Role of endoscopic surveillance for intestinal metaplasia limited to the antrum.

Abstract

The work by Shichijo et al1Shichijo S. Hirata Y. Niikura R. et al.Histological intestinal metaplasia and endoscopy atrophy are predictors of gastric cancer development after Helicobacter pylori eradication.Gastrointest Endosc. 2016; 84: 618-624Abstract Full Text Full Text PDF PubMed Scopus (135) Google Scholar showed a cumulative 5-year gastric cancer (GC) incidence of 3.2% in a cohort of 543 patients without history of GC, treated for Helicobacter pylori, and followed for 6.2 ± 4.8 years. In addition to severe endoscopic atrophy (hazard ratio [HR], 9.3) and corporal intestinal metaplasia (HR, 3.7), surprisingly, intestinal metaplasia limited to the antrum (HR, 3.6) was associated with GC development at follow-up. These data raise 2 concerns. First, the success of eradication therapy was assessed by the 13C-urea breath test (13CUBT) only, which has been reported to be unreliable in corporal atrophy.2Lahner E. Vaira D. Figura N. et al.Role of noninvasive tests (C-urea breath test and stool antigen test) as additional tools in diagnosis of Helicobacter pylori infection in patients with atrophic body gastritis.Helicobacter. 2004; 9: 436-442Crossref Scopus (48) Google Scholar False-negative 13CUBT results were shown in 31.8% of endoscopically proven H pylori–positive patients, which were associated with corpus-predominant gastritis (odds ratio, 5.6).3Capurso G. Carnuccio A. Lahner E. et al.Corpus-predominant gastritis as a risk factor for false-negative 13C-urea breath test results.Aliment Pharmacol Ther. 2006; 24: 1453-1460Crossref Scopus (24) Google Scholar In the study by Shichijo et al, 19% and 9.9% of patients had severe endoscopic atrophy and corporal intestinal metaplasia, respectively; thus, false-negative 13CUBT and ongoing H pylori infection may not be reliably excluded, possibly influencing the reported incidence rate of GC after H pylori eradication. Second, the significant association of intestinal metaplasia limited to the antrum and GC at follow-up (HR, 3.6), comparable with that of patients with corporal intestinal metaplasia (HR, 3.7), is in strict contrast to a solid body of evidence showing that precancerous mucosal changes in the antrum only are not linked to an increased GC risk.4Uemura N. Okamoto S. Yamamoto S. et al.Helicobacter pylori infection and the development of gastric cancer.N Engl J Med. 2001; 345: 784-789Crossref PubMed Scopus (3673) Google Scholar, 5Rugge M. de Boni M. Pennelli G. et al.Gastritis OLGA-staging and gastric cancer risk: a twelve-year clinico-pathological follow-up study.Aliment Pharmacol Ther. 2010; 31: 1104-1111PubMed Google Scholar, 6Dinis-Ribeiro M. Areia M. de Vries A.C. et al.Management of precancerous conditions and lesions in the stomach (MAPS): guideline from the European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter Study Group (EHSG), European Society of Pathology (ESP), and the Sociedade Portuguesa de Endoscopia Digestiva (SPED).Endoscopy. 2012; 44: 74-94Crossref PubMed Scopus (540) Google Scholar, 7Malfertheiner P. The intriguing relationship of Helicobacter pylori infection and acid secretion in peptic ulcer disease and gastric cancer.Dig Dis. 2011; 29: 459-464Crossref Scopus (71) Google Scholar In about 6% to 8% of patients with duodenal ulcers, who will never develop GC, antral intestinal metaplasia is detected.8Hong J.B. Xia L. Zuo W. et al.Risk factors for intestinal metaplasia in concomitant gastric and duodenal ulcer disease.Exp Ther Med. 2014; 7: 929-934Google Scholar, 9Leung W.K. Lin S.R. Ching J.Y. et al.Factors predicting progression of gastric intestinal metaplasia: results of a randomised trial on Helicobacter pylori eradication.Gut. 2004; 53: 1244-1249Crossref PubMed Scopus (347) Google Scholar In the study by Shichijo et al, patients with only antral intestinal metaplasia might have concomitant extensive atrophy, possibly explaining the odd association with GC at follow-up, but describing atrophy by endoscopy and intestinal metaplasia by histology splits information, limiting its usefulness. The need for GC surveillance has been raised recently in the United States.10Kim G.H. Liang P.S. Bang S.J. et al.Screening and surveillance for gastric cancer in the United States: is it needed?.Gastrointest Endosc. 2016; 84: 18-28Abstract Full Text Full Text PDF PubMed Scopus (132) Google Scholar These data suggest that we should reassess and standardize methods for atrophy and intestinal metaplasia description before starting GC surveillance in the intestinal metaplasia limited to the antrum. Histologic intestinal metaplasia and endoscopic atrophy are predictors of gastric cancer development after Helicobacter pylori eradicationGastrointestinal EndoscopyVol. 84Issue 4PreviewHelicobacter pylori eradication therapy is effective at reducing the incidence of gastric cancer; however, gastric cancer still develops after eradication. We conducted a cohort study to elucidate the risk factors for gastric cancer development after successful H pylori eradication therapy. Full-Text PDF Response:Gastrointestinal EndoscopyVol. 84Issue 5PreviewWe thank Lahner et al for their comments on our cohort study1 of the risk stratification for gastric cancer in Helicobacter pylori–eradicated patients. They commented on the 13C-urea breath test (C-UBT) and the risk of gastric cancer in patients with intestinal metaplasia limited to the antrum. Full-Text PDF