Complete and incomplete intestinal metaplasia at the oesophagogastric junction: prevalences and associations with endoscopic erosive oesophagitis andgastritis

Background/Aims-Intestinal metaplasia (IM) is a common finding at the oesop hagogastric junction, but the aetiopathogenesis of the different IM subtype s-that is, incomplete IA I (specialised columnar epithelium, SCE) and compl ete IM- and their associations with gastrooesophageal reflux disease and He licobacter pylori gastritis are unclear. Methods-1058 consecutive dyspeptic patients undergoing gastroscopy were enr olled. The gastric, oesophagogastric junctional, and oesophageal biopsy spe cimens obtained were stained with haematoxylin and eosin, alcian blue (pH 2 .5)-periodic acid Schiff, and modified Giemsa. Results-Complete junctional IM was detected in 196 (19%) of the 1058 subjec ts, and in 134 (13%) was the sole IM subtype. Incomplete junctional IM. (SC E) was detected in 101 (10%) subjects, of whom 62 (61%) also had the comple te IM subtype. Of patients with normal gastric histology (n = 426), 6% had complete IM and 7% junctional SCE. The prevalence of both types of IM incre ased with age in patients with either normal gastric histology or chronic g astritis (n = 611). Epithelial dysplasia was not detected in any patients w ith junctional IM. In multivariate analysis, independent risk factors for i ncomplete junctional INT were age (odds ratio (OR) 1.3 per decade, 95% conf idence interval (CI) 1.2 to 1.6), endoscopic erosive oesophagitis (OR 1.9, 95% CI 1.1 to 3.2), and chronic cardia inflammation (OR 2.9, 95% CI 1.3 to 6.2), but not gastric H pylori infection (OR 1.0, 95% CI 0.6 to 1.7). In un ivariate analysis, junctional incomplete IM was not associated with cardia H pylori infection. Independent risk factors for "pure" complete junctional IM (n = 134) were age (OR 1.2 per decade, 95% CI 1.0 to 1.4), antral predo minant non-atrophic gastritis (OR 2.6, 95% CI 1.3 to 5.2), antral predomina nt atrophic gastritis (OR 2.1, 95% CI 1.1 to 5.2), and multifocal atrophic gastritis (OR 7.1, 95% CI 2.5 to 19.8), In univariate analysis, junctional complete IM was strongly associated with chronic cardia inflammation and ca rdia H pylori infection (p<0.001). Conclusions-Both complete and incomplete junctional IR I are independent ac quired lesions that increase in prevalence with age. Although Im subtypes o ften occur simultaneously, they show remarkable differences in their associ ations with gastritis and erosive oesophagitis: junctional complete IM is a manifestation of multifocal atrophic gastritis, while the incomplete form (SCE) may result from carditis and gastro-oesophageal reflux disease. The f requency of dysplasia in intestinal metaplasia at the oesophagogastric junc tion appears to be low.