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Acid Suppression and Gastric Atrophy: Sifting Fact

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Acid Suppression and Gastric Atrophy: Sifting Fact Gut 1998;43(suppl 1):S35–S38 S35 Acid suppression and gastric atrophy: sifting fact from fiction Gut: first published as 10.1136/gut.43.2008.S35 on 1 July 1998. Downloaded from R M Genta Summary tuted with either intestinal metaplastic epithe- Prolonged pharmacological acid suppression is lium or fibroblasts and extracellular matrix, or associated with various histological changes in a combination of the two. In such cases the the gastric mucosa, particularly in Helicobacter glands are invisible for the obvious reason that pylori infected patients. In a number of subjects they are not there—that is, they are truly “lost”. these changes include a shift in the gastric Most definitions of gastric atrophy, including inflammation from the antrum to the corpus. Whitehead’s,1 Correa’s,2 the original Sydney This finding has been interpreted as gastric System,3 and the updated Sydney System4 have atrophy, and the possibility that acid suppres- emphasised gland loss without specifying what sion accelerates the progress of lesions that may replaces the missing glands. Therefore, mucosa lead to gastric cancer has been considered. Two showing the histopathological features de- recent studies on the relation between treat- picted in figure 1B would be considered ment with proton pump inhibitors and atrophic by many observers, but not by those atrophic gastritis have yielded apparently con- who would want to know whether the missing tradictory results. These studies are reviewed in glands are really lost or just displaced by the detail here and some of the possible reasons for inflammation. Functional studies do not help the discrepant conclusions are explored. In clarify the issue: inflammation in the oxyntic particular, the way the terms “gastric atrophy” mucosa interferes with the somatostatin– and “atrophic gastritis” are used is examined gastrin axis and depresses acid production.56 critically. Of course, the destruction of oxyntic glands results in hypochlorhydria. Consequently, these two types of gland loss (one apparent and What is gastric atrophy? one real, but both with similar pathophysiologi- As seen in histological preparations, the cal consequences) have not been considered as mucosa of the normal gastric corpus consists of separate entities in studies that have looked at Departments of a layer of mucous cells invaginating into the relation between structure and function of Pathology, Medicine, shallow pits, which merge with the oxyntic http://gut.bmj.com/ and Microbiology and the gastric mucosa. In the absence of stringent Immunology, glands. The latter are separated by little or no histopathological criteria, it is hardly surprising Pathology 113, extracellular matrix in which few mononuclear that pathologists have generally failed to agree Veterans AVairs cells may be interspersed (fig 1A). When the with one another in the evaluation of atrophy.7 Medical Center and mucosa is infiltrated by inflammatory cells Baylor College of (mostly plasma cells and lymphocytes, in the Medicine, case of H pylori infection) the glands become The importance of being atrophic 2002 Holcombe Blvd, Soon after was recognised as the cause on September 29, 2021 by guest. Protected copyright. Houston, TX 77030, separated and pushed aside, and may become H pylori USA invisible, or “lost” (fig 1B). In some circum- of chronic gastritis, it became apparent that the R M Genta stances glands may be destroyed and substi- epidemiological paradigms that linked atrophic gastritis and gastric cancer could be applied to H pylori infection.8–10 Populations with a high prevalence of H pylori infection and atrophic gastritis (such as Colombia11 and Japan12)have a high incidence of gastric cancer; in contrast, populations with low prevalence of H pylori13 or low prevalence of atrophic gastritis14 15 have low a incidence of gastric cancer. Furthermore, several studies have shown quite convincingly that long-standing H pylori infection results in atrophy and intestinal metaplasia in a portion of the infected subjects.16 The association between atrophic gastritis and gastric cancer detected in pre-helicobacter studies could just as well be applied to H pylori infection: no longer gastritis, but its principal cause—H pylori—could be named as the carcinogen, and both epidemiological and bio- logical evidence became available to support this role. The former consist of a large body of data Figure 1 (A) Normal gastric corpus mucosa. Glands are tightly packed and there are few showing that infection with H pylori increases inflammatory cells in the subepithelial area and in between the glands. (B) Severe corpus gastritis with probable atrophy. Islands of glands are separated by large numbers of the cancer risk between three- and 10-fold, inflammatory cells and fibrous tissue. depending on the population studied.17 18 The S36 Genta latter include a broad variety of observations treated with omeprazole (20 to 40 mg once linking particular histopathological features of daily). The presence of H pylori was assessed at the gastric mucosa with the development of the first visit by histological evaluation in the Gut: first published as 10.1136/gut.43.2008.S35 on 1 July 1998. Downloaded from intestinal-type adenocarcinoma.9 19–21 These fundoplication group and by histological and histopathological features include alterations of serological evaluation in the omeprazole group; the mucosal architecture, loss of glands, fibro- however, none of the patients was treated for H sis, and replacement of epithelial elements by pylori infection. In both cohorts, the patients an intestinal-type metaplastic epithelium (“in- were followed for three to eight years; all testinal metaplasia”). The constellation of patients underwent a gastroscopy at the begin- these features has been variously called ning of the study as well as repeated gastro- “atrophic gastritis” and “gastric atrophy,” but scopies during the follow up period. At each these terms remain poorly defined and, conse- gastroscopy biopsy specimens were obtained quently, loosely used.22 The same lack of from the gastric corpus for blinded histological agreement that exists on the definition of atro- evaluation. The histological examination in- phy also exists about the concept of atrophic cluded the semi-quantitative evaluation of the gastritis. What is atrophic gastritis? What is the features of H pylori gastritis according to the atrophic gastritis considered a precursor of Sydney System.3 The criteria used by the gastric cancer? The classic studies that defined authors for the diagnosis of atrophic gastritis atrophic gastritis (also called “multifocal were not stated. However, they did state that atrophic gastritis”) were performed on gastrec- among the patients treated with fundoplica- tomy specimens. With the entire stomach tion, atrophic gastritis did not develop in any of available for examination it was possible to see the 31 who were infected with H pylori at base- large patches of atrophic and metaplastic line or the 41 who were not infected. Among epithelium extending proximally and distally the patients treated with omeprazole, none of along the lesser curvature. The extension of whom had atrophic gastritis at baseline, these patches was so obvious that there atrophic gastritis developed in 18 of the 59 appeared to be no need for a strict topographi- infected with H pylori and two of the 46 who cal definition. In the past two decades, were not infected. None of the patients in however, eVective antacid therapies and treat- either group developed intestinal metaplasia. ment for H pylori have greatly reduced the need Based on these observations, the authors for gastrectomy and, consequently, the avail- concluded that patients with reflux oesophagi- ability of resected stomachs for histopathologi- tis and H pylori infection who are treated with cal examination. The diagnosis of atrophic gas- omeprazole are at increased risk of atrophic tritis must now be made based on the gastritis. examination of a limited number of biopsy specimens that, even in the most audacious The Swedish study sampling protocols,23 still represent only a In this study, patients with chronic gastro- http://gut.bmj.com/ minimal portion of the gastric mucosa. When oesophageal reflux were initially treated with only two or three samples from the stomach are 20–40 mg/day omeprazole for <4 months to available for examination it may be imprudent control symptoms and heal the oesophagitis.25 to make a diagnostic statement which has Patients who had symptom relief were then much broader topographical implications, such randomised and allocated to either omeprazole as “multifocal atrophic gastritis.” Although it is maintenance therapy or antireflux surgery very diYcult to produce an accurate topo- without vagotomy. All patients underwent gas- on September 29, 2021 by guest. Protected copyright. graphical definition of atrophic gastritis (the troscopy at the beginning of the study as well as multifocal type associated with chronic H pylori during the follow up period, which lasted infection, unknown environmental factors, and approximately 3.5 years. At each endoscopy, gastric cancer), the best approximation can multiple mucosal biopsy specimens were ob- only result from studies involving the observa- tained from the gastric corpus according to a tion of multiple mapped biopsy samples. If pre-determined protocol. The biopsy speci- such a definition is generated, tested, and mens were then examined blindly by a single found to be satisfactory, it should then be dis- pathologist, who
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