Deep gastritis is more likely to be symptomatic (eg, vague dyspepsia). Mononuclear cells and neutrophils infiltrate the entire mucosa to the level of the muscularis, but exudate or crypt abscesses seldom result, as might be expected by such infiltration. Distribution may be patchy. Superficial gastritis may be present, as may partial gland atrophy and metaplasia.
Atrophy of gastric glands may follow in gastritis, most often long-standing antral (sometimes referred to as type B) gastritis. Some patients with gastric atrophy have autoantibodies to parietal cells, usually in association with corpus (type A) gastritis and pernicious anemia.
Atrophy may occur without specific symptoms. Endoscopically, the mucosa may appear normal until atrophy is advanced, when submucosal vascularity may be visible. As atrophy becomes complete, secretion of acid and pepsin diminishes and intrinsic factor may be lost, resulting in vitamin B12 malabsorption.
Two types of metaplasia are common in chronic nonerosive gastritis:
Mucous gland metaplasia (pseudopyloric metaplasia) occurs in the setting of severe atrophy of the gastric glands, which are progressively replaced by mucous glands (antral mucosa), especially along the lesser curve. Gastric ulcers may be present (typically at the junction of antral and corpus mucosa), but whether they are the cause or consequence of these metaplastic changes is not clear.
Intestinal metaplasia typically begins in the antrum in response to chronic mucosal injury and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa—with goblet cells, endocrine (enterochromaffin or enterochromaffin-like) cells, and rudimentary villi—and may even assume functional (absorptive) characteristics.
Intestinal metaplasia is classified histologically as complete (most common) or incomplete. With complete metaplasia, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits dysplasia. Intestinal metaplasia may lead to stomach cancer.
Most patients with H. pylori–associated gastritis are asymptomatic, although some have mild dyspepsia or other vague symptoms.
Often, the condition is discovered during endoscopy done for other purposes. Testing of asymptomatic patients is not indicated. Once gastritis is identified, testing for H. pylori is appropriate.
Treatment of chronic nonerosive gastritis is H. pylori eradication. Treatment of asymptomatic patients is somewhat controversial given the high prevalence of H. pylori–associated superficial gastritis and the relatively low incidence of clinical sequelae (ie, peptic ulcer disease). However, H. pylori is a class 1 carcinogen; eradication removes the cancer risk.
In H. pylori–negative patients, treatment is directed at symptoms using acid-suppressive drugs (eg, H2 blockers, proton pump inhibitors) or antacids.