GASTROENTEROLOGY 1996;111:1206 – 1211 Adherence of Helicobacter pylori to Areas of Incomplete Intestinal Metaplasia in the Gastric Mucosa ROBERT M. GENTA,* ,‡,§ INANC ¸ E. GU ¨ RER,* ,‡ DAVID Y. GRAHAM, ‡,x BHUVANESWARI KRISHNAN,* ANA MARIA SEGURA,* ,‡ OSCAR GUTIERREZ, Ø JONG G. KIM, # and JAMES L. BURCHETTE, Jr.** Departments of *Pathology, ‡ Medicine, § Microbiology and Immunology, and x Molecular Virology, Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas; Ø Universidad Nacional de Colombia, Bogota ´, Colombia; # Guro Hospital, Korea University College of Medicine, Seoul, Korea; and **Department of Pathology, Duke University Medical Center, Durham, North Carolina Background & Aims: Helicobacter pylori is not usually at the border between gastric and intestinalized epithe- found in areas of intestinal metaplasia. Thus, the devel- lium, as if the mucus or some other product secreted by opment of intestinal metaplasia has been viewed as a the goblet cells rendered the area utterly inhospitable for mechanism by which the stomach eliminates H. pylori. the bacteria. The aim of this study was to evaluate the frequency of The histogenesis of intestinal metaplasia is unknown. H. pylori adherence to intestinal metaplasia in different Nevertheless, the observations that H. pylori seems to populations. Methods: Mapped gastric biopsy speci- avoid metaplastic areas and that, in advanced atrophic mens from 378 H. pylori – positive subjects from various metaplastic gastritis, bacteria are frequently undetectable geographical regions were examined. Intestinal meta- despite serological evidence of infection 6 have prompted plasia was typed by staining with periodic acid – Schiff/ the teleological speculation that intestinal metaplasia alcian blue and high-iron diamine/alcian blue. Results: may represent a mechanism through which the gastric In 32 patients, H. pylori was found in intimate contact with intestinal metaplasia. This was documented by mucosa eliminates H. pylori. In truth, epidemiological electron microscopy. All areas of intestinal metaplasia studies in populations with widely diverse prevalences showing adherence contained sulfomucins and had no of atrophic gastritis do not always suggest a causal rela- brush border. Posttreatment biopsy specimens from 4 tionship between H. pylori and intestinal metaplasia. 3,7–9 patients whose infection was not cured showed persis- However, the metaphor of intestinal metaplasia as a mech- tence of H. pylori in intestinal metaplasia. Conclusions: anism for self-cure is conceptually attractive and reconciles These patients may have a strain of H. pylori with un- well with a carcinogenic role for H. pylori. It is therefore usual adhesion characteristics, or their type of intesti- not surprising that it has gained wide acceptance. nal metaplasia may have biochemical properties that Recently we developed a staining technique that make it hospitable for H. pylori. The exclusive associa- allows visualization of H. pylori while simultaneously af- tion of H. pylori adherence with incomplete intestinal fording an excellent view of the histological features of metaplasia (a putative precursor of carcinoma) and its greater frequency in Koreans (a population at risk for the gastric mucosa, including intestinal metaplasia (Fig- gastric cancer) suggest that this phenomenon may play ure 1). 10 While conducting a study designed to compare a role in the hypothetical sequence metaplasia ú dys- the histopathologic features of H. pylori gastritis in popu- plasia ú carcinoma. lations with different incidences of gastric carcinoma and peptic ulcer disease, we encountered a gastric biopsy specimen in which the gastric mucosa, entirely replaced I by intestinal-type epithelium, was lined by innumerable nfection with Helicobacter pylori is the most important cause of chronic active gastritis worldwide. One of H. pylori. The organisms were not only situated in the the possible evolutions of chronic active gastritis is the overlaying mucus, a common and insignificant finding development of atrophic gastritis, a condition almost uni- possibly caused by the displacement of mucus and bacte- versally associated with extensive intestinal metaplasia. 1 ria occurring during the endoscopic procedure;. rather, Many investigators, including ourselves, have believed they were located deep in the lumen of the metaplastic that H. pylori is not encountered in areas of intestinal foveae, intimately connected with the metaplastic epithe- metaplasia, and photomicrographs have been published to support this contention. 2–5 Figure 1 is representative Abbreviation used in this paper: DAB, 3,3-diaminobenzidinetet- of this iconography: it shows a heavily infected gastric rahydrochloride. mucosa adjacent to a segment of intestinalized epithe-  1996 by the American Gastroenterological Association 0016-5085/96/$3.00 lium with no bacteria. 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