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atrophic gastritis
Sunday 4 March 2012
Definition: Gastric atrophy is a preneoplastic condition, especially in populations where gastric carcinoma is prevalent. It develops following gastric injury induced by various factors.
Images
Atrophic gastritis with megaloblastic change due to B12 deficiency
Sydney system of grading
| Feature | Definition | Grading Guidelines |
| Chronic inflammation | Increased lymphocytes and plasma cells in the lamina propria | Mild, moderate, or severe increase in density |
| Activity | Neutrophilic infiltrates of the lamina propria, pits, or surface epithelium | Less than one third of pits and surface infiltrated = mild; one third to two thirds = moderate; more than two thirds = severe |
| Atrophy | Loss of specialized glands from either antrum or corpus | Mild, moderate, or severe loss |
| Intestinal metaplasia | Intestinal metaplasia of the epithelium | Less than one third of mucosa involved = mild; one third to two thirds = moderate; more than two thirds = severe |
| Helicobacter pylori | H. pylori density | Scattered organisms covering less than one third of the surface = mild colonization; large clusters or a continuous layer over two thirds of surface = severe; intermediate numbers = moderate colonization |
There are substantial geographic and ethnic variations in the prevalence and severity of atrophic gastritis and its distribution within the stomach.
Its features differ, primarily determined by the clinical setting in which it arises, the lesion location, and etiologic, environmental, and host factors.
One may also grade chronic atrophic gastritis as active or quiescent based on the presence or absence of acute inflammation.
Because extensive atrophy and metaplasia appear to increase the risk of gastric cancer, it is important to determine the severity of these lesions in biopsies.
However, the definition of gastric atrophy is controversial and there is poor agreement in grading its severity, especially when it is only mild or moderate in nature.
It is more difficult to appreciate minor degrees of atrophy in the antrum than in the corpus.
This is due to the fact that in the antrum the gastric pits tend to be long and the antral glands normally lie in a loose connective tissue stroma.
The interpretation is made more difficult due to the presence of an intense antral inflammatory infiltrate that typically complicates HP
gastritis and expands the lamina propria.
In contrast, the glands of the oxyntic mucosa are normally tightly packed and lined bya population of parietal and chief cells that occupy well-established positions from the neck zone to the deepest portion of the gland.
In advanced atrophic gastritis, the glands disappear, the inflammation recedes, and the cellularity of the lamina propria returns to normal.
Pre-existing reticulin fibers collapse on one another between the pits.
There is a large section of literature devoted to defining and quantifying gastric atrophy, particularly since atrophy is an early step in the carcinogenic process.
It has been recommended that the term atrophic gastritis be restricted to those cases in which there is glandular loss that is replaced by extracellular matrix and fibroblasts, and/or when intestinal metaplasia is present.
The revised Sydney classification
The revised Sydney classification for gastritis provides guidelines for grading different histopathologic changes in gastric biopsies.
It aims to produce a standardized, consistent histologic interpretation of gastritis based on topography, morphology, and etiology and includes a morphologic component by which five histologic variables are graded:
chronic inflammation
neutrophil activity
glandular atrophy
intestinal metaplasia,
HP density
If one chooses to use this system, the pathology report should note the presence or absence of each variable and when present, each ofthese variables can be graded on a mild, moderate, or marked scale using the published visual guidelines.
The HP density should be evaluated in non-metaplastic areas.
The degree of atrophy can be graded as mild, moderate, or severe by estimating the thickness of the glands in relationship to the entire mucosal thickness.
This is facilitated by examining properly oriented biopsies containing the muscularis mucosae.
Increasing degrees of atrophy associate with glandular cystic dilation, epithelial atypia, and intestinal metaplasia.
Loss of all the glands qualifies for the diagnosis of severe atrophic gastritis.
Intestinal and pyloric metaplasia commonly develop.
A confident diagnosis of atrophy can be made when epithelial metaplasia and/or gastric gland loss affects at least 50% of the total area of gastric biopsy material, assuming that there has been adequate mucosal sampling as recommended by the updated Sydney classification.
Three features consistently discriminate atrophic from non atrophic lesions, particularly if one avoids areas of intestinal metaplasia and lymphoid follicles:
the ratio of the glandular length to total mucosal thickness,
the proportion of the secretory compartment area occupied by glands,
the number of glandular cross sections per 40 microscopic fields,
Most patients with intestinal metaplasia have enough non metaplastic areas that the degree of atrophy can be evaluated.
In patients in whom the entire stomach has been replaced by intestinal metaplasia, the patients are given the highest atrophy score.
One factor that may call attention to the presence of atrophy is the presence of intestinal metaplasia, since the two lesions are commonly found together, but in its absence, mild or focal atrophy is easily missed.
Both antral and autoimmune gastritis show a marked inflammatory infiltrate consisting of plasma cells, lymphocytes, and variable numbers of eosinophils in all levels of thelamina propria.
Initially, chronic inflammation fills the spaces left by glandular destruction and loss, thereby maintaining normal mucosal thickness.
Plasma cells tend to lie superficially in the lamina propria, whereas lymphocytes lie deeper in the mucosa.
Chronic progressive atrophy of the specialized epithelium results in an almost total loss of acid- and pepsinogen-secreting cells in the body ofthe stomach in autoimmune (type A) gastritis and ofthe antral glands in type B gastritis.
As the mucosa thins and glands disappear, the bases of the pits come to rest on the muscularis mucosae.
One must be careful not to mistake isolated residual cells seen in the setting of a gland-poor, stromal-rich mucosa, especially on a biopsy, as evidence ofan early diffuse carcinoma.
Variants
pediatric non-Helicobacter pylori atrophic gastritis
