Risk Of Gastric Cancer In Patients Research Articles

Physical Activity and Gastric Cancer Risk in Patients with and without Helicobacter pylori Infection in A Korean Population: A Hospital-Based Case-Control Study.

Although physical activity (PA) is beneficial for prolonging lifespan, evidence for the protective role of PA against the development of gastric cancer (GC) is not yet well established. This study assessed the association between PA and GC risk in patients with and without Helicobacter pylori (H. pylori) infection in a Korean population. In total, 415 GC patients and 830 controls were enrolled at the National Cancer Center, Korea. The International Physical Activity Questionnaire-Short Form was used to collect PA data. The odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression models. In the H. pylori-positive group, subjects who engaged in regular exercise showed a significantly reduced risk of GC in the entire population (OR = 0.52, 95% CI = 0.38–0.70) and in females (OR = 0.60, 95% CI = 0.21–0.64). Subjects who engaged in a high level of total PA showed a significantly reduced risk of GC relative to subjects in the lowest tertile in the fully adjusted model (OR = 0.46, 95% CI = 0.32–0.65, p-trend < 0.001). There was an inverse association between PA and GC risk in the entire population, and in the H. pylori-positive subgroup. Our data indicate the need for the promotion of all domains of PA, especially for Korean populations.

Su1227 - Metformin is Associated with a Reduced Gastric Cancer Risk in Patients with Diabetes Mellitus after Helicobacter Pylori Eradication: A Territory-Wide Study with Propensity Score Adjustment

Su1227 - Metformin is Associated with a Reduced Gastric Cancer Risk in Patients with Diabetes Mellitus after Helicobacter Pylori Eradication: A Territory-Wide Study with Propensity Score Adjustment

Metformin use and its effect on gastric cancer in patients with type 2 diabetes: A systematic review of observational studies

Increasing evidence suggests that metformin use is associated with a decreased risk of cancer. The traditional therapies for gastric cancer (GC) are gastrectomy and chemoradiotherapy; however, these therapies may cause certain adverse effects, which affect a patient's quality of life, and the overall survival rate is low. At present, little is known about whether the use of metformin decreases the risk of GC in patients with type 2 diabetes. Therefore, in the present study, a systematic review was performed to analyze the effect of metformin on GC. A literature search was conducted in PubMed, EMBASE, and the Cochrane Library databases for articles published up to June 30th, 2016. The studies that evaluated GC patients treated with metformin and compared them with GC patients treated with other antidiabetic drugs were reviewed. Eligible studies were evaluated using the Newcastle-Ottawa Scale. Adjusted hazard ratio and 95% confidence intervals were determined to evaluate the effect of metformin on GC. From the 422 articles evaluated, 5 studies involving a total of 1,804,479 patients met the inclusion criteria and were qualitatively analyzed. The quality of all selected articles was classified as moderate. These studies reported that the long-term use of metformin was associated with a lower risk of GC compared with the lack of use of metformin or the use of other hypoglycemic drugs. In GC patients with diabetes who were subjected to gastrectomy, the cumulative use of metformin reduced the rates of disease recurrence and of all-cause and cancer-specific mortality. Despite the limited number of studies on this subject, currently available evidence indicates that metformin is associated with a decreased risk of GC and improves survival in patients with type 2 diabetes. However, more well-designed trials are required to elucidate this association.

Association between metformin and the risk of gastric cancer in patients with type 2 diabetes mellitus: a meta-analysis of cohort studies

ObjectivesThe objective of this study was to evaluate the association between metformin therapy and the incidence of gastric cancer (GC) in patients with type 2 diabetes mellitus (T2DM).MethodsWe systemically searched the following databases for studies published between the databases’ dates of inception and Nov. 2016: PubMed, Embase, the Cochrane Library, the Web of Science, and the China National Knowledge Infrastructure (CNKI). Hazard ratios (HR)and corresponding 95% confidence intervals (CIs) for the association between metformin therapy and the incidence of GC in patients with T2DM were the outcome measures assessed in this study. STATA 12.0 (Stata Corporation, College Station, Texas, USA) was used to conduct the statistical analysis.ResultsA total of seven cohort studies including 591,077 patients met all the criteria for inclusion in the analysis. Our data showed that metformin therapy was associated with a significantly lower incidence of GC in patients with T2DM than other types of therapy (HR=0.763, 95% CI: 0.642˜0.905). Subgroup analysis showed that patients living in Taiwan benefitted more from metformin therapy than patients living in any other region, as metformin significantly decreased the risk of GC in patients living in Taiwan but did not significantly decrease the risk of GC in patients living in other regions (HR=0.514, 95% CI: 0.384-0.688). The results of the present analysis support the idea that metformin facilitates reductions in the risk of T2DM-related GC.ConclusionsThe risk of GC among patients with T2DM is lower in patients receiving metformin therapy than in patients not receiving metformin therapy.

Metformin reduces gastric cancer risk in patients with type 2 diabetes mellitus

This retrospective cohort study investigated whether metformin may reduce gastric cancer risk by using the reimbursement databases of the Taiwan's National Health Insurance. Patients with type 2 diabetes diagnosed during 1999-2005 and newly treated with metformin (n=287971, “ever users of metformin”) or other antidiabetic drugs (n=16217, “never users of metformin”) were followed until December 31, 2011. The effect of metformin (for ever versus never users, and for tertiles of cumulative duration of therapy) was estimated by Cox regression incorporated with the inverse probability of treatment weighting using propensity score. Results showed that the respective numbers of incident gastric cancer in ever and never users were 759 (0.26%) and 89 (0.55%), with respective incidences of 55.26 and 122.53 per 100,000 person-years. The overall hazard ratio (95% confidence intervals) of 0.448 (0.359-0.558) suggested a significantly lower risk among ever users. In tertile analyses, hazard ratios (95% confidence intervals) for the first (<21.47 months), second (21.47-45.97 months) and third (>45.97 months) tertile of cumulative duration was 0.973 (0.773-1.224), 0.422 (0.331-0.537) and 0.120 (0.090-0.161), respectively, while compared to never users. In conclusion, metformin significantly reduces gastric cancer risk, especially when the cumulative duration is more than approximately 2 years.

Gastric Cancer Risk in Patients with Precancerous Lesions

Gastric cancer is presumed to develop via precancerous mucosal changes called Correa's cascade, which includes successive stages of normal mucosa,

Long-Term Low-Dose Aspirin Use Reduces Gastric Cancer Incidence: A Nationwide Cohort Study.

PurposeThe aim of this study was to investigate whether aspirin use can reduce the incidence of gastric cancer in patients with hypertension or type 2 diabetes.Materials and MethodsA total of 200,000 patients with hypertension or type 2 diabetes were randomly selected from the Korean National Health Insurance claim database. Of these, 3,907 patients who used 100 mg of aspirin regularly (regular aspirin users) and 7,808 patients who did not use aspirin regularly (aspirin non-users) were selected at a frequency of 1:2, matched by age, sex, comorbid illnesses (type 2 diabetes and hypertension), and observation periods. The incidence of gastric cancer in this cohort was then assessed during the observation period of 2004 to 2010.ResultsIn the matched cohort, the incidence rates of gastric cancer were 0.8% (31/3,907) for regular aspirin users and 1.1% (86/7,808) for aspirin non-users, but the cumulative incidence rates were not significantly different between groups (p=0.116, log-rank test). However, in multivariate analysis, regular aspirin users had a reduced risk of gastric cancer (adjusted hazard ratio [aHR], 0.71; 95% confidential interval [CI], 0.47 to 1.08; p=0.107). Duration of aspirin use showed significant association with reduction of gastric cancer risk (aHR for each year of aspirin use, 0.85; 95% CI, 0.73 to 0.99; p=0.044), particularly in patients who used aspirin for more than 3 years (aHR, 0.40; 95% CI, 0.16 to 0.98; p=0.045).ConclusionLong-term low-dose aspirin use was associated with reduced gastric cancer risk in patients with hypertension or type 2 diabetes.

Acid Inhibitors Exacerbate H.pylori‐Induced Gastritis Both In Vitro And In Vivo

BackgroundGastric cancer (GC) is strongly associated with H.pylori infection. But, GC tends to develop in hypochlorhydric, but not in hyperchlorhydric patients. Since potent acid inhibitors, such as proton pump inhibitors (PPI) are widely used for the treatment of GERD, it seems reasonable to assume that potent acid inhibitors may excerbate H.pylori‐induced gastritis, promote gastric atrophy, and increase risk of GC. Based on these hypothesis, we examined (1) if the increased gastric luminal pH enhances toxicity of H.pylori‐derived ammonia in vitro, (2) if PPIs exacerbates gastritis in H.pylori‐infected mice in vivo.MethodsA:In vitro study: 1. Intact sheets of in vitro bullfrog gastric mucosa were incubated in Ussing chambers in vitro. Transmucosal electrical resistance (TER) was monitored to evaluate mucosal integrity. 2. GSM06 cells, derived from murine gastric mucosa, were cultured with or without 5 mM NH4Cl. Cell viablity and gastric mucosal apoptosis were evaluated by MTT, and by capase‐3 assay, respectively. B: In vivo study: Six‐wk‐old female mice were cultured for 8 wks after inoculated with H.pyloi, SS‐1. Degree of gastritis was evaluated using updated Sydney sysytem. Colonization of H.pylori was also examined.ResultsA‐1. NH4Cl decreased TER at high luminal pH (&gt;7.0), but not at low luminal pH (5.0). A‐2. NH4Cl decreased cell viality and enhanced apoptosis more at higher ambient pH (7.8), than at low pH (7.2). B‐1. PPI Tx exacerbated inflammation in corpus, but not in antral mucosa in H.pylori‐infected mice. B‐2. PPI Tx increased colonization of H.pylori only in corpus.ConclusionsHigh ambient pH induced by potent acid inhibitors enhances toxicity of H.pylori‐dervied ammonia, thereby exacerbates H.pylori‐induced gastritis. Potent acid inhibition may increase risk of GC in patients with H.pylori infection.

Increased Helicobacter pylori-associated gastric cancer risk in the Andean region of Colombia is mediated by spermine oxidase.

Helicobacter pylori infection causes gastric cancer, the third leading cause of cancer death worldwide. More than half of the world's population is infected, making universal eradication impractical. Clinical trials suggest that antibiotic treatment only reduces gastric cancer risk in patients with non-atrophic gastritis (NAG), and is ineffective once preneoplastic lesions of multifocal atrophic gastritis (MAG) and intestinal metaplasia (IM) have occurred. Therefore, additional strategies for risk stratification and chemoprevention of gastric cancer are needed. We have implicated polyamines, generated by the rate-limiting enzyme ornithine decarboxylase (ODC), in gastric carcinogenesis. During H. pylori infection, the enzyme spermine oxidase (SMOX) is induced, which generates hydrogen peroxide from the catabolism of the polyamine spermine. Herein, we assessed the role of SMOX in the increased gastric cancer risk in Colombia associated with the Andean mountain region when compared with the low-risk region on the Pacific coast. When cocultured with gastric epithelial cells, clinical strains of H. pylori from the high-risk region induced more SMOX expression and oxidative DNA damage, and less apoptosis than low-risk strains. These findings were not attributable to differences in the cytotoxin-associated gene A oncoprotein. Gastric tissues from subjects from the high-risk region exhibited greater levels of SMOX and oxidative DNA damage by immunohistochemistry and flow cytometry, and this occurred in NAG, MAG and IM. In Mongolian gerbils, a prototype colonizing strain from the high-risk region induced more SMOX, DNA damage, dysplasia and adenocarcinoma than a colonizing strain from the low-risk region. Treatment of gerbils with either α-difluoromethylornithine, an inhibitor of ODC, or MDL 72527 (N(1),N(4)-Di(buta-2,3-dien-1-yl)butane-1,4-diamine dihydrochloride), an inhibitor of SMOX, reduced gastric dysplasia and carcinoma, as well as apoptosis-resistant cells with DNA damage. These data indicate that aberrant activation of polyamine-driven oxidative stress is a marker of gastric cancer risk and a target for chemoprevention.

Estimación de riesgo de cáncer gástrico en pacientes con gastritis crónica asociada a la infección por Helicobacter pylori en un escenario clínico

Severity of chronic gastritis associated with Helicobacter pylori infection (CGAHpI) could play a role in evaluating the potential risk to develop gastric cancer. Our aim was to estimate the risk for gastric cancer in a clinical setting, according to histopathologic criteria, by applying the gastric cancer risk index (GCRI) METHODS: Histopathologic study of the gastric biopsies (corpus-antrum) from consecutive adult patients that underwent gastroesophageal duodenoscopy was carried out, and the GCRI was applied in patients presenting with CGAHpI. One hundred eleven patients (77% female) with a mean age of 38.6±13.1 years were included. Active Helicobacter pylori infection (aHpi) was diagnosed in 77 cases (69.40%). In 45% of the cases with aHpi, pangastritis (23%) or corpus-predominant gastritis (22%) was diagnosed. Nine cases were diagnosed with intestinal metaplasia (8%), 7 of which (77.70%) were in the aHpi group. Twenty one percent of the patients with aHpi had a GCRI of 2 (18.10%) or 3 (2.50%) points (high risk index), while 79.10% accumulated a GCRI of 0 or 1 points (low risk index). Of the patients with no aHpi, none of them had 3 points (p=0.001). Of the 18 patients that accumulated 2 or 3 points, 6 (33.30%) presented with intestinal metaplasia (all with pangastritis and corpus-predominant gastritis), of which 4 cases (66.60%) had aHpi. The estimated gastric cancer risk in patients with CGAHpI in the clinical setting studied was relatively low and 5% of the patients had a histopathologic phenotype associated with an elevated risk for developing gastric cancer.

P-0022 Association Between C3435T Single Nucleotide Polymorphism of Multi-Drug Resistance 1 Gene and Risk of Gastric Cancer

ABSTRACT Introduction Gastric cancer (GC) is the fourth most common cancer in the world and the second leading cause of death due to cancer. The Multi-Drug Resistance 1 (MDR1) gene encodes P-glycoprotein, which confers resistance to antineoplastic drugs, but also affects the kinetic disposition of some drugs and carcinogens. The C3435T polymorphism of the MDR1 gene may influence the transport and excretion of carcinogens, increasing the risk of cancer. The aim of this study was to evaluate the association between this polymorphism and the risk of gastric cancer and tumor aggressiveness. Methods A case-control study was conducted. The case group consisted of patients with non-cardia adenocarcinoma. The control group consisted of healthy subjects. Serology was performed by ELISA for the investigation of infection with Helicobacter pylori. DNA was extracted from peripheral venous blood leukocytes collected with EDTA. The MDR1 polymorphism was analyzed by PCR-RFLP. After amplification, the products were digested with 5 units of the restriction enzyme MboI (New England Biolabs). Genome sequencing was used to confirm the PCR and RFLP techniques using random samples of the two groups. The PCR product of the MDR1 gene was purified using the Big Dye XTerminator Kit and sequenced in an ABI Prism 3100 sequencer. The reverse primer was used for sequencing. The electropherogram was analyzed with the Sequence Scanner v1.0 program. Results Ninety eight patients with non-cardia GC and 203 healthy subjects participated in the study. There was no difference in gender (p=0.12) or age (p=0.125) between the two groups. The genotypes in the control group were in Hardy-Weinberg equilibrium and the frequency of TT, CC and CT genotypes was 19.2%, 33.0% and 47.8%, respectively. In the GC, the frequency of TT, CC and CT genotypes was 15.3%, 32.7% and 52.0%, respectively. No significant difference in the genotypes (p=0.668) or alleles (p=0.745) was observed between the groups. There was no association between the genotypes and the risk of GC in patients infected with H. pylori (p=0.662). Patient survival was not correlated with the genotypes studied (p=0.454). Conclusion The present results provide evidence that the C3435T polymorphism of the MDR1 gene is not associated with GC risk or prognosis in the population studied. No correlation was observed between this polymorphism and infection with H. pylori.

Association between the C3435T single-nucleotide polymorphism of multidrug resistance 1 gene and risk of gastric cancer

The multidrug resistance 1 (MDR1) gene encodes P-glycoprotein, which confers resistance to antineoplastic drugs, but also affects the kinetic disposition of certain drugs and carcinogens. The C3435T polymorphism of the MDR1 gene may influence the transport and excretion of carcinogens, increasing the risk of cancer. The aim of this study was to evaluate the association between this polymorphism and the risk of gastric cancer (GC). Ninety-eight patients with non-cardia GC and 203 healthy subjects participated in the study. DNA was extracted from leukocytes and the MDR1 polymorphism was analyzed using PCR-RFLP. Serology was performed by ELISA for the investigation of infection with Helicobacter pylori. No significant difference in the genotype (p=0.668) or allele (p=0.745) frequency of the C3435T polymorphism was observed between the GC and control groups. There was no association between the genotypes studied and the risk of GC in patients infected with H. pylori (p=0.662). Patient survival was not correlated with the genotypes studied (p=0.454). No correlation was observed between the C3435T polymorphism of the MDR1 gene and GC risk or prognosis in the population studied.

The staging of gastritis with the OLGA system by using intestinal metaplasia as an accurate alternative for atrophic gastritis

The OLGA (operative link on gastritis assessment) staging system is based on severity of atrophic gastritis (AG). AG remains a difficult histopathologic diagnosis with low interobserver agreement, whereas intestinal metaplasia (IM) is associated with high interobserver agreement. The aim of this study was to evaluate whether a staging system based on IM is preferable to estimate gastric cancer risk. Prospective multicenter study. A total of 125 patients previously diagnosed with gastric IM or dysplasia. Surveillance endoscopy with extensive biopsy sampling. Three pathologists graded biopsy specimens according to the Sydney classification. Interobserver agreement was analyzed by kappa statistics. In the OLGA, AG was replaced by IM, creating the OLGIM. Interobserver agreement was fair for dysplasia (kappa = 0.4), substantial for AG (kappa = 0.6), almost perfect for IM (kappa = 0.9), and improved for all stages of OLGIM compared with OLGA. Overall, 84 (67%) and 79 (63%) patients were classified as stage I-IV according to OLGA and OLGIM, respectively. Of the dysplasia patients, 5 (71%) and 6 (86%) clustered in stage III-IV of OLGA and OLGIM, respectively. Prospective studies should confirm the correlation between gastric cancer risk and OLGIM stages. Replacement of AG by IM in the staging of gastritis considerably increases interobserver agreement. The correlation with the severity of gastritis remains at least as strong. Therefore, the OLGIM may be preferred over the OLGA for the prediction of gastric cancer risk in patients with premalignant lesions.

Gastric cancer risk in patients with premalignant gastric lesions

Gastric cancer risk in patients with premalignant gastric lesions

Early Helicobacter pylori Eradication Decreases Risk of Gastric Cancer in Patients With Peptic Ulcer Disease

Helicobacter pylori (H pylori) is a risk factor for gastric cancer. We investigated whether early H pylori eradication is associated with gastric cancer risk in patients with peptic ulcer diseases. This nationwide cohort study was based on the Taiwan National Health Insurance Database (NHID), which provided data on 80,255 patients who were hospitalized for the first time between 1997 and 2004 with a primary diagnosis of peptic ulcer diseases and received H pylori eradication therapy. The patient population was divided into early (within 1 year) and late (after 1 year) eradication cohorts; standardized incidence ratios (SIRs) and hazards ratios (HRs) were determined. There was no significant difference in gastric cancer risk between patients who received early H pylori eradication and the general population (SIR, 1.05; 95% confidence interval [CI]: 0.96-1.14), but late eradication was associated with an increased risk (SIR, 1.36; 95% CI: 1.24-1.49). In gastric ulcer patients who received early eradication, SIRs of gastric cancer decreased from 1.60 at 3-4 years to 1.05 at 7-10 years after hospitalization; the SIRs decreased from 0.57 to 0.33 for duodenal ulcer patients over the same period. Among patients who received late eradication, SIRs decreased from 2.14 to 1.32 for those with gastric ulcers and from 0.90 to 0.66 for those with duodenal ulcers. Early H pylori eradication (HR, 0.77) and frequent aspirin or nonsteroidal anti-inflammatory drug use (HR, 0.65) were independent protective factors for gastric cancer. Early H pylori eradication is associated with decreased risk of gastric cancer in patients with peptic ulcer diseases.

M1988 Genetic and Epigenetic Alterations of Netrin Receptors in Gastric Cancer

Background: The recently proposed OLGA staging system (Gut 2007;56;631-636) is based on the extent and severity of atrophic gastritis (AG) and provides relevant clinical information regarding gastric cancer risk. However, AG is a difficult histopathological diagnosis of which the interobserver agreement is low. In contrast, intestinal metaplasia (IM) has better defined specific histopathological features and is associated with a much better interobserver agreement. The aim of this study was to evaluate interobserver agreement for AG, IM and dysplasia (DYS) and to assess whether a staging system based on IM instead of AG may be preferred to estimate gastric cancer risk. Methods: In a prospective multicenter study, patients with IM and DYS underwent surveillance endoscopy with extensive biopsy sampling. Three expert pathologists graded biopsy specimens according to the updated Sydney classification and the Vienna classification. Interobserver variation for these classifications was analysed by kappa (K) statistics. In the OLGA staging system AG was replaced by IM creating the IM staging system. Both classifications were evaluated for patient distribution and severe premalignant gastric lesions by stage. Results: In total, 125 patients (69 men and 56 women) with a mean (± SD) age of 61 ±11.7 years (range 23-81 years) were included in this study. DYS was diagnosed in 7 (6%) patients. For DYS interobserver variability was fair (K=0.4; low grade DYS K=0.2; and high gradeDYS K=0.5). The interobserver agreement was moderate for AG (K=0.6), whereas agreement was almost perfect for IM (K=0.9). Overall, 83 (66%) patients were classified in stage I-IV according to the OLGA staging system (stage I n=23; stage II n=29; stage III n=23; stage IV n=8) and 80 (64%) patients were classified in stage I-IV according to the IM staging system (stage I n=24; stage II n=25; stage III n=22; stage IV n=9). Of the dysplasia patients, 5 (71%) patients clustered in stage III-IV in the OLGA system, whereas 6 (86%) patients clustered in III-IV of the IM staging system. Conclusions: Replacement of AG by IM in the staging and grading of gastritis increases interobserver agreement considerably. Moreover, the correlation with the severity of gastritis remains at least as effective as the OLGA classification. Therefore, the intestinal metaplasia staging may be preferred over the OLGA system for the prediction of gastric cancer risk in patients with pre-malignant gastric lesions. Further research is needed to evaluate the use of this system for the selection of a small category of patients for more intense follow-up.

M1983 Grading and Staging Gastritis with the Olga System: Intestinal Metaplasia As a Reproducible Alternative

Background: The recently proposed OLGA staging system (Gut 2007;56;631-636) is based on the extent and severity of atrophic gastritis (AG) and provides relevant clinical information regarding gastric cancer risk. However, AG is a difficult histopathological diagnosis of which the interobserver agreement is low. In contrast, intestinal metaplasia (IM) has better defined specific histopathological features and is associated with a much better interobserver agreement. The aim of this study was to evaluate interobserver agreement for AG, IM and dysplasia (DYS) and to assess whether a staging system based on IM instead of AG may be preferred to estimate gastric cancer risk. Methods: In a prospective multicenter study, patients with IM and DYS underwent surveillance endoscopy with extensive biopsy sampling. Three expert pathologists graded biopsy specimens according to the updated Sydney classification and the Vienna classification. Interobserver variation for these classifications was analysed by kappa (K) statistics. In the OLGA staging system AG was replaced by IM creating the IM staging system. Both classifications were evaluated for patient distribution and severe premalignant gastric lesions by stage. Results: In total, 125 patients (69 men and 56 women) with a mean (± SD) age of 61 ±11.7 years (range 23-81 years) were included in this study. DYS was diagnosed in 7 (6%) patients. For DYS interobserver variability was fair (K=0.4; low grade DYS K=0.2; and high gradeDYS K=0.5). The interobserver agreement was moderate for AG (K=0.6), whereas agreement was almost perfect for IM (K=0.9). Overall, 83 (66%) patients were classified in stage I-IV according to the OLGA staging system (stage I n=23; stage II n=29; stage III n=23; stage IV n=8) and 80 (64%) patients were classified in stage I-IV according to the IM staging system (stage I n=24; stage II n=25; stage III n=22; stage IV n=9). Of the dysplasia patients, 5 (71%) patients clustered in stage III-IV in the OLGA system, whereas 6 (86%) patients clustered in III-IV of the IM staging system. Conclusions: Replacement of AG by IM in the staging and grading of gastritis increases interobserver agreement considerably. Moreover, the correlation with the severity of gastritis remains at least as effective as the OLGA classification. Therefore, the intestinal metaplasia staging may be preferred over the OLGA system for the prediction of gastric cancer risk in patients with pre-malignant gastric lesions. Further research is needed to evaluate the use of this system for the selection of a small category of patients for more intense follow-up.

This Month in Gastroenterology

This Month in Gastroenterology

Gastric Cancer Risk in Patients With Premalignant Gastric Lesions: A Nationwide Cohort Study in the Netherlands

A cascade of precursor lesions (eg, atrophic gastritis, intestinal metaplasia, and dysplasia) precedes most gastric adenocarcinomas. Quantification of gastric cancer risk in patients with premalignant gastric lesions is unclear, however. Consequently, endoscopic surveillance is controversial, especially in Western populations. To analyze current surveillance practice and gastric cancer risk in patients with premalignant gastric lesions, all patients with a first diagnosis between 1991 and 2004 were identified in the Dutch nationwide histopathology registry (PALGA); follow-up data were evaluated until December 2005. In total, 22,365 (24%) patients were diagnosed with atrophic gastritis, 61,707 (67%) with intestinal metaplasia, 7616 (8%) with mild-to-moderate dysplasia, and 562 (0.6%) with severe dysplasia. Patients with a diagnosis of atrophic gastritis, intestinal metaplasia, or mild-to-moderate dysplasia received re-evaluation in 26%, 28%, and 38% of cases, respectively, compared with 61% after a diagnosis of severe dysplasia (P < .001). The annual incidence of gastric cancer was 0.1% for patients with atrophic gastritis, 0.25% for intestinal metaplasia, 0.6% for mild-to-moderate dysplasia, and 6% for severe dysplasia within 5 years after diagnosis. Risk factors for gastric cancer development were increasing severity of premalignant gastric lesions at initial diagnosis (eg, severe dysplasia, hazard ratio 40.14, 95% confidence interval 32.2-50.1), increased age (eg, 75-84 years, hazard ratio 3.75, 95% confidence interval 2.8-5.1), and male gender (hazard ratio 1.50, 95% CI 1.3-1.7). Patients with premalignant gastric lesions are at considerable risk of gastric cancer. As current surveillance of these patients is inconsistent with their cancer risk, development of guidelines is indicated.