(See also Overview of Acid Secretion Overview of Acid Secretion Acid is secreted by parietal cells in the proximal two thirds (body) of the stomach. Gastric acid aids digestion by creating the optimal pH for pepsin and gastric lipase and by stimulating pancreatic... read more and Overview of Gastritis Overview of Gastritis Gastritis is inflammation of the gastric mucosa caused by any of several conditions, including infection (Helicobacter pylori), drugs (nonsteroidal anti-inflammatory drugs, alcohol),... read more .)
Pathology of Nonerosive Gastritis
Lymphocytes and plasma cells mixed with neutrophils are the predominant infiltrating inflammatory cells. Inflammation is superficial and may involve the antrum, body, or both. It is usually not accompanied by atrophy or metaplasia. Prevalence increases with age.
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 gastritis (sometimes referred to as type B gastritis). Some patients with gastric atrophy have autoantibodies to parietal cells, usually in association with corpus gastritis (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 Stomach Cancer Etiology of stomach cancer is multifactorial, but Helicobacter pylori plays a significant role. Symptoms include early satiety, obstruction, and bleeding but tend to occur late in the... read more .
Symptoms and Signs of Nonerosive Gastritis
Most patients with H. pylori–associated gastritis are asymptomatic, although some have mild dyspepsia Dyspepsia Dyspepsia is a sensation of pain or discomfort in the upper abdomen; it often is recurrent. It may be described as indigestion, gassiness, early satiety, postprandial fullness, gnawing, or burning... read more or other vague symptoms.
Diagnosis of Nonerosive Gastritis
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 Diagnosis Helicobacter pylori is a common gastric pathogen that causes gastritis, peptic ulcer disease, gastric adenocarcinoma, and low-grade gastric lymphoma. Infection may be asymptomatic or... read more is appropriate.
Treatment of Nonerosive Gastritis
Eradication of H. pylori
Sometimes acid-suppressive drugs
Treatment of chronic nonerosive gastritis is H. pylori eradication Treatment Helicobacter pylori is a common gastric pathogen that causes gastritis, peptic ulcer disease, gastric adenocarcinoma, and low-grade gastric lymphoma. Infection may be asymptomatic or... read more . 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 group 1 carcinogen (1 Treatment reference Nonerosive gastritis refers to a variety of histologic abnormalities that are mainly the result of Helicobacter pylori infection. Most patients are asymptomatic. Diagnosis is by endoscopy. Treatment... read more ); eradication removes the cancer risk.
In H. pylori–negative patients, treatment is directed at symptoms using acid-suppressive drugs Drug Treatment of Gastric Acidity Drugs for decreasing acidity are used for peptic ulcer, gastroesophageal reflux disease (GERD), and many forms of gastritis. Some drugs are used in regimens for treating Helicobacter pylori... read more (eg, H2 blockers, proton pump inhibitors) or antacids.