Endoscopy 2013; 45(04): 249-256
DOI: 10.1055/s-0032-1326379
Original article
© Georg Thieme Verlag KG Stuttgart · New York

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

C. M. den Hoed
1   Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands
,
I. L. Holster
1   Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands
,
L. G. Capelle
1   Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands
,
A. C. de Vries
1   Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands
,
B. den Hartog
2   Department of Gastroenterology and Hepatology, Rijnstate Hospital, Arnhem, The Netherlands
,
F. ter Borg
3   Department of Gastroenterology and Hepatology, Deventer Hospital, Deventer, The Netherlands
,
K. Biermann
4   Department of Pathology Erasmus MC University Medical Center, Rotterdam, The Netherlands
,
E. J. Kuipers
1   Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands
5   Department of Internal Medicine, Erasmus MC University Medical Center, Rotterdam, The Netherlands
› Author Affiliations
Further Information

Publication History

submitted 05 April 2012

accepted after revision 08 November 2012

Publication Date:
26 March 2013 (online)

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.

 
  • References

  • 1 Karim-Kos HE, de Vries E, Soerjomataram I et al. Recent trends of cancer in Europe: a combined approach of incidence, survival and mortality for 17 cancer sites since the 1990s. Eur J Cancer 2008; 44: 1345-1389
  • 2 de Vries AC, van Grieken NC, Looman CW et al. Gastric cancer risk in patients with premalignant gastric lesions: a nationwide cohort study in the Netherlands. Gastroenterology 2008; 134: 945-952
  • 3 Gotoda T. Endoscopic resection of early gastric cancer: the Japanese perspective. Curr Opin Gastroenterol 2006; 22: 561-569
  • 4 Whiting JL, Sigurdsson A, Rowlands DC et al. The long term results of endoscopic surveillance of premalignant gastric lesions. Gut 2002; 50: 378-381
  • 5 Dinis-Ribeiro M, Areia M, de Vries AC 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: 74-94
  • 6 Lee CW, Rickman B, Rogers AB et al. Helicobacter pylori eradication prevents progression of gastric cancer in hypergastrinemic INS-GAS mice. Cancer Res 2008; 68: 3540-3548
  • 7 Mera R, Fontham ET, Bravo LE et al. Long term follow up of patients treated for Helicobacter pylori infection. Gut 2005; 54: 1536-1540
  • 8 You WC, Brown LM, Zhang L et al. Randomized double-blind factorial trial of three treatments to reduce the prevalence of precancerous gastric lesions. J Natl Cancer Inst 2006; 98: 974-983
  • 9 Correa P, Houghton J. Carcinogenesis of Helicobacter pylori. Gastroenterology 2007; 133: 659-672
  • 10 El-Zimaity HM. Gastric atrophy, diagnosing and staging. World J Gastroenterol 2006; 12: 5757-5762
  • 11 El-Zimaity HM, Graham DY. Evaluation of gastric mucosal biopsy site and number for identification of Helicobacter pylori or intestinal metaplasia: role of the Sydney System. Human pathology 1999; 30: 72-77
  • 12 Farinati F, Cardin R, Cassaro M et al. Helicobacter pylori, inflammation, oxidative damage and gastric cancer: a morphological, biological and molecular pathway. Eur J Cancer Prev 2008; 17: 195-200
  • 13 Motta CR, Cunha MP, Queiroz DM et al. Gastric precancerous lesions and Helicobacter pylori infection in relatives of gastric cancer patients from northeastern Brazil. Digestion 2008; 78: 3-8
  • 14 Xia HH, Kalantar JS, Talley NJ et al. Antral-type mucosa in the gastric incisura, body, and fundus (antralization): a link between Helicobacter pylori infection and intestinal metaplasia?. Am J Gastroenterol 2000; 95: 114-121
  • 15 Eidt S, Stolte M. Prevalence of intestinal metaplasia in Helicobacter pylori gastritis. Scand J Gastroenterol 1994; 29: 607-610
  • 16 Meining ARB, Stolte M. Features of gastritis predisposing to gastric adenoma and early gastric cancer. J Clin Pathol 2002; 55: 770-773
  • 17 Schultze V, Hackelsberger A, Gunther T et al. Differing patterns of Helicobacter pylori gastritis in patients with duodenal, prepyloric, and gastric ulcer disease. Scand J Gastroenterol 1998; 33: 137-142
  • 18 Sakitani K, Hirata Y, Watabe H et al. Gastric cancer risk according to the distribution of intestinal metaplasia and neutrophil infiltration. J Gastroenterol Hepatol 2011; 26: 1570-1575
  • 19 Kuipers EJ, Uyterlinde AM, Pena AS et al. Long-term sequelae of Helicobacter pylori gastritis. Lancet 1995; 345: 1525-1528
  • 20 Cassaro M, Rugge M, Gutierrez O et al. Topographic patterns of intestinal metaplasia and gastric cancer. Am J Gastroenterol 2000; 95: 1431-1438
  • 21 Tava F, Luinetti O, Ghigna MR et al. Type or extension of intestinal metaplasia and immature/atypical “indefinite–for–dysplasia” lesions as predictors of gastric neoplasia. Hum Pathol 2006; 37: 1489-1497
  • 22 Mastracci L, Bruno S, Spaggiari P et al. The impact of biopsy number and site on the accuracy of intestinal metaplasia detection in the stomach: A morphometric study based on virtual biopsies. Dig Liver Dis 2008; 40: 632-640
  • 23 Rugge M, Correa P, Dixon MF et al. Gastric dysplasia: the Padova international classification. Am J Surg Pathol 2000; 24: 167-176
  • 24 Capelle LG, de Vries AC, Haringsma J et al. The staging of gastritis with the OLGA system by using intestinal metaplasia as an accurate alternative for atrophic gastritis. Gastrointest Endosc 2010; 71: 1150-1158
  • 25 Dixon MF, Genta RM et al. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol 1996; 20: 1161-1181
  • 26 Dixon MF. Gastrointestinal epithelial neoplasia: Vienna revisited. Gut 2002; 51: 130-131
  • 27 Genta RM, Graham DY. Comparison of biopsy sites for the histopathologic diagnosis of Helicobacter pylori: a topographic study of H. pylori density and distribution. Gastrointest Endosc 1994; 40: 342-345
  • 28 Rugge M, Correa P, Di Mario F et al. OLGA staging for gastritis: a tutorial. Dig Liver Dis 2008; 40: 650-658
  • 29 de Vries AC HJ, de Vries RA, ter Borg F et al. The use of clinical, histologic, and serologic parameters to predict the intragastric extent of intestinal metaplasia: a recommendation for routine practice. Gastrointest Endosc 2009; 70: 18-25
  • 30 Fleiss J. Statistical methods for rates and proportions. 2nd. . edition New York: Wiley; 1981
  • 31 de Vries AC, Meijer GA, Looman CW et al. Epidemiological trends of premalignant gastric lesions: a long term nationwide study in the Netherlands. Gut 2007; 56: 1665-1670
  • 32 den Hoed CM, van Eijck BC, Capelle LG et al. The prevalence of premalignant gastric lesions in asymptomatic patients: predicting the future incidence of gastric cancer. Eur J Cancer 2011; 47: 1211-1218
  • 33 den Hoed CM, Vila AJ, Holster IL et al. Helicobacter pylori and the birth cohort effect: evidence for stabilized colonization rates in childhood. Helicobacter 2011; 16: 405-409