Gastric cancer in patients with gastric atrophy and intestinal metaplasia: A systematic review and meta-analysis

Abstract

Aim Intestinal metaplasia (IM) and gastric atrophy (GA) are precancerous lesions in the stomach. There is a large debate on natural course of these lesions and surveillance strategy in these patients. This meta-analysis was aimed to find the most appropriate follow up and the rate of progression from IM and GA to GC. Methods This meta-analysis is followed and reported according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Electronic databases including EMBASE, PubMed, Web of Science databases, Scopus, and the Cochrane Library were searched until July 2018. Cochran’s Q test and I-square (I 2 ) test were used to examine heterogeneity across included studies. We pooled data using random-effect or fixed effect models indicated as incidence rate or proportion with 95% confidence intervals (CI). The variables of study included demographic data, endoscopy interval, follow up interval and time, GA and IM type and GC stage. Moreover, incidence rate of GC and progress rate, regress and persistence proportion in both GA and IM patients were assessed. Results Overall, 68 original articles out of 32981 citations were included in our meta-analysis. The pooled GC incidence rate in patients with GA was 1.24 (95% CI, 0.80, 1.76; I 2 : 83.6%) cases per 1,000 person-years. The rates of later diagnosis of IM and gastric dysplasia in patients with GA were estimated as 41.42 (95% CI, 3.11, 64.45; I 2 : 95.6%) and 6.23 (95% CI, 2.34, 11.46; I 2 : 83.0%) cases per 1,000 person-years, respectively. The pooled regressed proportion was 32.23 (95% CI, 18.07–48.02; I 2 : 94.0%) and the persistence proportion was 38.83 (95% CI, 20.20–59.13; I 2 : 97.0%) per 100 observations in GA patients. In IM studies, the pooled incidence rate of GC was 3.38 (95% CI, 2.13, 4.85; I 2 : 93.4%) cases per 1,000 person-years. The progressed rate to dysplasia in IM patient was estimated to be 12.51 (95% CI, 5.45, 22.03; I 2 : 95.1%) cases per 1,000 person-years. The pooled regressed proportion was 31.83 (95% CI, 25.48–38.51; I 2 : 91.0%) and the persistence proportion was 43.46 (95% CI, 32.52–54.71; I 2 : 96.0%) per 100 observations in IM patients. Conclusion Overall, the incidence of GC in patients with IM and GA are low but there is heterogeneity in data with the highest rate in Asian, males with those with incomplete IM. There is probability of regression or persistence without progression in patients with IM and GA who receive appropriate management.

Follow-Up Study Confirms the Presence of Gastric Cancer DNA Methylation Hallmarks in High-Risk Precursor Lesions

“…In our studies, we obtained 9 cases that progressed to cancer, which represents an incidence rate of 2.5 per 1000/person/year. The number of cases that progress to cancer obtained in our study is in accordance with previous estimations in European populations (1.75 cases per person/year) [39]. It should be noted that detection of the CpG methylation of a specific region could be easily performed by simple approaches without complex handling requirements and within an acceptable cost/effectiveness margin.…”

Screening and eradication of Helicobacter pylori for gastric cancer prevention: the Taipei global consensus

“…138 A meta-analysis showed that the incidence rates of gastric cancer in patients with atrophic gastritis and intestinal metaplasia are 1.24 (95% CI 0.80 to 1.76) and 3.38 (95% CI 2.13 to 4.85) cases per 1000 person-years, respectively. 139 Advanced-stage atrophy and intestinal metaplasia are defined as OLGA stage III/IV and OLGIM stage III/IV, respectively. The definition is based on the study following the "MAnagement of Precancerous conditions and lesions in the Stomach (MAPS)" guideline, which showed that 3.8% of patients with OLGIM stages III/IV and/or serum pepsinogen I/II ratio ≤3 progressed to high-grade dysplasia or cancer.…”

Insights into Effects/Risks of Chronic Hypergastrinemia and Lifelong PPI Treatment in Man Based on Studies of Patients with Zollinger–Ellison Syndrome

“…Gastritis increases the risk of GC when it effects the oxyntic mucosa of the stomach, principally when its presence results in the development of oxyntic atrophy and with time the development of intestinal metaplasia [79,223]. More recent studies demonstrate that treatment with PPIs resulting in reduced acidity leads to the migration of H. pylori from the antrum to the corpus resulting in an increased colonization of the gastric corpus, which is associated with the development of corpus inflammation, gastritis, and an increase risk of developing atrophic gastritis [139,243,244]. The atrophy of the corpus area resulting in chronic hypergastrinemia has been shown to be a significant risk factor for the development of GC [244,245].…”

“…More recent studies demonstrate that treatment with PPIs resulting in reduced acidity leads to the migration of H. pylori from the antrum to the corpus resulting in an increased colonization of the gastric corpus, which is associated with the development of corpus inflammation, gastritis, and an increase risk of developing atrophic gastritis [139,243,244]. The atrophy of the corpus area resulting in chronic hypergastrinemia has been shown to be a significant risk factor for the development of GC [244,245]. The role of chronic hypergastrinemia in development of GC was further supported by studies on insulin-gastrin (INS-GAS) transgenic mice [223].…”