Alimentary Tract
Gastric metaplasia and chronic inflammation at the duodenal bulb mucosa

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Abstract

Background. Chronic inflammation and gastric metaplasia are often observed in biopsy specimens from the duodenal bulb of Heliobacter pylori positive patients with duodenal ulcer disease (DU).

Aims. We set out to investigate the prevalence of these lesions and their associations with other gastric and duodenal histopathological lesions.

Patients. A total of 1255 consecutive patients who underwent upper gastrointestinal endoscopy were recruited into the present study.

Methods. Two biopsy specimens were obtained from each of the following sites: duodenal bulb, gastric antrum, gastric body, and distal to the superior duodenal angle. These specimens were stained with hematoxylin-eosin, alcian blue periodic acid Schiff (pH 2.5) and modified Giemsa (Heliobacter pylori infection was determined only by histology).

Results. The mean age of the study population was 57 years, and male:female ratio 1:1.6. Overall, 235 (19%) had gastric metaplasia and/or chronic inflammation in the duodenal bulb mucosa, and H. pylori organisms could be found in 17 (1%). In univariate analyses, gastric metaplasia and/or chronic duodenal bulb inflammation positively associated with male sex (p=0.046), Heliobacter pylori-positive chronic gastritis (p=0.033), villous atrophy of distal duodenal mucosa, i.e., coeliac disease (p<0.001), duodenal ulcer (p<0.001), and duodenal bulb deformity and scarring in endoscopy (p<0.001), but not with age (p=0.7) nor use of nonsteroidal anti-inflammatory drugs (p=0.055). Multivariate analysis revealed that independent risk factors for gastric metaplasia and chronic inflammation in duodenal bulb were duodenal Heliobacter pylori infection (odds ratio 1.6, 95% confidence interval CI 1.1–2.1), and villous atrophy of the distal duodenal mucosa (odds ratio 12.7, 95% CI 4.4–36.5), while chronic atrophic gastritis was protective against them (odds ratio 0.5, 95% CI 0.3–0.8).

Conclusions. In addition to Heliobacter pylori infection, duodenal bulb gastric metaplasia and chronic inflammation may result from predisposition to toxic dietary components in gluten-sensitive subjects.

Introduction

Gastric metaplasia—patches of gastric type mucous cells interspersed between duodenal cells—and chronic inflammation at the duodenal bulb mucosa are common findings [1]. The central role of acid and Heliobacter pylori in the development of these lesions is well known [2], [3], [4]. There are data to suggest that gastric metaplasia of the duodenum is colonized by H. pylori resulting in inflammation (duodenitis/bulbitis) [5].

Apart from H. pylori infection, data is sparse on other factors involved in the development of gastric metaplasia and chronic inflammation of the duodenal bulb. However, gastric metaplasia and duodenitis are also detected in H. pylori-negative subjects, in whom hypergastrinemia, increased acid secretion, and rapid gastric emptying may play a role in the pathogenesis of duodenal ulcer [6]. Correspondingly, different types of chronic gastritis have dissimilar influences on gastric acid secretion [7], and may thereby exert positive or negative influences on the appearance of metaplasia and inflammation in the duodenal bulb. In this study we set out to examine the prevalences and associations of duodenal bulb gastric metaplasia and chronic inflammation with other gastroduodenal lesions.

Section snippets

Patients and methods

Cases were drawn from 1562 consecutive patients sent for upper gastrointestinal endoscopy in Jyväskylä Central Hospital referral area between September 1 and December 31 1996. Those without previous peptic ulcer treatment and/or H. pylori eradication therapy, and with adequate biopsy specimens from the distal duodenum, duodenal bulb, gastric antrum, and gastric body were included in the present study population, which finally numbered 1255 patients. The demographic and clinical data (e.g. data

Results

Of the 1255 patients included in the present analysis, 492 were males and 763 females (male:female 1:1.6), mean age 57 years (95% CI 56–58 years). The mean age of the male patients was 55 years (95% CI 53–56 years), and of female patients 58 years (95% CI 57–59 years). At endoscopy, duodenal ulcer was observed in 36 (3%) patients and duodenal bulb deformity and scarring in 28 (2%). In male and female patients the prevalence of duodenal ulcer was 5% (N=22) and 2% (N=14, p=0.006), respectively,

Discussion

Duodenal gastric metaplasia, i.e., the presence of gastric-type mucus-secreting cells in the surface epithelium of the duodenum, is considered as an acquired condition resulting from gastric acid injury [10]. H. pylori infection intensifies gastrin secretion probably leading to increased duodenal acid load [11]. Duodenal gastric metaplasia is considered, however, as a nonspecific response to mucosal injury. This opinion is supported by findings that duodenal ulcer patients with and without

Conflict of interest statement

None declared.

Acknowledgements

In addition to the authors, the following investigators participated in the present study: Liisa Ahlskog-Muraja, Teuvo Antikainen, Sirpa Antila, Jorma Anttinen, Matti Hallikas, Kari-Pekka Hämäläinen, Heikki Janhonen, Matti Kairaluoma, Kerkko Karjalainen, Pekka Kauranen, Matti Kolu, Heikki Korhonen, Jari Korhonen, Ritva Koskela, Raimo Krees, Ilkka Kunnamo, Vesa Kärjä, Päivi Laaksonen, Matti Laukkanen, Reino Liisanantti, Marja Lohman, Jukka-Pekka Mecklin, Timo Mäntynen, Kyösti Nuorva, Antero

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