Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2010 Mar;105(3):493-8.
doi: 10.1038/ajg.2009.728.

Pathology of gastric intestinal metaplasia: clinical implications

Pelayo Correa  1 , M Blanca Piazuelo, Keith T Wilson
Affiliations
Review

Pathology of gastric intestinal metaplasia: clinical implications

Pelayo Correa et al. Am J Gastroenterol. 2010 Mar.
No abstract available

PubMed Disclaimer

Conflict of interest statement

CONFLICT OF INTEREST

Guarantor of the article: Pelayo Correa, MD.

Specific author contributions: All authors participated in the review of the literature and in the drafting and editing of the article for intellectual content and approved the final draft submitted.

Potential competing interests: None.

Figures

Figure 1
Figure 1
Photomicrographs of gastric intestinal metaplasia. (a) Complete type with well-defined goblet cells alternating with eosinophilic enterocytes displaying well-developed brush border (inset) and Paneth cells (arrow). (b) Incomplete type showing multiple intracytoplasmic mucin droplets of varying sizes and shapes, and absence of a brush border. (Hematoxylin and eosin; original magnification, ×400; inset, ×1,000.)
Figure 2
Figure 2
Histochemical staining of gastric intestinal metaplasia (IM). (a, c) Periodic acid–Schiff–Alcian blue staining. Neutral mucins are stained magenta (arrows show normal epithelium), and acid mucins are blue (or purple when combined with neutral). (b, d) Alcian blue–high-iron diamine technique differentiates acid mucins. Sialomucins are stained blue, and sulfomucins are brown. (a, b) Complete IM (type I) shows sialomucins in goblet cells, and absence of sulfomucins. (c, d) Incomplete IM (type III) with sialomucins in goblet cells and a mixture of neutral and sulfomucins in columnar cells. (Original magnification, ×400.)
Figure 3
Figure 3
Diagrammatic representation of the sequential steps in intestinal metaplasia (IM), indicating the mucin types expressed in each step. Staining intensities are represented by the symbols + to ++++.
Figure 4
Figure 4
Proposed algorithm for the management and surveillance of gastric intestinal metaplasia (IM). *Definition of extensive IM: (i) IM present in at least two gastric locations or (ii) moderate or marked IM in at least two biopsy specimens (see refs. and 36). **Definition of extensive atrophy: serum pepsinogen I (PGI) level <70 μg/l and PGI/PGII ratio <3.
See this image and copyright information in PMC

References

    1. Correa P. Human gastric carcinogenesis: a multistep and multifactorial process. First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention. Cancer Res. 1992;52:6735–40. - PubMed
    1. Fennerty MB. Gastric intestinal metaplasia on routine endoscopic biopsy. Gastroenterology. 2003;125:586–90. - PubMed
    1. Brown LM, Devesa SS. Epidemiologic trends in esophageal and gastric cancer in the United States. Surg Oncol Clin N Am. 2002;11:235–56. - PubMed
    1. Devesa SS, Blot WJ, Fraumeni JF., Jr Changing patterns in the incidence of esophageal and gastric carcinoma in the United States. Cancer. 1998;83:2049–53. - PubMed
    1. Goldblum JR, Richter JE, Vaezi M, et al. Helicobacter pylori infection, not gastroesophageal reflux, is the major cause of inflammation and intestinal metaplasia of gastric cardiac mucosa. Am J Gastroenterol. 2002;97:302–11. - PubMed

Publication types