Castritis represents a nonspecific inflammation of the stomach. Clinically, the three most common and important causes of gastritis are infection with the bacteria Helicobacter pylori, ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs), and stress-related mucosal changes.

Helicobacter pylori H. pylori is a gram-negative, curved, flagellated rod found only in gastric epithelium or in gastric metaplastic epithelium. H. pylori clearly causes histo-logic gastritis and is found in 80% to 95% of patients with duodenal ulcers and 70 % to 90 % of patients with gastric ul-cers. However, only a minority of patients with H. pylori gas-tritis develop peptic ulcer disease or gastric cancer. There is a clear age-related prevalence of H. pylori infection in healthy subjects, increasing from 10 % in those younger than age 30 to 60% in subjects older than age 60 in the Western world. The majority are infected early in life, although the mode of trans. mission remains unknown. H. pylori colonization is more com-mon in blacks, individuals in lower socioeconomic classes, and inhabitants of custodial institutions. In the developing world, infection is far more common, with over 80% of the popula-tion infected by age 20. Infection with H. pylori typically is lifelong unless treated.

H. pylori is a noninvasive organism that colonizes the mu-cus layer overlying gastric epithelium. Factors important in the organism's ability to colonize the stomach include its flagellae, which facilitate locomotion, ability to adhere to the mucus lay-er, and production of urease. Urease increases juxtamucosal pH, creating a more hospitable microclimate than that of the acidic stomach. Colonization causes acute and chronic inflam-mation consisting of neutrophils, plasma cells, T cells, and macrophages accompanied by varying degrees of epithelial cell injury, all of which resolve after treatment.

The ultimate clinical outcome of infection depends on a complex interplay between virulence factors of the organism, the host response, environmental factors, and age at the time of infection. It is now clear that there are many different strains of H. pylori with different virulence factors. Two such virulence factors are the vacA and cagA genes. The vacA gene encodes a vacuolating cytotoxin that directly damages epithelial cells and is more common in patients with peptic ulcer disease. There is a strong association between production of the vacuo-lating cytotoxin and presence of the cagA gene, both of which are more common in patients with peptic ulcer disease. The most common endpoint of H. pylori infection is chronic super-ficial gastritis, which may persist for years. Duodenal and gas-tric ulcers develop in the minority of infected patients. Atroph-ic gastritis is another end result of infection that may increase the risk of gastric cancer. Finally, the mucosal lymphocytic response to H. pylori infection may lead to a monoclonal B cell proliferation in mucosa-associated lymphoid tissue (MALT) lymphoma.

Nonsteroidal Anti-inflammatory Drugs The NSAIDs are among the most widely used classes of drugs. There is a clear relationship between ingestion of NSAIDs and injury to the gastrointestinal tract. Two types of mucosal injury are caused by NSAIDs. The first form develops after acute inges-tion and is related to direct topical injury to mucosal cells. A-cute ingestion of aspirin enhances mucosal permeability by low-ering the mucosal potential difference and enhancing back-dif-fusion of hydrogen ions. Hyperemia, subepithelial hemor-rhage, and superficial erosions are seen endoscopically, al-though these lesions are typically asymptomatic. Microscopi-cally, there is a "reactive" pattern of injury characterized by little or no increase in inflammatory cells, With longer term NSAID use, these lesions disappear and frank ulceration may develop. Chronic NSAID ingestion results in inhibition of gas-troduodenal mucosal prostaglandin synthesis caused by inhibi-tion of the enzyme eyclooxygenase, and hence a decrease in mucus and bicarbonate production and mucosal blood flow.

Stress-Related Gastric Mucosal Damage Whereas mu-cosal damage develops in the majority of critically ill patients, there is a low incidence of clinically significant upper gastroin-testinal bleeding. The etiology of stress-related mucosal injury is multifactorial. Mucosal ischemia caused by decreased blood flow (from shock, hypotension, or catecholamine release) im-pairs mucosal resistance to acid back-diffusion, Hyperemia of the mucosa evolves into erosions and then frank ulceration in the stomach and duodenum, which may go on to bleed.

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