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Metaplastic (chronic) atrophic gastritis

Authors
Pamela J Jensen, MD
Mark Feldman, MD, MACP, AGAF, FACG
Section Editor
J Thomas Lamont, MD
Deputy Editor
Shilpa Grover, MD, MPH

INTRODUCTION

Gastritis is a term used to denote inflammation-associated mucosal injury. Gastritis is commonly secondary to infectious or autoimmune etiologies, although it can also result from drugs or hypersensitivity reactions. This topic review will discuss the different types of metaplastic atrophic gastritis (also called chronic atrophic gastritis) [1,2]. The other forms of gastritis and gastropathy are presented separately.

METAPLASTIC ATROPHIC GASTRITIS

The term atrophic gastritis, sometimes referred to as gastric atrophy, has been used since the nineteenth century. It is still commonly used to describe chronic gastritis that, in addition to inflammation, is associated with mucosal thinning, gland loss, and changes in epithelial cell types (ie, metaplasia).

The classification of atrophic gastritis has varied. In one system proposed by Strickland and colleagues, the designation type A and B gastritis were used to describe immune, endocrine, and functional changes in the body and antrum, respectively [3,4]. However, these alphabetic designations have been used inconsistently among authors.

A more precise classification system uses the term "metaplastic atrophic gastritis" to specify the presence of metaplastic epithelial changes. It recognizes two main subtypes, autoimmune and environmental metaplastic atrophic gastritis (AMAG and EMAG). The location and histologic features defining autoimmune and environmental metaplastic atrophic gastritis are similar to those of type A and B atrophic gastritis, respectively [3,5,6]. This classification system has several advantages:

Metaplasia, especially of the intestinal type, is virtually a universal feature of atrophic gastritis and is often the most dependable defining morphologic feature.

                      

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Literature review current through: May 2016. | This topic last updated: Dec 17, 2015.
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