Intestinal Metaplasia Surveillance

Intestinal metaplasia (IM) of the stomach is a risk factor in developing intestinal-type gastric cancer. It occurs as a result of reduced acidity within the stomach, with gastric mucosa changing its appearance more in keeping with intestinal mucosa. IM is much more common in those with Helicobacter pylori infection, and smokers and alcohol drinkers, and those deficient in essential vitamins including vitamin C found in fresh fruit and vegetables [1]. Bile reflux is also a risk factor for IM. When Helicobacter pylori is present, this needs to be treated with eradication therapy with good evidence that this causes regression of IM [2]. Patients should be encouraged to quit smoking, reduce alcohol intake and there is some evidence that antioxidants (fresh fruit and vegetables and vitamin C) can be protective and reverse IM.

Ongoing Surveillance

Patients with gastric intestinal metaplasia (GIM) may have a greater than 10-fold increased risk of gastric cancer than the general population [3]. GIM is recognized as a premalignant condition that may be the result of an adaptive response to environmental stimuli such as H pylori infection, smoking, and high salt intake [3]. The potential benefits of surveillance were evaluated in 2 retrospective studies from the United Kingdom [4,5]. The incidence of gastric cancer was reported to be as high as 11% [5]. Endoscopic surveillance was associated with earlier stage cancer detection and improved survival [4,5]. Additionally, patients with GIM and high-grade dysplasia (HGD) were at significant risk of harbouring a prevalent or incident cancer [5]. In both retrospective [6,7] and prospective [8-10] European studies of patients with GIM and HGD, the cancer detection rate with endoscopic surveillance ranged from 33% to 85%. A review of the management of patients with GIM suggests that for most U.S. patients, the risk of progression to cancer is low, and surveillance is not clinically indicated unless other risk factors for gastric cancer are present, such as a family history of gastric cancer and Asian heritage [11]. A recent European consensus statement suggested that if low-grade dysplasia is detected in a patient with GIM, a repeat surveillance EGD with a topographic mapping biopsy strategy should be performed within 1 year [12]. The optimal frequency of subsequent endoscopic evaluation is not known. Surveillance may be suspended when 2 consecutive endoscopies are negative for dysplasia. Patients with confirmed HGD should undergo surgical or endoscopic resection due to the high probability of coexisting invasive adenocarcinoma. Twenty- five percent of patients with HGD will progress to adenocarcinoma within a year [13]. If Helicobacter pylori infection is identified, eradication should be performed. It remains controversial whether empiric Helicobacter pylori treatment should be administered when GIM is diagnosed.

References

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  2. Sung JJ, Lin SR, Ching JY, et al Atrophy and intestinal metaplasia one year after cure of H. pylori infection: a prospective, randomized study. Gastroenterology 2000;119:7–14.
  3. Vannella L, Lahner E, Osborn J, et al. Risk factors for progression to gastric neoplastic lesions in patients with atrophic gastritis. Aliment Pharmacol Ther 2010;31:1042-50.
  4. den Hoed CM, Holster IL, Capelle LG, et al. Follow-up of premalignant lesions in patients at risk for progression to gastric cancer. Endoscopy 2013;45:249-56.
  5. Whiting JL, Sigurdsson A, Rowlands DC, et al. The long term results of endoscopic surveillance of premalignant gastric lesions. Gut 2002;50:378-81.
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  7. Lansdown M, Quirke P, Dixon MF, et al. High grade dysplasia of the gastric mucosa: a marker for gastric carcinoma. Gut 1990;31:977-83.
  8. Farinati F, Rugge M, Di Mario F, et al. Early and advanced gastric cancer in the follow-up of moderate and severe gastric dysplasia patients. A prospective study. I.G.G.E.D.–Interdisciplinary Group on Gastric Epithelial Dysplasia. Endoscopy 1993;25:261-4.
  9. Fertitta AM, Comin U, Terruzzi V, et al. Clinical significance of gastric dysplasia: a multicenter follow-up study. Gastrointestinal Endoscopic Pathology Study Group. Endoscopy 1993;25:265-8.
  10. Rugge M, Leandro G, Farinati F, et al. Gastric epithelial dysplasia. How clinicopathologic background relates to management. Cancer 1995;76:376-82.
  11. Fennerty MB. Gastric intestinal metaplasia on routine endoscopic biopsy. Gastroenterology 2003;125:586-90.
  12. 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.
  13. Cassaro M, Rugge M, Gutierrez O, et al. Topographic patterns of intestinal metaplasia and gastric cancer. Am J Gastroenterol 2000;95: 1431-8. 54. Toh BH, va.