Intestinal metaplasia developsinbothformsofchronicgastritisandisariskfactorfordevelopmentofgastricdysplasiaandadenocarcinoma.
PepticulcerdiseasecanbecausedbyH. pylori chronicgastritisandtheresultanthyperchlorhydriaorNSAIDuse.Ulcerscandevelopinthestomachorduodenumandusuallyhealaftersuppressionofgastricacidproduction,discontinuationofNSAIDuse,or,ifpresent,H. pylori eradication.
Polyps are nodules or masses that project above the level of the surrounding mucosa. They are identified in up to 5% of upper gastrointestinal tract endoscopies. Polyps may develop as a result of epithelial or stromal cell hyperplasia, inflammation, ectopia, or neoplasia. Although many different types of polyps can occur in the stomach, only hyper-plastic and inflammatory polyps, fundic gland polyps, and adenomas are considered here.
Up to 75% of all gastric polyps are inflammatory or hyperplastic polyps. In the stomach, inflammatory and hyperplastic polyps represent opposite ends of the morphologic spectrum of a single entity; the distinction is based solely on the degree of inflammation. They most commonly affect individuals between 50 and 60 years of age, usually arising in a background of chronic gastritis that initiates the injury and reactive hyperplasia that cause polyp growth. If associated with H. pylori gastritis, polyps may regress after bacterial eradication.
The frequency with which dysplasia, a precancerous in situ lesion, develops in these polyps correlates with size; there is a significant increase in risk with polyps larger than 1.5 cm.
Fundic gland polyps occur sporadically and in individuals with familial adenomatous polyposis (FAP) Polyps associated with FAP (but not sporadic) may show dysplasia, but they almost never progress to become malignant. The incidence of sporadic lesions has increased markedly as a result of the widespread use of proton pump inhibitors. This likely results from increased gastrin secretion, in response to reduced acidity, and glandular hyperplasia driven by gastrin. Fundic gland polyps are nearly always asymptomatic, and are usually an incidental finding. These well-circumscribed polyps occur in the gastric body and fundus, often are multiple, and are composed of cystically dilated, irregular glands lined by flattened parietal and chief cells.
Gastric adenomas represent up to 10% of all gastric polyps. Their incidence increases with age and varies among different populations in parallel with that of gastric adenocarcinoma. Patients usually are between 50 and 60 years of age, and males are affected three times more often than females. Adenomas almost always occur on a background of chronic gastritis with atrophy and intestinal metaplasia. All gastrointestinal adenomas exhibit epithelial dysplasia, which can be classified as low-or high-grade. The risk for development of adenocarcinoma in gastric adenomas is related to the size of the lesion and is particularly elevated with lesions greater than 2 cm in diameter. Overall, the malignant potential of gastric adenomas is far greater than that of their colonic counterparts. Carcinoma may be present in up to 30% of gastric adenomas.
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Adenocarcinoma is the most common malignancy of the stomach, comprising more than 90% of all gastric cancers. Early symptoms resemble those of chronic gastritis, including dyspepsia, dysphagia, and nausea. As a result, the cancer is often diagnosed at advanced stages when clinical manifestations such as weight loss, anorexia, altered bowel habits, anemia, and hemorrhage trigger diagnostic evaluation.