Pathology of Gastric Intestinal Metaplasia: Clinical Implications


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IntroductionIntestinal metaplasia (IM) of the gastric mucosa is a relatively frequent precancerous lesion (1). The inclusion of IM in a gastric biopsy pathology report often creates uncertainty for the gastroenterologist about the appropriate management. Although the risk of gastric cancer is increased in the presence of IM, the overall risk of gastric cancer in a patient with IM is extremely low compared with the risk of adenocarcinoma in a patient with Barrett's esophagus (BE)(2). Although the incidence of gastric cancer is high in certain regions, such as Asia and Latin America, it is much lower in the United States and other Western countries, making it difficult to justify broad surveillance programs. The aims of this article are (i) to assist the clinician in identifying subgroups of patients with IM at increased risk for gastric cancer and (ii) to propose an algorithm for gastric IM management, considering the lack of universally accepted guidelines that can be applied to any population.Intestinal metaplasia of the gastric cardiaThe gastric cardia is a poorly defined region whose anatomy and pathology are a subject of controversy. The cardiac mucosa, located immediately distal to the squamocolumnar junction (Z line) and proximal to the oxyntic mucosa, consists of columnar epithelium on the surface and mucous glands with morphology similar to that of the antrum. The diagnosis and management of IM of the gastric cardia are especially challenging in Western affluent societies because of the increasing incidence of adenocarcinoma of the cardia and lower esophagus (3,4) and its precursors, gastroesophageal reflux and BE. Carcinomas arising in the cardia or the lower esophagus tend to involve the gastroesophageal junction, making it often difficult to determine the site of origin of the tumor.Esophageal adenocarcinoma has been causally related to gastroesophageal reflux. The risk factors for adenocarcinoma of the cardia are less well defined. A dual etiology, linking some tumors to Helicobacter pylori infection and others to reflux injury, is favored (5,6). IM of the cardia and BE differ in their risk for malignant transformation, and there are different implications for patient management (3). It is therefore important to distinguish between the two entities in biopsies from the gastroesophageal junction area. Several histopathology features have been found to be of special value (7). The presence of overlying squamous epithelium, esophageal gland ducts, and hybrid glands is seen exclusively in BE. IM of the incomplete type and multilayered epithelium also favor BE (7). However, in some cases the histology of BE and cardia IM is identical, and it is the endoscopic location of the biopsy that determines whether the patient is more likely to have BE rather than cardia IM.Distal (noncardia) IMAlthough the incidence of distal gastric cancer has decreased steadily in Westernized countries over the past century, this disease is still the second leading cause of cancer deaths worldwide (8). The International Agency for Research on Cancer categorized H. pylori infection as a type I carcinogen (9), and it is considered the primary cause of gastric cancer. The infection induces a chronic inflammatory process in the gastric mucosa. Over time, atrophy and IM may develop (10,11). IM is frequently identified in distal gastric biopsies, especially in populations at high risk for gastric cancer, such as those of eastern Asia, eastern Europe, and Andean Latin America. In the United States, the majority of the population is at low risk for gastric cancer, but there are several ethnic populations at high cancer risk, such as African Americans, Native Americans, and immigrants from Asia and Latin America (12,13).

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