Results

The study population consisted of 1058 patients (mean age 57.3 years, 95% CI 56.3 to 58.3 and male to female ratio 1:1.5), of whom 134 (13%) had complete IM and 39 (4%) incomplete IM (SCE) as the sole type of IM at the oesophagogastric junction. The mean age of the “pure” complete IM group was 65.0 (95% CI 62.5 to 67.4) years and that of the “pure” incomplete IM group 62.9 (95% CI 58.5 to 67.3) years. A total of 62 patients harboured both types of IM simultaneously, giving overall prevalence for complete IM of 19% (n = 196), and for incomplete IM or SCE of 10% (n = 101). Henceforth patients with complete IM denotes the patients with this type of IM only (n = 134), whereas the incomplete IM or SCE group refers to patients with SCE only plus those with complete IM as well as SCE (n = 101).

The patients with complete or incomplete IM were older than those without either lesion (table 1, both patients with chronic gastritis and normal stomach included). In subjects with normal stomach, the mean age of the non-IM-non-SCE group was 50.8 (95% CI 48.4 to 53.2) years, that of the junctional complete IM group 62.4 (95% CI 56.3 to 68.5) years, (p = 0.001), and that of the junctional SCE group 54.0 (95% CI 46.3 to 61.7) years (p = 0.003). The difference in mean age between the complete IM and SCE group was insignificant (p = 0.1). Both types of junctional IM correlated with age in patients with normal gastric histology or with chronic gastritis (fig 2). The sex ratios of patients with either type of junctional IM were not significantly different from that of the control group. In patients with multifocal atrophic gastritis, complete junctional IM was significantly more common than incomplete junctional IM (table 2). On the other hand, in patients with histologically normal stomach, junctional incomplete IM was more common than complete IM, although the difference did not reach statistical significance (table 2). Junctional epithelial dysplasia was not observed in any patient with complete or incomplete junctional IM.

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Figure 2

Prevalences of junctional complete and incomplete (specialised columnar epithelium, SCE) intestinal metaplasia (IM) in different age groups. NH, normal gastric histology (n = 426); CG, chronic gastritis (n = 632). The correlation of age with both IM types was significant in the CG (p<0.001 for complete IM and incomplete IM) and NH (p = 0.001 for complete IM and p = 0.002 for incomplete IM) group.

Reflux symptoms, smoking habits, or the use of non-steroidal anti-inflammatory drugs did not correlate with the presence of either type of IM (table 1). Hiatal hernia or histological oesophagitis did not predict the presence of junctional IM of either type.

Multivariate analysis showed that age, antral predominant non-atrophic gastritis, antral predominant atrophic, and multifocal atrophic gastritis were independent risk factors for “pure” complete junctional IM (table 3). Independent risk factors for junctional SCE were age, endoscopic erosive oesophagitis, and chronic cardia inflammation (“carditis”) (table 3).

Discussion

This study showed complete and incomplete IM to be common findings at the oesophagogastric junction in a consecutive series of dyspeptic patients: almost a quarter of our study population had either or both forms of the lesion. Previously reported prevalence rates varied from 5.3 to 36%.2-4 ,6 ,21 ,22 The width of this range may be due to patient selection or to different methods of biopsy sampling or staining for histology. Haematoxylin-eosin stain yields lower IM rates than the simultaneous application of alcian blue(pH 2.5)-periodic acid Schiff, which also enables differentiation between complete and incomplete IM.6 ,19 ,20 ,23

The prevalence of junctional complete IM and SCE at the oesophagogastric junction increased with age, and both IM subtypes were also found in patients without concomitant gastritis, indicating that junctional IM and SCE are acquired local lesions. Complete IM and SCE seemed to occur in men and women at similar frequencies, contrasting with Barrett’s oesophagus and oesophagogastric junctional adenocarcinomas which are strongly male predominant diseases.12 ,24 ,25

An important finding was that, in multivariate analysis, endoscopic erosive oesophagitis, but not H pyloriinfection or antral predominant gastritis, was an independent risk factor for junctional SCE. In contrast, complete junctional IM was associated with gastritis, and particularly with multifocal atrophic gastritis, but not with endoscopic erosive oesophagitis. These observations suggest that at least some subjects with junctional SCE suffer this lesion as a consequence of gastro-oesophageal reflux disease, while complete junctional IM is a manifestation of multifocal atrophic gastritis and H pylori infection. However, in patients with normal stomach, complete junctional IM may result from gastro-oesophageal reflux disease, because this IM subtype was detected in 6% of this subgroup.

In the stomach, IM represents a sequence of progressive lesions from complete (type I or “small bowel type IM”) to incomplete (types II and III or “colonic type IM”) IM.26 ,27 This may also be the case with IM at the oesophagogastric junction. However, this hypothesis was not supported by the finding that junctional complete IM and SCE were detected at a similar age in subjects with normal gastric histology. Proper and correct analysis of the background factors for junctional IM subtypes is difficult because obviously there are varying degrees of overlap with regard to the pathogenic factors for junctional complete IM and SCE.

The present findings suggest important clinical and practical conclusions on junctional SCE: the presence of SCE at the oesophagogastric junction in subjects with a normal stomach—that is, histologically normal antral and gastric corpus mucosa—may predict gastro-oesophageal reflux disease with high certainty. This could also apply to junctional SCE patients with chronic gastritis. The presence of complete junctional IM may not indicate reflux, but is a manifestation of multifocal atrophic gastritis. These conclusions are concordant with an earlier study indicating that junctional SCE is related to gastro-oesophageal reflux disease detected by 24 hour oesophageal pH monitoring.28

In this study, none of the patients with junctional IM showed dysplasia, which accords with an earlier report.5Dysplasia is quite a common finding at Barrett’s epithelium and precedes the appearance of adenocarcinoma.12 This may also be the case in the adenocarcinomas of the oesophagogastric junction, which are on the increase in many western countries.24 ,25 ,29 The low rate of dysplasias in junctional IM suggests that neither junctional SCE nor complete IM are as high risk carcinoma precursor lesions as Barrett’s oesophagus is for oesophageal adenocarcinoma. On the other hand, junctional complete IM and SCE are common lesions, and the absence of dysplasia in a limited number of patients does not exclude the possibility that junctional SCE or complete IM could progress to dysplasia and carcinoma in some patients.

In conclusion, this study indicates that complete and incomplete IM at the oesophagogastric junction are common acquired lesions. They may not be directly related to Barrett’s oesophagus or junctional adenocarcinomas because of the differences in their basic demographics. It seems that incomplete junctional IM (SCE) and complete IM are dissimilar lesions in terms of their pathogenesis: the former seems to be a consequence of gastro-oesophageal reflux disease and the latter a manifestation of multifocal atrophic gastritis.