is inflammation of the gastric mucosa caused by any of several conditions,
including infection (Helicobacter
pylori), drugs (NSAIDs, alcohol), stress, and autoimmune phenomena
(atrophic gastritis). Many cases are asymptomatic, but dyspepsia
and GI bleeding sometimes occur. Diagnosis is by endoscopy. Treatment
is directed at the underlying cause but often includes acid suppression
and, for H. pylori infection,
Gastritis is classified as erosive or nonerosive based on the severity of mucosal injury. It is also classified according to the site of involvement (ie, cardia, body, antrum). Gastritis can be further classified histologically as acute or chronic based on the inflammatory cell type. No classification scheme matches perfectly with the pathophysiology; a large degree of overlap exists. Some forms of gastritis involve acid-peptic and H. pylori disease. Additionally, the term is often loosely applied to nonspecific (and often undiagnosed) abdominal discomfort and gastroenteritis.
Acute gastritis is characterized by PMN infiltration of the mucosa of the antrum and body.
Chronic gastritis implies some degree of atrophy (with loss of function of the mucosa) or metaplasia. It predominantly involves the antrum (with subsequent loss of G cells and decreased gastrin secretion) or the corpus (with loss of oxyntic glands, leading to reduced acid, pepsin, and intrinsic factor).
is gastric mucosal erosion caused by damage to mucosal defenses.
It is typically acute, presenting with bleeding, but may be subacute
or chronic with few or no symptoms. Diagnosis is by endoscopy. Treatment
is supportive, with removal of the inciting cause. Certain ICU patients
(eg, ventilator-bound, head trauma, burn, multisystem trauma) benefit from
prophylaxis with acid suppressants.
Causes of erosive gastritis include NSAIDs, alcohol, stress, and less commonly radiation, viral infection (eg, cytomegalovirus), vascular injury, and direct trauma (eg, nasogastric tubes).
Superficial erosions and punctate mucosal lesions occur. These may develop as soon as 12 h after the initial insult. Deep erosions, ulcers, and sometimes perforation may occur in severe or untreated cases. Lesions typically occur in the body, but the antrum may also be involved.
stress gastritis, a form of erosive gastritis, occurs in about 5% of critically ill patients. The incidence increases with duration of ICU stay and length of time the patient is not receiving enteral feeding. Pathogenesis likely involves hypoperfusion of the GI mucosa, resulting in impaired mucosal defenses. Patients with head injury or burns may also have increased secretion of acid.
Signs, and Diagnosis
Patients with mild erosive gastritis are often asymptomatic, although some complain of dyspepsia, nausea, or vomiting. Often, the first sign is hematemesis, melena, or blood in the nasogastric aspirate, usually within 2 to 5 days of the inciting event. Bleeding is usually mild to moderate, although it can be massive if deep ulceration is present, particularly in acute stress gastritis. Acute and chronic erosive gastritis are diagnosed endoscopically.
In severe gastritis, bleeding is managed with IV fluids and blood transfusion as needed. Endoscopic hemostasis should be attempted, with surgery (total gastrectomy) a fallback procedure. Angiography is unlikely to stop severe gastric bleeding because of the many collateral vessels supplying the stomach. Acid suppression should be started if the patient is not already receiving it.
For milder gastritis, removing the offending agent and using drugs to reduce gastric acidity (see Gastritis and Peptic Ulcer Disease: Drug Treatment of Gastric Acidity) may be all that is required.
Prophylaxis with acid-suppressive drugs can reduce the incidence of acute stress gastritis. However, it mainly benefits certain high-risk ICU patients, including those with severe burns, CNS trauma, coagulopathy, sepsis, shock, multiple trauma, mechanical ventilation for > 48 h, hepatic or renal failure, multiorgan dysfunction, and history of peptic ulcer or GI bleeding.
Prophylaxis consists of IV H2 blockers, proton pump inhibitors, or oral antacids to raise intragastric pH > 4.0. Repeated pH measurement and titration of therapy are not required. Early enteral feeding also can decrease the incidence of bleeding.
Acid suppression is not recommended for patients simply taking NSAIDs unless they have previously had an ulcer.
gastritis refers to a variety of histologic abnormalities that are
mainly the result of H. pylori infection.
Most patients are asymptomatic. Diagnosis is by endoscopy. Treatment is
eradication of H. pylori and
sometimes acid suppression.
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 (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 and intestinal.
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 performed 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 (see Gastritis and Peptic Ulcer Disease: Treatment). 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 J 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.
gastritis is gastric atrophy developing after partial or subtotal
gastrectomy (except in cases of gastrinoma).
Metaplasia of the remaining corpus mucosa is common. The degree of gastritis is usually greatest at the lines of anastomosis.
Several mechanisms are responsible: bile reflux, which is common after such surgery, damages the gastric mucosa; loss of antral gastrin decreases stimulation of parietal and peptic cells, causing atrophy; and vagotomy may result in a loss of vagal trophic action.
There are no specific symptoms of gastritis. Postgastrectomy gastritis often progresses to severe atrophy and achlorhydria. Production of intrinsic factor may cease with resultant vitamin B12 deficiency (which may be worsened by bacterial overgrowth in the afferent loop). The relative risk of gastric adenocarcinoma seems to increase 15 to 20 yr after partial gastrectomy; however, given the low absolute incidence of postgastrectomy cancer, routine endoscopic surveillance is probably not cost effective, but upper GI symptoms or anemia in such patients should prompt endoscopy.
This rare idiopathic disorder affects adults aged 30 to 60 and is more common among men. It manifests as a significant thickening of the gastric folds of the gastric body but not the antrum. Gland atrophy and marked foveolar pit hyperplasia occur, often accompanied by mucous gland metaplasia and increased mucosal thickness with little inflammation. Hypoalbuminemia (the most consistent laboratory abnormality) caused by GI protein loss may be present (protein-losing gastropathy). As the disease progresses, the secretion of acid and pepsin decreases, producing hypochlorhydria.
Symptoms are nonspecific and commonly include epigastric pain, nausea, weight loss, edema, and diarrhea. Differential diagnosis includes (1) lymphoma, in which multiple gastric ulcers may occur; (2) mucosa-associated lymphoid tissue (MALT) lymphoma, with extensive infiltration of monoclonal B lymphocytes; (3) Zollinger-Ellison syndrome with associated gastric fold hypertrophy; and (4) Cronkhite-Canada syndrome, a mucosal polypoid protein-losing syndrome associated with diarrhea. Diagnosis is made by endoscopy with deep mucosal biopsy or full-thickness laparoscopic gastric biopsy.
Various treatments have been used, including anticholinergics, antisecretory drugs, and corticosteroids, but none have proven fully effective. Partial or complete gastric resection may be necessary in cases of severe hypoalbuminemia.
Extensive infiltration of the mucosa, submucosa, and muscle layers with eosinophils often occurs in the antrum. It is usually idiopathic but may result from nematode infestation. Symptoms include nausea, vomiting, and early satiety. Diagnosis is by endoscopic biopsy of involved areas. Corticosteroids can be successful in idiopathic cases; however, if pyloric obstruction develops, surgery may be required.
tissue (MALT) lymphoma:
This rare condition is characterized by massive lymphoid infiltration of the gastric mucosa, which can resemble Ménétrier's disease.
caused by systemic disorders:
Sarcoidosis, TB, amyloidosis, and other granulomatous diseases can cause gastritis, which is seldom of primary importance.
caused by physical agents:
Radiation and ingestion of corrosives (especially acidic compounds) can cause gastritis. Exposure to > 16 Gy of radiation produces marked deep gastritis, usually involving the antrum more than the corpus. Pyloric stenosis and perforation are possible complications of radiation-induced gastritis.
Except for H. pylori infection, bacterial invasion of the stomach is rare and mainly occurs following ischemia, ingestion of corrosives, or exposure to radiation. On x‑ray, gas outlines the mucosa. The condition can present as an acute surgical abdomen and has a very high mortality rate. Surgery is often necessary.
Debilitated or immunocompromised patients may develop viral or fungal gastritis with cytomegalovirus, Candida, histoplasmosis, or mucormycosis; these diagnoses should be considered in patients with exudative gastritis, esophagitis, or duodenitis.
Last full review/revision January 2007 by Sidney Cohen, MD
Content last modified January 2007