Gastritis: General, Erosive, and Acute


Gastritis

Gastritis is inflammation of the gastric mucosa, submucosa, or muscularis ( Fig. 33.1 ). A gastritis classification proposed in 1991 by an international convention in Sydney, Australia, has not gained support in the past two decades, reflecting the clinical confusion in this area. However, the basic pathologic entity of “inflammation in the mucosa” is considered gastritis. It may be acute or chronic, or it may result in atrophy. Each condition is associated with a clear endoscopic clinical picture.

Fig. 33.1, Gastritis and Erosive Gastritis With Acute Gastric Ulcers.

Gastritis may be chronic, may be associated with disease (e.g., Helicobacter pylori, autoimmune), or may be a progressive atrophic form. It may be associated with all forms of infectious disease (viral, bacterial, parasitic, fungal), or it may be granulomatous and associated with chronic disease (e.g., Crohn, tumors). Gastritis may be erosive (often referred to as reactive ) because of foreign agents such as aspirin, nonsteroidal antiinflammatory drugs (NSAIDs), bile reflux, alcohol, and caffeine. It may be classified as rare entities such as collagenous, lymphocytic, and eosinophilic gastritis (referred to as distinctive ). A hypertrophic form is known as Ménétrier disease, and a postgastric surgery form is known as gastritis cystica profunda. A form now appearing in patients who have had grafts or transplants is known as graft-versus-host disease, in which the stomach and other parts of the gastrointestinal (GI) tract are involved.

Recent attempts to classify gastritis according to topography, morphology, and etiology have not changed clinical practice. In the most recent consensus, gastritis was categorized into nonatrophic, atrophic, and special forms. H. pylori gastritis is classified as nonatrophic.

Clinical Picture

The clinical picture of gastritis can be specific in that patients have abdominal pain, nausea, and anorexia. Patients may report bloating or a burning discomfort in the epigastrium. In severe acute gastritis, patients may vomit and have food intolerance. In chronic gastritis, patients may have anorexia with weight loss. Many academicians believe that gastritis can exist without symptoms; therefore symptoms often will not be attributed to the mucosal inflammation. Nevertheless, if a cause such as H. pylori or an associated disease can be identified and treated, symptoms can be resolved. Gastritis is often part of another disease process.

Diagnosis

The history of onset of symptoms is important. When symptoms are acute and the gastritis is associated with infection, symptoms usually subside within days, and evaluation is unnecessary. The use of NSAIDs must be evaluated. However, when symptoms persist longer than 7 to 14 days, an investigation is necessary. The standard evaluation includes upper GI endoscopy with biopsy to determine the disease process.

When atrophy is present, a test for parietal cell antibodies is indicated. Serum gastrin levels may be elevated if atrophy is diffuse. Evaluation for vitamin B 12 is necessary.

The most common cause of gastritis is H. pylori (see Chapter 32 ). Finding the organism through endoscopy and biopsy confirms the diagnosis. When present, other organisms can be identified on biopsy, but careful histologic staining must be done to identify chronic infections, such as tuberculosis and fungi. Anisakiasis can be diagnosed on endoscopy; with the increased ingestion of raw fish, Anisakis infection should be considered in patients with an appropriate history. Other parasites also may be identified in the stomach.

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