Factors associated with the progression of gastric intestinal metaplasia: a multicenter, prospective cohort study.

Background and study aims Gastric cancer (GC) is usually preceded by premalignant gastric lesions (GPLs) such as gastric intestinal metaplasia (GIM). Information on risk factors associated with neoplastic progression of GIM are scarce. This study aimed to identify predictors for progression of GIM in areas with low GC incidence. Patients and methods The Progression and Regression of Precancerous Gastric Lesions (PROREGAL) study includes patients with GPL. Patients underwent at least two upper endoscopies with random biopsy sampling. Progression of GIM means an increase in severity according to OLGIM (operative link on gastric intestinal metaplasia) during follow-up (FU). Family history and lifestyle factors were determined through questionnaires. Serum Helicobacter pylori infection, pepsinogens (PG), gastrin-17 and GC-associated single nucleotide polymorphisms (SNPs) were determined. Cox regression was performed for risk analysis and a chi-squared test for analysis of single nucleotide polymorphisms. Results Three hundred and eight patients (median age at inclusion 61 years, interquartile range (IQR: 17; male 48.4 %; median FU 48 months, IQR: 24) were included. During FU, 116 patients (37.7 %) showed progression of IM and six patients (1.9 %) developed high-grade dysplasia or GC. The minor allele (C) on TLR4 (rs11536889) was inversely associated with progression of GIM (OR 0.6; 95 %CI 0.4-1.0). Family history (HR 1.5; 95 %CI 0.9-2.4) and smoking (HR 1.6; 95 %CI 0.9-2.7) showed trends towards progression of GIM. Alcohol use, body mass index, history of H. pylori infection, and serological markers were not associated with progression. Conclusions Family history and smoking appear to be related to an increased risk of GIM progression in low GC incidence countries. TLR4 (rs11536889) showed a significant inverse association, suggesting that genetic information may play a role in GIM progression.

Follow-up of premalignant lesions in patients at risk for progression to gastric cancer.

BACKGROUND AND STUDY AIMS: A recent international guideline recommends surveillance of premalignant gastric lesions for patients at risk of progression to gastric cancer. The aim of this study was to identify the role of the distribution and severity of premalignant lesions in risk categorization. PATIENTS AND METHODS: Patients with a previous diagnosis of atrophic gastritis, intestinal metaplasia, or low grade dysplasia were invited for surveillance endoscopy with non-targeted biopsy sampling. Biopsy specimens were evaluated by pathologists (four general and one expert) using the Sydney and the operative link for gastric intestinal metaplasia (OLGIM) systems, and scores were compared using kappa statistics. RESULTS: 140 patients were included. In 37 % (95 % confidence interval [CI] 29 % - 45 %) the severity of premalignant lesions was less than at baseline, while 6 % (95 %CI 2 % - 10 %) showed progression to more severe lesions. Intestinal metaplasia in the corpus was most likely to progress to more than one location (57 %; 95 %CI 36 % - 76 %). The proportion of patients with multilocated premalignant lesions increased from 24 % at baseline to 31 % at surveillance (P = 0.014). Intestinal metaplasia was the premalignant lesion most frequently identified in subsequent endoscopies. Intestinal metaplasia regressed in 27 % compared with 44 % for atrophic gastritis and 100 % for low grade dysplasia. Interobserver agreement was excellent for intestinal metaplasia (k = 0.81), moderate for dysplasia (k = 0.42), and poor for atrophic gastritis (k < 0). CONCLUSIONS: Premalignant gastric lesions found in the corpus have the highest risk of progression, especially intestinal metaplasia, which has excellent interobserver agreement. This supports the importance of intestinal metaplasia as marker for follow-up in patients with premalignant gastric lesions.

The prevalence of premalignant gastric lesions in asymptomatic patients: predicting the future incidence of gastric cancer.

BACKGROUND: Helicobacter pylori is the main risk-factor for gastric cancer through a cascade from gastritis through atrophic gastritis (AG), intestinal metaplasia (IM), dysplasia (DYS) to malignancy. The presence of these lesions in the general population predicts the gastric cancer incidence in the coming decades. Prevalence data are mostly obtained from serological studies and endoscopy data in symptomatic patients. AIM: To investigate the prevalence of H. pylori infection and its related gastric changes in asymptomatic subjects. METHODS: 383 Patients undergoing routine colonoscopy were included. All subjects underwent upper GI endoscopy and completed the Gastrointestinal Symptom Rating Scale (GSRS). Biopsies were taken from antrum and corpus. RESULTS: H. pylori infection was present in 22%. Non-Caucasian subjects had a significantly higher H. pylori prevalence (p < 0.001). AG, IM and DYS were together found in 9.3% of subjects. Subjects with AG, IM or DYS were significantly older (p < 0.001). No differences were found with respect to gender, presence of GI symptoms as scored by GSRS, lifestyle and medication use. CONCLUSIONS: The prevalence of premalignant gastric lesions is considerable in general Western population with increasing age as the main risk factor. One time screening for premalignant lesions at the age of 60 years is a reasonable strategy since the numbers found imply that gastric cancer will remain a prevalent disease.

Comparison of patient and proxy responses on risk factors for stroke.

BACKGROUND: For studies on chronic risk factors and trigger (i.e. acute risk) factors, stroke researchers often have to rely on proxies. The reliability of proxy responses regarding trigger factors for stroke is unknown. METHODS: Thirty patients with stroke and their proxies were interviewed about chronic risk factors and trigger factors. We assessed the completeness of proxy-derived data by calculating the level of non-response and the level of agreement using Cohen kappa statistics. RESULTS: For most chronic risk factors and trigger factors, the response rate to whether or not exposure had taken place in the past year was 87% or higher. If couples agreed on exposure, patient and proxy could also provide a comparable estimate of the average frequency of exposure. Although the non-response on last time of exposure was higher, proxies who could answer provide a reasonably good estimate for most trigger factors. CONCLUSIONS: Proxies provide reliable information on exposure to chronic risk factors and trigger factors for stroke. For exposure and average frequency of exposure, non-response is low and the level of agreement is high for most chronic risk factors; for last time of exposure non-response is higher, but proxies who could respond provided reliable estimates of last time of exposure to most trigger factors.

Gastric MALT lymphoma: epidemiology and high adenocarcinoma risk in a nation-wide study.

BACKGROUND: Gastric marginal zone non-Hodgkin lymphomas MALT type (gMALT) and gastric adenocarcinomas (GC) are long-term complications of chronic Helicobacter pylori gastritis, however, the incidence of gMALT and the GC risk in these patients is unclear. OBJECTIVE: To evaluate epidemiological time trends of gMALT in the Netherlands and to estimate GC risk. METHODS: Patients with a first diagnosis of gMALT between 1991 and 2006 were identified in the Dutch nation-wide histopathology registry (PALGA). Age-standardised incidence rates were calculated. The incidences of GC in patients with gMALT and in the Dutch population were compared. Relative risks were calculated by a Poisson Model. RESULTS: In total, 1419 patients were newly diagnosed with gMALT, compatible with an incidence of 0.41/100,000/year. GC was diagnosed in 34 (2.4%) patients of the cohort. Patients with gMALT had a sixfold increased risk for GC in comparison with the general population (p<0.001). This risk was 16.6 times higher in gMALT patients aged between 45 and 59 years than in the Dutch population (p<0.001). CONCLUSIONS: GC risk in patients with gMALT is six times higher than in the Dutch population and warrants accurate re-evaluation after diagnosis and treatment for gMALT.