Diagnosis and Management of Gastric Intestinal Metaplasia: Current Status and Future Directions

Abstract

Gastric intestinal metaplasia (GIM) is a known premalignant condition of the human stomach along the pathway to gastric cancer (GC). Histologically, GIM represents the replacement of normal gastric mucosa by mucin-secreting intestinal mucosa. Helicobacter pylori infection is the most common etiologic agent of GIM development worldwide. The prevalence of GIM is heterogeneous among different regions of the world and correlates with the population endemicity of H. pylori carriage, among other environmental factors. GC remains the third leading cause of cancer-related mortality globally. GIM is usually diagnosed by upper endoscopy with biopsy, and histologic scoring systems have been developed to risk-stratify patients at highest risk for progression to GC. Several recent endoscopic imaging modalities may improve the optical detection of GIM and early GC. Appropriate surveillance of GIM may be cost effective and represents an opportunity for the early diagnosis and therapy of GC. Certain East Asian nations have established population-level programs for the screening and surveillance of GIM; guidelines regarding GIM surveillance have also recently been published in Europe. By contrast, few data exist regarding the appropriateness of surveillance of GIM in the United States. In this review, we discuss the pathogenesis, epidemiology, diagnosis, and management of GIM with an emphasis on the role of appropriate endoscopic surveillance.

Keywords: Epidemiology; Helicobacter pylori; Stomach.

Fig. 1

Correa’s cascade, a model for the histologic progression towards gastric cancer. Infection with Helicobacter pylori is the single most common etiologic environmental factor that precipitates the cascade.

Fig. 2

High-power view (H&E, ×100) of intestinal metaplasia showing metaplastic goblet cells on the surface and in the foveolar epithelium.

Fig. 3

Updated the Sydney System biopsy protocol, with two biopsies taken from the antrum, one biopsy taken from the incisura, one biopsy taken along the lesser curvature of the gastric body, and one biopsy taken along the greater curvature of the gastric body.

Fig. 4

On magnified narrow-band imaging, the normal gastric mucosa (A) should demonstrate a regular circular pattern and homogeneously spaced gastric pits. In contrast, gastric intestinal metaplasia (B) is characterized by the presence of features such as a tubule-villous mucosal pattern, irregular mucosal pattern, and variable vascular density.

Fig. 5

With probe-based confocal laser endomicroscopy, intestinal cells can clearly be identified by the presence of mucin-containing vesicles within the cytoplasm, which appear dark due to absence of fluorescein uptake (white arrows).

Fig. 6

Recommended surveillance strategy following a gastric biopsy that shows intestinal metaplasia (IM). H, pylori, Helicobacter pylori. *Increaed risk race/ethinicity defined as African Americans, Asian Americans, and Hispanic Americans of any race. Increased risk immigration status defined as 1st or 2nd (with at least one parent) generation immigrants from high-incidence areas (South America, Central America, Mexico, Caribbean, East Asia, Southeast Asia, post-Soviet states, Iran, and Turcky). Family history defined as at least one first-degree relative with gastric cancer; ^†Based upon biopsies from antrum and corpus, and from lesser and greater curvatures, in separate bottles. Extensive IM involving both antrum and corpus.