Gastric Intestinal Metaplasia Cases Research Articles

Validation of a pre-endoscopy risk score for predicting the presence of gastric intestinal metaplasia in a U.S. population

Surveillance of gastric intestinal metaplasia (GIM) may lead to early gastric cancer detection. Our purpose was to externally validate a predictive model for endoscopic GIM previously developed in a veteran population in a second U.S. We previously developed a pre-endoscopy risk model for detection of GIM using 423 GIM cases and 1796 control subjects from the Houston Veterans Affairs Hospital. The model included sex, age, race/ethnicity, smoking, and Helicobacter pylori infection with an area under the receiver-operating characteristic curve (AUROC) of .73 for GIM and .82 for extensive GIM. We validated this model in a second cohort of patients from 6 Catholic Health Initiative (CHI)-St Luke's hospitals (Houston, Tex, USA) from January to December 2017. Cases were defined as having GIM on any gastric biopsy sample and extensive GIM as involving both the antrum and corpus. We further optimized the model by pooling both cohorts and assessing discrimination using AUROC. The risk model was validated in 215 GIM cases (55 with extensive GIM) and 2469 control subjects. Cases were older than control subjects (59.8 vs 54.7 years) with more nonwhites (59.1% vs 42.0%) and H pylori infections (23.7% vs 10.9%). The model applied to the CHI-St Luke's cohort had an AUROC of .62 (95% confidence interval [CI], .57-.66) for predicting GIM and of .71 (95% CI, .63-.79) for predicting extensive GIM. When the Veterans Affairs and CHI-St Luke's cohorts were pooled, discrimination of both models improved (GIM vs extensive GIM AUROC: .74 vs .82). A pre-endoscopy risk prediction model was validated and updated using a second U.S. cohort with robust discrimination for endoscopic GIM. This model should be evaluated in other U.S. populations to risk-stratify patients for endoscopic GIM screening.

Inverse Association Between Gluteofemoral Obesity and Risk of Non-Cardia Gastric Intestinal Metaplasia

It is unclear whether obesity confers increased risk of non-cardia gastric adenocarcinoma and its precursor, gastric intestinal metaplasia. Here, we examined whether various dimensions of adiposity independently predispose to the development of non-cardia gastric intestinal metaplasia. We compared data from 409 non-cardia gastric intestinal metaplasia cases and 1748 controls without any gastric intestinal metaplasia from a cross-sectional study at the VA Medical Center in Houston, Texas. Participants completed standardized questionnaires, underwent anthropometric measurements, and underwent a study endoscopy with gastric mapping biopsies. Non-cardia gastric intestinal metaplasia cases included participants with intestinal metaplasia on any non-cardia gastric biopsy. We calculated odds ratios (ORs) and 95% confidence intervals (95% CIs) using logistic regression models. Increasing body mass index (BMI) was not associated with risk of non-cardia gastric intestinal metaplasia (per unit BMI adjusted OR, 0.98; 95% CI, 0.96-1.00). Similarly, we found no associations with increase in waist circumference (per 10-cm increase adjusted OR, 0.94; 95% CI, 0.87-1.03) and waist-to-hip ratio (WHR) (per unit WHR adjusted OR, 2.34; 95% CI, 0.37-14.7). However, there was a significant inverse association with gastric intestinal metaplasia and increasing hip circumference, reflecting gluteofemoral obesity (per 10-cm increase adjusted OR, 0.89; 95% CI, 0.80-0.98). The inverse association was observed for both extensive and focal gastric intestinal metaplasia. The independent dimensions of adiposity (BMI, waist circumference) are not associated with increased risk of non-cardia gastric intestinal metaplasia. The inverse association between gluteofemoral obesity and risk of gastric intestinal metaplasia warrants additional study.

Performance status of targeted biopsy alone versus Sydney protocol by non-NBI expert gastroenterologist in gastric intestinal metaplasia diagnosis.

Background and study aims According to a recent guideline, patients with gastric intestinal metaplasia (GIM) should have at least five biopsies performed under the Sydney protocol to evaluate for risk of extensive GIM. However, only narrow-band imaging (NBI)-targeted biopsy may be adequate to diagnose extensive GIM. Patients and methods A cross-sectional study was conducted between November 2019 and October 2020. Patients with histology-proven GIM were enrolled. All patients underwent standard esophagogastroduodenoscopy performed by a gastroenterology trainee. The performing endoscopists took biopsies from either a suspected GIM area (NBI-targeted biopsy) or randomly (if negative for GIM read by NBI) to complete five areas of the stomach as per the Sydney protocol. The gold standard for GIM diagnosis was pathology read by two gastrointestinal pathologists with unanimous agreement. Results A total of 95 patients with GIM were enrolled and 50 (52.6%) were men with a mean age of 64 years. Extensive GIM was diagnosed in 43 patients (45.3%). The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of NBI-targeted biopsy vs. the Sydney protocol were 88.4% vs.100 %, 90.3% vs. 90.3%, 88.4% vs. 89.6%, 90.3% vs. 100%, and 89.5% vs. 94.7%, respectively. The number of specimens from NBI-targeted biopsy was significantly lower than that from Sydney protocol (311vs.475, P < 0.001). Conclusions Both NBI-targeted biopsy and Sydney protocol by a gastroenterologist who was not an expert in NBI and who has experience with diagnosis of at least 60 cases of GIM provided an NPV higher than 90%. Thus, targeted biopsy alone with NBI, which requires fewer specimens, is an alternative option for extensive GIM diagnosis.

Ethnicity Is an Important Consideration in Screening for Gastric Intestinal Metaplasia.

Gastric intestinal metaplasia (GIM) is a precursor to gastric adenocarcinoma, making it an attractive target for early detection by endoscopy. The aim of this study was to determine the prevalence, risk factors, and associated histologic findings of GIM among patients undergoing endoscopy in a diverse US population. We conducted a retrospective, cross-sectional study of patients undergoing elective endoscopy with gastric biopsies at 6 academic and community centers in Houston, Texas. GIM prevalence was estimated with a 95% confidence interval (CI), and patient demographic and clinical characteristics were summarized using mean with standard deviation, or frequency with percentage. Generalized estimating equations (GEE) were used to compare characteristics between those with and without GIM. Our final cohort consisted of 2685 patients, including 216 cases with GIM and 2469 controls. The prevalence of GIM in our cohort was 8.04% (95% CI 7.07%, 9.14%). The mean age of GIM cases was higher than in the control group (59.8 vs 54.7years, p < 0.0001). The prevalence of GIM in Asians, Hispanic, Black and Non-Hispanic Whites (NHW) was 14.7%, 11.7%, 9.8% and 5.8%, respectively. On multivariable analysis, factors associated with GIM include age (adj. OR 1.32 per 10year increase, p < 0.0001), habitual smoking (adj. OR 1.68, p < 0.0001), and race (compared to NHW: Asian, adj. OR 2.34, p = 0.010; Hispanic, adj. OR 2.15, p < 0.001; Black, adj. OR 1.61, p < 0.001). Asians, Hispanics, and African Americans have higher rates of GIM than NHW. Ethnicity should be an important consideration on determining who to screen for GIM in the US.

Index diagnoses of gastric intestinal metaplasia in the United States: patient characteristics, endoscopic findings, and clinical practice patterns at a large tertiary care center.

Background:Gastric intestinal metaplasia (GIM) is a premalignant gastric mucosal change that is often incidentally detected during esophagogastroduodenoscopy (EGD). Despite the established higher risk of gastric cancer associated with GIM, the incidence, prevalence, and outcomes data for GIM are limited in the United States (US), and practice patterns are highly variable.Objectives:Our primary objectives were to accurately identify incident histology-confirmed GIM cases and determine patient characteristics, endoscopy findings, Helicobacter pylori (HP) detection, and eradication treatment outcomes, as well as surveillance and follow-up recommendations.Design:We conducted a retrospective cohort study using administrative data.Methods:We first developed and validated a rule-based natural language processing tool to identify the patients with GIM on gastrointestinal pathology reports between 2011 and 2016. We then performed a manual chart review of all EGD procedures and associated pathology notes to confirm cases and obtain clinically relevant data.Results:In all, 414 patients with an index diagnosis of GIM were confirmed (prevalence = 2.5% of patients undergoing any EGD). A majority (52.4%) of patients were non-Hispanic white. The most common indication for EGD was abdominal pain (46.9%). A majority (55%) did not receive specific follow-up recommendations or were asked to see their primary care provider. HP testing was documented in 86% of patients, and detected in 94 patients (prevalence = 26.4%). Treatment was documented in 94.7% of cases, and eradication confirmed in only 34.8% of these cases.Conclusion:A large group of US patients with an index diagnosis of GIM was accurately identified. There was wide variability in clinical practice patterns including biopsy practice, HP treatment and eradication confirmation testing, and surveillance recommendations. This work demonstrates that there is a major unmet need for quality improvement efforts to standardize care for patients with GIM, a premalignant condition, and inform future prospective studies in a US population.

Risk Score Using Demographic and Clinical Risk Factors Predicts Gastric Intestinal Metaplasia Risk in a U.S. Population.

Screening for gastric intestinal metaplasia (GIM) may lead to early gastric cancer detection. We developed and validated a pre-endoscopy risk prediction model for detection of GIM based on patient-level risk factors in a U.S. We used data from 423 GIM cases and 1796 controls from a cross-sectional study among primary care and endoscopy clinic patients at the Houston VA. We developed the model using backwards stepwise regression and assessed discrimination using area under the receiver operating characteristic (AUROC). The model was internally validated using cross-validation and bootstrapping. The final expanded model was compared to a model including H. pylori infection alone and a baseline model including remaining terms without H. pylori. Male sex, older age, non-white race/ethnicity, smoking status, and H. pylori were associated with GIM risk. The expanded model including these terms had AUROC 0.73 (95%CI 0.71-0.76) for predicting GIM and AUROC 0.82 (95%CI 0.79-0.86) for extensive GIM. This model discriminated better than a model including only H. pylori (AUROC 0.66; 95%CI 0.63-0.68) and the baseline model (AUROC 0.67; 95%CI 0.64-0.70). The expanded model performed similarly among primary care (AUROC 0.75) and endoscopy (AUROC 0.73) patients. The expanded model showed sufficient internal validity (cross-validation AUROC 0.72) with little evidence of over-fitting. We develop and validate a non-invasive risk model for GIM detection in a U.S. population that included terms for sex, age, race/ethnicity, smoking status, and H. pylori infection. Validated risk models would identify individuals with GIM who should be referred for endoscopic screening.

Gastric Intestinal Metaplasia: Demographic and Epidemiological Characterization in Puerto Rican Hispanics (2012-2014).

Background and Aims Gastric cancer is the 5th leading cause of cancer mortality worldwide and the leading infection-associated cancer. Helicobacter pylori is the most common chronic bacterial infection in humans and the major predisposing factor for the development of gastric intestinal metaplasia (GIM), the principal preneoplastic lesion in the gastric carcinogenesis pathway. GIM surveillance is now recommended for individuals among high-risk subgroups by three major gastroenterology societies in Europe, England, and U.S. Our objective was to provide the initial epidemiologic data for GIM among Hispanics in Puerto Rico. Methods Using a cross-sectional study design, we analyzed an extensive pathology database (n = 43,993) that captured approximately 50% of all endoscopy biopsies taken during 2012-2014 at academic, public, and private sectors in Puerto Rico. Prevalence estimates of GIM, GIM subgroups, and H. pylori status were estimated using logistic regression models. Results A total of 4,707 GIM cases were identified during the study period for a prevalence rate of 10.7%. H. pylori was detected in 26.9% (95% CI: 25.7-28.2) of the GIM cases. The majority of the pathology reports lacked information regarding the high-risk subtypes (99.6%) and extension (71.2%). Conclusions The prevalence of GIM among Hispanics living in Puerto Rico may be higher than in U.S. mainland non-Hispanic populations. The prevalence of H. pylori detected in our study population was comparable to the rates reported in the mainland U.S. Standardization of the endoscopy biopsy protocol and pathology reporting is needed to characterize and risk stratify GIM surveillance programs in Puerto Rico.

Associations of Duration, Intensity, and Quantity of Smoking With Risk of Gastric Intestinal Metaplasia.

Determine whether various dimensions of smoking increase risk for gastric intestinal metaplasia. Cigarette smoking has been implicated in the etiology of gastric cancer, but it is not clear if smoking is a risk factor for gastric intestinal metaplasia, a precursor lesion of gastric cancer. We compared data from 385 gastric intestinal metaplasia cases and 1577 controls without gastric intestinal metaplasia recruited into a cross-sectional study at the Michael E. DeBakey VA Medical Center in Houston, Texas. All participants completed standardized questionnaires and underwent a study endoscopy with gastric mapping biopsies. Gastric intestinal metaplasia cases included participants with intestinal metaplasia on any noncardia gastric biopsy. We calculated odds ratios and associated 95% confidence intervals using multivariable logistic regression models. Compared with never smokers, current smokers had 2-fold increased risk for gastric intestinal metaplasia (odds ratio, 2.05; 95% confidence interval, 1.47-2.85). Among ever smokers, increasing duration and total dose were significantly associated with increased risk for gastric intestinal metaplasia (P-trend, 0.004 and 0.01, respectively). Among former smokers, risk for gastric intestinal metaplasia decreased over time and was no different to never smokers after 15 years smoking cessation. Cases with gastric intestinal metaplasia were more likely than controls to have Helicobacter pylori infection (53.2% vs. 21.7%); however, smoking effect on gastric intestinal metaplasia was not different by H. pylori infection status. Cigarette smoking is a risk factor for gastric intestinal metaplasia. Risk of gastric intestinal metaplasia among former smokers remained significantly elevated until 15 years postcessation.

Dietary Factors and Gastric Intestinal Metaplasia Risk Among US Veterans.

Studies on diet and gastric intestinal metaplasia (GIM) risk are lacking in US populations. To determine the associations of dietary factors and risk of GIM among aUS population with typical American diet. We analyzed data from a cross-sectional study of veterans attending primary care and endoscopy clinics at the Houston VA Medical Center. Patients completed a 110-item Block Food Frequency Questionnaire then underwent upper endoscopy with gastric mapping biopsies. We compared cases defined by GIM on ≥ 1 non-cardia gastric biopsy to controls without GIM. Associations of dietary factors and GIM were estimated using logistic regression models as odds ratios (OR) and 95% confidence intervals (CI). Among 423 GIM cases and 1796 controls, cases were older (62.1 vs. 59.9years) and more likely to be male (97.2% vs. 90.8%) and non-White (58.6% vs. 39.0%). GIM cases had lower fat intake (percent kcal from fat tertile 1: 43.6% vs. 33.4%) and higher carbohydrate intake (percent kcal from carbohydrate T3: 41.8% vs. 33.3%) than controls. Adjusting for age, gender, race, smoking, and Helicobacter pylori, percent kcal from carbohydrates (T3 vs. T1: OR 1.35, 95% CI 1.08-1.67), fruit intake (T3 vs. T1: OR 1.28, 95% CI 1.02-1.61), and fiber intake (T3 vs. T1: OR 1.37, 95% CI 1.04-1.80) were associated with GIM. In subgroup analyses, these associations were primarily seen in non-White patients. Few dietary factors, including high carbohydrate intake, are associated with increased risk of GIM in US populations, independent of H. pylori or smoking.

Abstract C059: A case-control study of risk factors for advanced gastric intestinal metaplasia in a multiethnic United States population (The Stanford GAPS Study)

Abstract Introduction Gastric intestinal metaplasia (GIM) is a precursor to gastric cancer (GC). It is not cost effective to survey the general American population for progression from GIM onto GC; however, development of risk-stratification models may allow for targeted surveillance. There exist very limited data regarding GIM epidemiology or risk derived from North American populations. The Stanford Gastric Precancerous Conditions Study (GAPS) is an ongoing, prospective study incorporating both 1) a cross-sectional, case-control study of subjects with GIM compared to controls, and 2) a longitudinal evaluation of subjects with GIM to evaluate risk factors for progression. The purpose of GAPS is to both improve the detection of GIM, and to predict risk for progression of GIM onto dysplasia or GC. Methods At time of enrollment in GAPS, all patients complete a standardized questionnaire inquiring about medical, family, dietary, and exposure history. Biopsies are performed from both antrum and body, and bio-specimens from the gastric mucosa, blood, and saliva are collected. Subjects are assigned an operative link for GIM (OLGIM) score based on adjudication by an expert pathologist. Demographic, clinical, and environmental covariates are compared between cases of GIM and controls. Subgroup analysis is performed to compare cases of advanced GIM (defined as OLGIM &amp;gt;=2) and controls. Continuous variables are analyzed using Student’s T-test, and categorical variables are analyzed using the Chi-squared test. Results As of July 2019, 44 cases and 49 controls have undergone questionnaire administration, endoscopy, and bio-specimen collection. Of cases, 23 demonstrate advanced GIM. Subjects with GIM were older (65 vs 56 years, p&amp;lt;0.001), more likely to have a history of H. pylori treatment (48% vs 20%, p=0.005), and more likely to be first-generation immigrants (p=0.03) compared to controls. Subjects with advanced GIM were older (65 vs 58 years, p=0.03), and more likely to be first-generation immigrants (p=0.04) compared to subjects without advanced GIM. Differences in family history, smoking status, presence of symptoms, presence of medical comorbidity, and dietary patterns did not reach statistical significance. Discussion Age and immigration status, known risk factors for GC, may also be risk factors for advanced GIM. As advanced GIM significantly increases risk for GC, detection of advanced GIM may improve GC morbidity and mortality. With ongoing enrollment in GAPS, it is hoped that additional environmental risk factors may be isolated from this cohort. Additional research should be focused on non-invasive testing to detect advanced GIM in North American populations. Citation Format: Robert J Huang, Sungho Park, Tanvi Chitre, Jeanne Shen, Teri Longacre, Joo Ha Hwang. A case-control study of risk factors for advanced gastric intestinal metaplasia in a multiethnic United States population (The Stanford GAPS Study) [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr C059.

Accuracy of biopsies for Helicobacter pylori in the presence of intestinal metaplasia of the stomach.

Gastric cancer is the second leading cause of cancer-related death worldwide. The majority of gastric cancers is "intestinal-type" adenocarcinoma, caused in part by H. pylori infection. Chronic gastritis leading to atrophy and intestinal metaplasia (IM) can result in cancer. Studies have demonstrated reversibility of mucosal atrophy following H. pylori eradication. Concern has been raised regarding the sensitivity of gastric biopsy for H. pylori detection in the context of IM. All cases of IM on gastric biopsy from a single gastroenterologist's outpatient practice were retrospectively reviewed from February 1, 2006 until May 31, 2012. In total, 105 IM cases were found, of which 37 (35.2%, 95% CI: 26.3-45.2) were H. pylori-positive on biopsy. Charts of the remaining 68 patients were reviewed for availability of other tests, namely urea breath test (UBT) and serology. Of 43 H. pylori-negative patients who underwent a UBT, 10 were positive for the infection (23.3%, 95% CI: 12.3-39.0). Amongst patients with coexisting autoimmune gastritis (AIG), 4 out of 9 (44.4%, 95% CI: 15.3-77.3) also had evidence of H. pylori infection by UBT, despite negative histology. For cases of gastric IM with negative histology for H. pylori, UBT should be considered, even in cases of AIG, as this may alter the management and clinical course for patients.

Demographic and Lifestyle Risk Factors for Gastric Intestinal Metaplasia Among US Veterans.

The risk of noncardia gastric cancer is increased in the presence of gastric intestinal metaplasia. We aimed to identify demographic and lifestyle factors independently associated with the risk of gastric intestinal metaplasia. We used data from a cross-sectional study of patients attending primary care and endoscopy clinics at the Michael E. DeBakey VA Medical Center in Houston, Texas, between February 2008 and August 2013. All patients completed standardized questionnaires and underwent endoscopy with gastric mapping biopsies. Gastric intestinal metaplasia cases included patients with intestinal metaplasia on any noncardia gastric biopsy; we defined extensive gastric intestinal metaplasia as antrum and corpus involvement. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) using multivariate logistic regression models. We identified 423 cases with gastric intestinal metaplasia and 1,796 controls without gastric intestinal metaplasia. Older age (vs <60 years: 60-69 years AdjOR, 1.50; 95% CI, 1.17-1.93; ≥70 years AdjOR, 2.12; 95% CI, 1.48-3.04), male sex (AdjOR, 2.76; 95% CI, 1.50-5.10), nonwhite race/ethnicity (vs non-Hispanic white: Hispanic, AdjOR, 2.66; 95% CI, 1.89-3.76; black, AdjOR, 2.36; 95% CI, 1.85-3.02), and current smoking status (AdjOR, 1.78; 95% CI, 1.29-2.48) were independently associated with gastric intestinal metaplasia. These risk factors remained statistically significantly associated with gastric intestinal metaplasia after adjusting for Helicobacter pylori infection, and their effect sizes were larger for associations with extensive gastric intestinal metaplasia compared with focal gastric intestinal metaplasia. Older age, male sex, nonwhite race/ethnicity, and current smoking status were the nonendoscopic factors independently associated with gastric intestinal metaplasia in a predominantly nonimmigrant US population.

Prevalence, risk factors, and surveillance patterns for gastric intestinal metaplasia among patients undergoing upper endoscopy with biopsy

Gastric intestinal metaplasia (GIM) is an important precursor lesion to gastric cancer (GC), the second leading cause of cancer death worldwide. There exist few data regarding the prevalence of, risk factors for, and clinical practice patterns regarding GIM in the United States. Furthermore, there are currently no U.S. guidelines regarding screening/surveillance for GIM. All consecutive upper endoscopic procedures from 2 academic medical centers in Seattle between 1999 and 2014 were reviewed. Demographic, clinical, and endoscopic covariates were recorded at time of endoscopy. Procedures with gastric biopsy were matched to final the histologic diagnoses, including the presence of Helicobacter pylori. Cases of GIM and dysplasia were recorded and compared with non-GIM controls using univariate and multivariable regression. Surveillance patterns for cases of GIM were recorded. Data from 36,799 upper endoscopies, 17,710 gastric biopsies, 2073 cases of GIM, 43 cases of dysplasia, and 78 cases of GC were captured. The point prevalence of GIM was 11.7% in patients who underwent gastric biopsy. Non-white race (P< .001), increasing age (P< .001), and presence of H pylori (P< .001) were associated with GIM. If GIM was present, increasing age (P< .001) and male gender (P< .001) were associated with progression, and the presence of H pylori (P< .001) was inversely associated with progression to dysplasia/GC. Few cases of GIM/dysplasia/GC were identified during procedures for GIM screening/surveillance. Only 16% of patients with a diagnosis of GIM received a recommendation for surveillance. There is a high prevalence of GIM among non-white and Hispanic Americans. Risk factors fordevelopment of GIM may be distinct from the risk factors for progression to GC.

Gastric Intestinal Metaplasia and Helicobacter pylori Testing

Introduction: Gastric Intestinal metaplasia (GIM) is a frequent precancerous lesion, with 6-10 fold increase in gastric cancer risk. Helicobacter pylori (H. pylori) is believed to be the cause of majority of intestinal-type gastric adenocarcinoma by causing chronic active gastritis, which may evolve to atrophic gastritis, IM, dysplasia, and cancer. Whether H. Pylori eradication leads to reversal of IM remains controversial. Since H. pylori exhibits tissue tropism, we believe that IM drives H.pylori out of the gastric mucosa. Biopsy alone for the detection of H. pylori may be less accurate in the context of IM, especially if biopsies fail to sample non-metaplastic tissue. Hence, another method of H. Pylori testing must be performed. Methods: A retrospective chart review was conducted using Electronic Medical Records (EMR) at one hospital. After Institutional Review Board approval, a list of patients with a histological diagnosis of GIM over the past 10 years was obtained. The EMR was reviewed for patients with biopsy proven gastric intestinal metaplasia and H. Pylori testing status was documented. Results: A total of 54 patients were identified with GIM. The median age was 68 year, 94.4% were male, 83.3% were Caucasian, 79.6% were present or former smokers. Documentation of pathologic testing for H. Pylori was found for all patients with 22.2% testing positive in pathology specimen. Of the remaining 42 patients, serologic testing was done in 19 % with 50% testing positive, 25% testing negative and 25% equivocal. There were 34 patients with GIM and H pylori negative biopsies who did not have serological testing done, 2 had empiric anti-H Pylori treatment and 2 had protocol biopsies done 2 years later. Both the patientswith equivocal results on serological testing had protocol biopsies. Only 25.9%npatients were treated for H. Pylori after the diagnosis of GIM. Conclusion: Our study shows that pathologic testing for H. Pylori was completed in almost all cases of GIM and only 22.2% of patients had H. Pylori identified from their biopsy. This is in accordance with our hypothesis that gastric biopsy has lower accuracy in the presence of IM because of inability of H. Pylori to grow on metaplastic tissue. H. Pylori eradication could reduce the risk of further development of dysplasia and subsequent gastric malignancy. Therefore, we recommend that patients with intestinal metaplasia should undergo additional diagnostic tests if the initial biopsy is negative for H. Pylori.Figure 1

Gastric intestinal metaplasia - age, ethnicity and surveillance for gastric cancer.

Determine the prevalence and distribution of gastric intestinal metaplasia (GIM) in a large cohort of patients subjected to esophagogastroscopy (EGD). Evaluate usefulness of grading the severity of gastritis, GIM and the impact of Helicobacter pylori (HP). Define the population at risk for gastric adenocarcinoma (GC) and assess the value of surveillance. In the course of 19 years, we performed 11,600 sequential EGDs in male veterans at Brooklyn, New York. Of all patients, 47 % had EGD only one time while 53 % had EGD repeated, 11 % of these had four or more EGDs. Patients with GIM were matched with equal number of controls with no GI symptoms. All gastric biopsies were processed in one laboratory, using the standardized protocol for histological staining and for grading the severity of epithelial changes. Of all patients subjected to EGD, 354 (3.05 %) were diagnosed with GIM. Compared to controls, GIM patients were older, 80 % were over 71. Regarding ethnicity, GIM was 5.4 % more frequent in 177 African Americans than in 159 Caucasians. Distribution of GIM did not differ with respect to age or ethnicity. As many as 6 %of GIM cases were diagnosed with GC. Grading of GIM severity had a predictive value, the average grade of severity in GC was 50 % higher than in non-cancer patients with GIM. Severity of gastritis was also a useful biomarker: patients with GC had more severe gastritis. Surprisingly, HP positivity had no predictive value: HP positive patients had similar distribution of GIM as the HP negative patients. Use of proton pump inhibitors in the past was unknown. Prevalence of GC in patients with GIM was more than 200 times higher than reported in normal population. Age more than 70 years and African Americans appeared to be at higher risk. Routine EGD and histological diagnosis, with simple grading of severity of epithelial changes provides a useful predictive information. Individuals with upper GI symptoms undergoing EGD with gastric biopsy benefited from routine clinical screening for GC. Patients with higher severity of GIM should enter surveillance (Tab. 1, Fig. 10, Ref. 45).

Alimentary factors in the development of gastric intestinal metaplasia in functional dyspeptic patients

Intestinal metaplasia of the stomach is a lesion in which metaplasia of gastric epithelial cells occurs for an intestinal phenotype. Gastric intestinal metaplasia is a lesion associated with an increase in the risk of gastric carcinoma development. Epidemiologic studies indicate a relation between dietary habits and stomach cancer development, some habits increasing the risk for it, and others have a protective effect, suggesting that antioxidants, such as vitamins A, C, and E, decrease the risk of this type of cancer. The relationship of these alimentary factors and intestinal metaplasia is unknown. It is a case-control, observational study in which 320 patients with functional dyspepsia, divided in two groups, were assessed. The case I group (individuals with intestinal metaplasia) had their dietary pattern compared to that of the control group, constituted of individuals similar to those in the case group but without intestinal metaplasia, through a food frequency questionnaire. The analysis of the dietary pattern of functional dyspeptic patients with intestinal metaplasia, and its comparison with those without intestinal metaplasia, showed a higher frequency of canned and smoked foods consumption in the first group and, on the other hand, a higher consumption of fruits and vegetables in patients without intestinal metaplasia. No effect of salt consumption was detected. The results obtained in this study suggest changes in the diet, with a decrease in the consumption of smoked and canned foods, and an increase in the consumption of fruits and vegetables, can lead to a diminution of gastric intestinal metaplasia cases.

Expression of p53, c-erbB-2 and Ki67 in intestinal metaplasia and gastric carcinoma

To compare two types of classification of intestinal metaplasia (IM) of the stomach and to explore their relationship to gastric carcinoma. Forty-seven cases of gastric IM were classified into type I, type II or type III according to mucin histochemical staining and compared with a novel classification in which the specimens were classified into simple IM (SIM) or atypical IM according to polymorphism in terms of atypical changes of the metaplastic epithelium. Forty-seven IM and thirty-seven gastric carcinoma samples were stained for p53, c-erbB-2 and Ki67 proteins by Envision immunohistochemical technique. There were no significant differences in the expression of p53 and c-erbB-2 among type I, type II, type III IM and gastric carcinomas. The positive expression rate of Ki67 was significantly higher in gastric carcinomas than in type I IM while no significant Ki67 expression differences were observed among type II, type III IM and gastric carcinomas. The expression of p53, c-erbB-2 and Ki67 proteins in 20 SIM, 27 Atypical IM and 37 gastric carcinomas showed significant differences between SIM and gastric carcinomas while no significant differences were observed between Atypical IM and gastric carcinomas. Atypical IM may better reveal the precancerous nature of IM and could be a helpful indicator in the clinical follow up of patients.

Differences in genetic instability and cellular phenotype among Barrett’s, cardiac, and gastric intestinal metaplasia in a Japanese population with Helicobacter pylori

Intestinal metaplasia is considered to be a precursor lesion in both Barrett's and intestinal-type gastric cancer. The aim was to clarify the differences in molecular pathology between specialized intestinal metaplasia (SIM) in Barrett's oesophagus (BO), cardiac (CIM) and gastric intestinal metaplasia (GIM). Eighty-eight SIM cases with BO, 30 CIM cases and 52 GIM cases in patients with or without Helicobacter pylori infectionwere analysed for genetic instability and Das-1. Microsatellite instability and a loss of heterozygosity were evaluated at five microsatellite loci. The incidence of genetic instability was 55.7% in SIM, 40.0% in CIM and 23.1% in GIM, revealing a significant difference between SIM and GIM (P < 0.0005). For each microsatellite marker analysed, there were obvious differences in frequency among the three conditions. Das-1 reactivity was significantly higher in SIM than in CIM or GIM (P < 0.0001, both). Interestingly, both genetic instability and Das-1 reactivity in SIM showed a significantly higher incidence in patients with H. pylori infection than in those without (P < 0.005 and P < 0.01, respectively). SIM is distinct from CIM and GIM, and the pathogenesis of SIM, like that of GIM, is associated to some degree with H. pylori infection in a Japanese population.

Patterns of intestinal metaplasia in gastric biopsies. A comparison of different histochemical classifications

A total of 217 cases of gastric intestinal metaplasia (IM), out of 491 cases of consecutive multiple gastric biopsies, were examined using various histochemical methods. Three classifications were adopted (1) Jass and Filipe's (1979), (2) Segura and Montero's (1983), and (3) our own distinguishing two types of small intestine IM (incomplete and complete) and two types of colonic IM (incomplete and complete). Our classification revealed (1) a group of 'pure' IM cases (44%), (2) a group of 'combined' IM cases (15%), either small intestinal or colonic, expressing a maturating line, and (3) a conspicuous group of mixed 'mosaic' IM cases (41%) consisting of all possible combinations between the basic IM types. No significant correlations were found between each IM type and associated diseases (i.e. gastritis, stump gastritis, ulcer, adenoma and adenocarcinoma). However, a suggestive association between colonic IM and malignancy was observed. Our results confirmed the heterogeneity of IM and indicated two differentiation cell lines (ileal and colonic), thus providing additional evidence of impaired maturation and aberrant differentiation along various cell lines, supporting Leblond's (1976) unifying theory on the origin of intestinal epithelial cells.