection to assess associations between 25-hydroxyvitamin D levels and gastric incomplete intestinal metaplasia. Results: A majority of case subjects were male, Hispanic, and did not have hypertension or diabetes mellitus. The average serum 25-hydroxyvitamin D level was significantly lower in the intestinal metaplasia group than the control group (19.7 ng/dL vs. 34.7 ng/dL; p < 0.001). Hypovitaminosis D was more common in subjects with incomplete intestinal metaplasia in a multivariable regression model (OR 54.1, 95% CI 21.8–134.3; p < 0.001). VDd (OR 129.0, 95% CI 43.7–381.2; p < 0.001) and VDi (OR 31.0, 95% CI 11.9–80.3; p < 0.001) were more common in patients with incomplete intestinal metaplasia than healthy subjects, with VDd slightly more prevalent than VDi (OR 4.0, 95% CI 1.7–9.6; p < 0.001). Conclusions: Vitamin D deficiency and insufficiency are more common in patients with gastric incomplete intestinal metaplasia than healthy subjects and may play a role in the development of premalignant phenotypes related to gastric adenocarcinoma.

Circulating microRNA-22-3p Predicts the Malignant Progression of Precancerous Gastric Lesions from Intestinal Metaplasia to Early Adenocarcinoma.

Gastric cancer has a poor outcome and identifying useful biomarkers from peripheral blood or tissue could allow its early detection, or potentially precancerous changes, thus improving the curative rates. MicroRNAs (miRNAs) have been shown to offer great potential in cancer diagnosis and prediction. Here, we investigated the role of plasma miRNAs in the natural course of gastric cancer, from intestinal metaplasia to early cancer. The findings were used to understand whether patients at a high risk of malignancy could be given appropriate interventions in the early disease process, such as using endoscopic submucosal dissection to treat gastric dysplasia or early gastric cancer. Participants were divided into healthy control, intestinal metaplasia (IM), and dysplasia/early cancer (pT1a/b) groups. Microarray was used to select potential markers in tissue. Quantitative real-time polymerase chain reaction data showed circulating miRNA-22-3p had significantly different expression in patients with precancerous lesions or gastric adenocarcinoma. The areas under the curve of incomplete IM versus healthy control, low-grade/high-grade dysplasia, early gastric cancer, and GED were 0.8080, 0.8040, 0.8494, and 0.8095, respectively (all P values < 0.05). Circulating miRNA-22-3p could be a potential biomarker for gastric precancerous dysplasia and early cancer detection.

The Distribution of Incomplete Gastric Intestinal Metaplasia (GIM) Subtype among Biopsy Sites according to the Updated Sydney System and Its Association with GIM Extension.

Background Current guidelines recommend that extensive gastric intestinal metaplasia (GIM) be considered as a high-risk marker for the development of gastric cancer (GC). But there is emerging evidence that the incomplete GIM subtype is also a high-risk marker. Aims To evaluate the performance of biopsy sites according to the updated Sydney system on detecting the incomplete GIM subtype and to assess its association with GIM extension. Patients and methods A cross-sectional study was conducted on 280 Vietnamese patients with nonulcer dyspepsia. Biopsy specimens were taken from gastric sites according to the updated Sydney system, and sections were routinely stained with Giemsa and hematoxylin and eosin. Biopsy specimens with intestinalization were further evaluated for GIM subtypes with alcian blue 2.5 and periodic acid Schiff stainings. Two experienced pathologists jointly examined all the specimens and reached consensus. Results The rates of patients with GIM and the incomplete GIM subtype were 81 (28.9%) and 24 (8.4%), respectively. There was no GIM in specimens taken from the greater curvature of corpus. The proportions of the incomplete GIM subtype detected at the incisura angularis, lesser curvature of corpus, lesser curvature of antrum, and greater curvature of antrum were 34.3% (12/35), 34.5% (10/29), 40.5% (17/42), and 31.6 (6/19), respectively, which were not significantly different (p = 0.89). The presence of an incomplete GIM subtype was associated with multifocal GIM (i.e., ≥3 out of 5 biopsy sites with GIM) (OR = 4.02, CI 95%, 1.33–12.16, p = 0.022) and extensive GIM (i.e., GIM in specimens from both of corpus and antrum) (OR = 2.89, CI 95% 1.04–8.02, p = 0.045). Conclusions The proportions of an incomplete GIM subtype were not significantly different among gastric biopsy sites with intestinalization. The association between an incomplete GIM subtype and GIM extension, therefore, may be due to an sum accumulation effect.

Helicobacter pylori as a crucial factor in intestinal metaplasia development of gastric mucosa

&lt;p class="BodyText1"&gt;&lt;em&gt;Helicobacter pylori&lt;/em&gt; (&lt;em&gt;H. pylori&lt;/em&gt;) is detected on the surface of gastric epithelium and in goblet cells, predominantly in patients with chronic atrophic gastritis and incomplete intestinal metaplasia (IM). &lt;em&gt;H. pylori&lt;/em&gt; infection persistence leads to the formation of gastrointestinal phenotype of IM. &lt;em&gt;H. pylori&lt;/em&gt; can be considered as an etiological factor of IM. It inhibits the expression of SOX2 in gastric epithelial cells, hence activating transcription factor CDX2 as a counterpart to &lt;em&gt;MUC5AC&lt;/em&gt; gene inhibition and &lt;em&gt;MUC2&lt;/em&gt; gene induction. Thus, in metaplastic cells, programming differentiation after intestinal phenotype will develop. The role of &lt;em&gt;H. pylori&lt;/em&gt; in the origin of intestinal metaplasia of gastric mucosa was defined in this study to elucidate the probable mechanism of cell reprogramming. The activation of CDX2, with simultaneous inactivation and decreased number of genes (&lt;em&gt;e.g.&lt;/em&gt;, &lt;em&gt;SHH&lt;/em&gt;, &lt;em&gt;SOX2&lt;/em&gt;, and &lt;em&gt;RUNX3&lt;/em&gt;) responsible for gastric differentiation, was identified to cause the appearance of IM. &lt;/p&gt;

Is there any association between colonic polyps and gastric intestinal metaplasia?

Chronic gastritis progression is a multistep process of atrophy, intestinal metaplasia (IM), and dysplasia, which may lead to invasive carcinoma. In this study, we identified an association of colonic polyps with gastric IM in patients undergoing colonoscopy. This retrospective case-control, cross-sectional study was conducted in a tertiary-care institution in Turkey. Pathology and endoscopy reports were reviewed. The study group comprised 400 patients with colonic adenomatous polyps, and the control group comprised 360 patients without colonic adenomatous polyps on colonoscopy. The risk of gastric IM was 1.42-fold higher in the study group (p<0.05). The risk of IM in patients aged ≥50 years with colonic polyps was 3.35-fold higher than in those aged <50 years (p<0.05). The risk of Helicobacter pylori infection in the study group was 1.07-folder higher than that in the control group (p<0.05). H. pylori infection prevalence was higher only in patients with high-grade colonic polyp dysplasia (p<0.05). There were no statistically significant differences in the proportion of incomplete IM between the groups (p<0.05). This study observed increased rates of gastric IM with colonic polyps. An increased risk of gastric IM was associated with higher grades of polyp dysplasia.

SCHLAFEN 5 expression correlates with intestinal metaplasia that progresses to gastric cancer.

Intestinal metaplasia (IM) is a gastric cancer precursor lesion (GCPL) and an extremely high risk factor for progression to gastric cancer (GC). Clinical guidelines recommend that patients with extensive IM undergo a gastroscopy every 3years. However, protein biomarkers that indicate a transition from IM to GC are lacking. Our group recently identified an interferon-alpha (IFNα)-responsive gene, Schlafen 4 (Slfn4), in immune cells that correlates with metaplastic changes in Helicobacter-infected mice. We therefore tested the hypothesis that a human homolog of Slfn4, namely, Schlafen 5 (SLFN5), correlates with progression of GCPL to GC. Jurkat T-lymphoid and HL-60 myeloid cell lines were treated with IFNα, and SLFN5 mRNA was quantified by quantitative PCR. SLFN5 protein expression in the inflamed gastric mucosa was co-localized to specific immune cell types by immunohistochemistry using CD20, CD2, and MAC2 antibodies. SLFN5 expression was also determined by immunohistochemistry in formalin-fixed paraffin-embedded samples from individuals with non-atrophic gastritis, atrophic gastritis, complete IM, incomplete IM, and GC, respectively. The IFNα treatment of Jurkat and HL-60 cells induced SLFN5 mRNA. SLFN5 protein was expressed mainly by T lymphocytes in inflamed gastric mucosa. The highest level of SLFN5 expression was observed in patients with IM that progressed to GC. Receiver operating characteristic curves demonstrated that correlating SLFN5 expression with the histologic diagnosis of IM significantly increased the probability of identifying patients who may progress to GC. In this study population, elevated SLFN5 protein expression in patients with IM correlated with progression to GC.

Regression of gastric intestinal metaplasia after the eradication of Helicobacter pylori infection in a hospital in Mexico.

Intestinal metaplasia is a precursor lesion of gastric cancer. Infection by Helicobacter pylori is the principal cause of metaplasia. While evidence of the regression of metaplasia after treatment to eradicate this infection has been demonstrated, controversy remains with regard to this subject. The objective of this study was to determine the frequency of the regression of gastric intestinal metaplasia one year after the eradication of Helicobacter pylori. A prospective longitudinal designed study was carried out. The population studied in this research consisted of patients attending the Endoscopy Unit to undergo an upper endoscopy, in whom various symptoms indicated intestinal metaplasia associated with Helicobacter pylori, and who received standard empiric triple therapy to eradicate the bacteria. An upper endoscopy was performed in which four gastric biopsy samples were taken (two from the antrum and two from the body) before and after the eradicating treatment, with the endoscopic and histological findings studied after one year of monitoring. The statistical analysis was conducted using the Fisher's exact test and the McNemar's test. Forty-six patients were studied, of whom 20 (43.5%) were men and 26 (56.5%) were women, with an average age of 58.9 (DE 11.2). Intestinal metaplasia was found in 46 (100%) patients before treatment and in 21 (45.7%) patients post-eradication. Complete intestinal metaplasia (type I) was found in 35 patients (76.1%) before treatment and in 11 (23.9%) patients post-eradication (p = 0.000), while incomplete intestinal metaplasia (type II) was found in 10 (21.7%) patients before treatment and in 10 (21.7%) patients post-eradication. Non-atrophic chronic gastritis was found in 35 (76.1%) patients before treatment and in 32 (69.6%) patients post-eradication. In this study, gastric intestinal metaplasia associated with Helicobacter pylori infection showed a regression of 54.3% one year after the eradication of this microorganism. This treatment could modify the natural history of the development of gastric cancer.

Helicobacter pylori associated gastric intestinal metaplasia: Treatment and surveillance.

Gastric cancer (GC) is one of the leading causes of cancer related death in the world, particularly in East Asia. According to the Correa's cancer cascade, non-cardia GC is usually developed through a series of mucosal changes from non-atrophic gastritis to atrophic gastritis (AG), intestinal metaplasia (IM), dysplasia and adenocarcinoma. Atrophic gastritis and IM are therefore generally considered to be pre-neoplastic gastric lesions. Helicobacter pylori (H. pylori) infection is an important initiating and promoting step of this gastric carcinogenesis cascade. Emerging long-term data showed that eradication of H. pylori reduced the risk of subsequent cancer development. It however remains confusing whether eradication of the bacterium in individuals with pre-neoplastic gastric lesions could regress these changes as well as in preventing cancer. Whilst H. pylori eradication could likely regress AG, the presence of IM may be a point of no return in this cascade. Hence, surveillance by endoscopy may be indicated in those with extensive IM or those with incomplete IM, particularly in populations with high GC risk. The optimal interval and the best tool of surveillance endoscopy remains to be determined in future studies.

The Prevalence of Gastric Intestinal Metaplasia and Distribution of Helicobacter pylori Infection, Atrophy, Dysplasia, and Cancer in Its Subtypes.

Objectives. Gastric intestinal metaplasia (IM) is frequently encountered and is considered a precursor of gastric adenocarcinoma. In the Van region of Turkey, gastric adenocarcinoma incidence is high but the prevalence of gastric IM is not known. Helicobacter pylori (H. pylori) infection is a main factor leading to atrophy, IM, and cancer development in the stomach. The aim of the current study was to investigate the prevalence of IM and its subtypes and the prevalence of H. pylori infection, atrophy, dysplasia, and cancer in gastric IM subtypes. Materials and Methods. This retrospective study was conducted on 560 IM among the 4050 consecutive patients who were undergoing esophagogastroduodenoscopy (EGD) with biopsy between June 2010 and October 2014. Clinical records and endoscopic and histopathologic reports of patients with IM were analyzed. Results. The prevalence of gastric IM was 13.8%. The prevalence of incomplete IM was statistically significantly higher than complete IM. Type III IM was the most frequent subtype. Conclusions. Gastric IM is a common finding in patients undergoing EGD with biopsy in this region. High prevalence of incomplete type IM, especially type III, can be associated with the high prevalence of gastric cancer in our region.

Differentiation reprogramming in gastric intestinal metaplasia and dysplasia: role of SOX2 and CDX2.

Intestinal metaplasia (IM), which results from de-novo expression of CDX2, and dysplasia are precursor lesions of gastric cancer that are associated with an increased risk for cancer development. There is much evidence suggesting a role for the transcription factor SOX2 in gastric differentiation. The aim of this study was to attempt to establish the relationship of SOX2 with CDX2 and with the differentiation reprogramming that characterizes gastric carcinogenesis, to assess their involvement in IM and dysplasia. Characterization of gastric (SOX2, MUC5AC, and MUC6) and intestinal (CDX2 and MUC2) markers in normal gastric mucosa, in 55 foci of IM and in 26 foci of dysplasia, was performed by immunohistochemistry. SOX2 was expressed in the normal gastric mucosa, in the presumptive stem cell compartment, and was maintained in 7% of the complete (MUC5AC-negative) and 85% of the incomplete (MUC5AC-positive) IM subtypes. Twelve per cent of the dysplastic lesions expressed SOX2, and the association with MUC5AC was lost. CDX2 was present in all IMs and dysplastic lesions. SOX2 is associated with gastric differentiation in incomplete IM and is lost in the progression to dysplasia, whereas CDX2 is acquired denovo in IM and maintained in dysplasia. This suggests that the balance between gastric and intestinal differentiation programmes impacts on the gastric carcinogenesis cascade progression.

Screening for and surveillance of gastric cancer.

Although the prevalence of gastric cancer (GC) progressively decreased during the last decades, due to improved dietary habit, introduction of food refrigeration and recovered socio-economic level, it still accounts for 10% of the total cancer-related deaths. The best strategy to reduce the mortality for GC is to schedule appropriate screening and surveillance programs, that rises many relevant concerns taking into account its worldwide variability, natural history, diagnostic tools, therapeutic strategies, and cost-effectiveness. Intestinal-type, the most frequent GC histotype, develops through a multistep process triggered by Helicobacter pylori (H. pylori) and progressing from gastritis to atrophy, intestinal metaplasia (IM), and dysplasia. However, the majority of patients infected with H. pylori and carrying premalignant lesions do not develop GC. Therefore, it remains unclear who should be screened, when the screening should be started and how the screening should be performed. It seems reasonable that screening programs should target the general population in eastern countries, at high prevalence of GC and the high-risk subjects in western countries, at low prevalence of GC. As far as concern surveillance, currently, we are lacking of standardized international recommendations and many features have to be defined regarding the optimal diagnostic approach, the patients at higher risk, the best timing and the cost-effectiveness. Anyway, patients with corpus atrophic gastritis, extensive incomplete IM and dysplasia should enter a surveillance program. At present, screening and surveillance programs need further studies to draw worldwide reliable recommendations and evaluate the impact on mortality for GC.

Outcome of Intestinal Metaplasia in Gastric Biopsy of Patients with Dyspepsia in Guilan Province, North Iran

It is generally accepted that gastric carcinomas are preceded by a sequential multistage process that includes chronic gastritis, gastric atrophy, usually with intestinal metaplasia (IM), and dysplasia. This series of changes in gastric carcinogenesis is often initiated by Helicobacter pylori (H pylori) infection. The aim of the present study was determination of gastric histopathologic changes in IM patients after at least one year in Guilan province, Iran. This case-series study was conducted in Guilan Gastrointestinal and Liver Disease Research Center (GLDRC) during 2010 to 2011. Gastric biopsy was performed for all 71 known cases of IM and precanceric lesions including gastric atrophy, IM, dysplasia and H pylori infection were determined after at least one year. Of the total of 71 patients with established IM who were enrolled, 50 had complete-type IM and 21 had incomplete-type IM. Fifty two people had H pylori infection. H pylori eradication was achieved in 39 patients (75%). Secondary pathology findings of patients with IM were complete metaplasia (39.4%), incomplete metaplasia (32.4%), dysplasia (23.9%) and other precanceric lesions (4.2%). Dysplasia (20%vs 33%) occurred in patients who had complete and incomplete IM at baseline respectively (p>0.05). Age, gender, family history of gastric cancer(GC); smoking habits and NSAIDs use were not associated with gastric premalignant lesions in initial and secondary pathologies (p>0.05). The difference became statistically significant between H pylori infection in patients with more than 3 years diagnostic intervals (p<0.05). Statistical difference between eradicators and non-eradicators was not significant. We found that incomplete IM increased the risk of subsequent dysplasia in this study.

Intestinal Metaplasia of the Stomach

Intestinal metaplasia (IM) of the stomach is associated with a very small increased risk of developing gastric cancer. Endoscopic surveillance has been proposed and advocated for populations at risk. Risk factors for IM include Helicobacter pylori infection, high salt intake, smoking, alcohol consumption, and chronic bile reflux. IM tends to appear initially at the antrum–corpus junction, especially at the gastric angularis. As atrophy and metaplastic changes advance, they extend to the antrum and corpus. Gastric IM is categorized histopathologically into incomplete and complete types. Patients with incomplete IM should undergo endoscopic gastric mapping to define the extent of IM and rule out dysplasia or adenocarcinoma. In this video presentation, endoscopic and pathological findings in gastric IM and gastric mapping techniques has been described. This article is part of an expert video encyclopedia.

Utility of subtyping intestinal metaplasia as marker of gastric cancer risk. A review of the evidence

The identification and surveillance of patients with preneoplastic lesions at high risk of progressing to gastric cancer (GC) represents the most effective way of reducing the burden of GC. The incomplete type of intestinal metaplasia (IM) could be considered as the best candidate for surveillance. However, the usefulness of subtyping of IM has been considered by some authors as limited and inconsistent. A search was carried out to identify all cross-sectional (n=14) and follow-up (n=10) studies that assessed the risk of GC among subjects with different types of IM. Out of the 14 cross-sectional studies, 13 reported that the prevalence of incomplete IM was statistically significantly higher in GC than in other gastric lesions. Out of the ten follow-up studies, six found a statistically significant association between incomplete IM and subsequent GC risk. The relative risks of GC were from 4- to 11-fold higher for the presence of incomplete type in comparison to complete type or in comparison to the absence of incomplete type, among the studies that reported the magnitude of the risk. According to this comprehensive review, most of the scientific evidence supports the utility of subtyping IM as a predictor of GC risk. Recognizing its usefulness by gastroenterologists should encourage pathologists to subtype IM.

Gastric precancerous lesions are associated with gene variants inHelicobacter pylori-susceptible ethnic Malays

To identify genes associated with gastric precancerous lesions in Helicobacter pylori (H. pylori)-susceptible ethnic Malays. Twenty-three Malay subjects with H. pylori infection and gastric precancerous lesions identified during endoscopy were included as "cases". Thirty-seven Malay subjects who were H. pylori negative and had no precancerous lesions were included as "controls". Venous blood was collected for genotyping with Affymetrix 50K Xba1 kit. Genotypes with call rates < 90% for autosomal single nucleotide polymorphisms (SNPs) were excluded. For each precancerous lesion, associated SNPs were identified from Manhattan plots, and only SNPs with a χ² P value < 0.05 and Hardy Weinberg Equilibrium P value > 0.5 was considered as significant markers. Of the 23 H. pylori-positive subjects recruited, one sample was excluded from further analysis due to a low genotyping call rate. Of the 22 H. pylori-positive samples, atrophic gastritis only was present in 50.0%, complete intestinal metaplasia was present in 18.25%, both incomplete intestinal metaplasia and dysplasia was present in 22.7%, and dysplasia only was present in 9.1%. SNPs rs9315542 (UFM1 gene), rs6878265 (THBS4 gene), rs1042194 (CYP2C19 gene) and rs10505799 (MGST1 gene) were significantly associated with atrophic gastritis, complete intestinal metaplasia, incomplete metaplasia with foci of dysplasia and dysplasia, respectively. Allele frequencies in "cases" vs "controls" for rs9315542, rs6878265, rs1042194 and rs10505799 were 0.4 vs 0.06, 0.6 vs 0.01, 0.6 vs 0.01 and 0.5 vs 0.02, respectively. Genetic variants possibly related to gastric precancerous lesions in ethnic Malays susceptible to H. pylori infection were identified for testing in subsequent trials.