GASTRITIS



Gastritis does not represent, strictly speaking, an acid-peptic group of diseases, but it will be discussed here for convenience, since it does re­flect a breakdown in the interaction of injurious agents and mucosal defense mechanisms. Gastri­tis can be acute or chronic, specific or nonspecific.

Acute Gastritis. In acute gastritis there is infil­tration of the lamina propria by inflammatory cells, often accompanied by superficial erosions that may be diffuse or localized. The mechanism of the mucosal injury is often unclear. Certain drugs, especially aspirin, nonsteroidal anti-in­flammatory agents, and ethanol, are thought to disrupt the mucosal barrier to back-diffusion of acid and thereby to initiate chemical injury. “Stress ulcers” represent acute erosive injury to the stomach in many severe surgical or medical conditions with complicating bleeding. Stress ul­cers are thought to result from ischemia, but again back-diffusion of acid may be the common final pathway of injury. Gastritis can sometimes be at­tributed’ to specific events such as irradiation, ingestion of alkali, or rarely bacteria] infection (phlegmonous gastritis). Following surgery, reflux of bile salts and/or pancreatic enzymes mav pro­duce acute gastritis.

Most cases of acute gastritis are probably mild and escape diagnosis. The diagnosis is established by endoscopic examination. When present, symp­toms are usually those of dyspepsia, epigastric pain, nausea, and vomiting. The most important complication of acute gastritis is that of bleeding from the superficial erosions. This usually re­sponds to conservative management and omission of the precipitating agent if known (aspirin, al­cohol). Antacids and/or cimetidine or ranitidine is often used as well but has not been shown to affect healing. The overall prognosis of acute, ero-•sive gastritis is excellent with rapid healing of the lesions within days.
Chronic Gastritis. Chronic gastritis has been classified by the histological severity of the pro­cess (superficial, atrophic, or gastric atrophy) and by the anatomical location in the stomach where it is most manifest (Type Afundus and body of the stomach; Type B—antrum). In most patients no pathogenesis can be firmly established, al­though chronic use of the same drugs implicated in acute gastritis and chronic exposure to bile salts and pancreatic enzymes are postulated to be of importance in some patients. In Type A atrophic gastritis there are usually circulating antibodies against parietal cells whether or not pernicious anemia is present; in some patients with Type B atrophic gastritis antibodies against gastrin-pro-ducing cells have been reported.

There are no definite clinical manifestations of idiopathic chronic gastritis. Patients with Type A gastritis may have pernicious anemia alone or linked with one or more other autoimmune dis­eases. Chronic gastritis may be associated with a higher incidence of benign gastric ulcer and gas­tric cancer. No specific treatment is indicated for idiopathic chronic gastritis.