Supplement Abstracts Submitted for the 70th Annual Scientific Meeting of the American College of Gastroenterology: ESOPHAGUS
Purpose: The etiology and significance of cardiac intestinal metaplasia (CIM) is disputed. CIM may represent a form of Barrett's esophagus (BE) due to reflux or could reflect generalized gastric intestinal metaplasia (GIM) due to H. pylori. The aim of this study was to utilize gene expression data to compare CIM to BE and GIM.
Methods: Biopsies were first classified by endoscopic and histologic criteria as CIM (n = 40), BE (n = 26), or GIM (n = 23). The squamocolumnar and gastroesophageal junctions were aligned in CIM patients. H. pylori status was tested in antral biopsies of all patients. After laser-capture microdissection, quantitative RT-PCR was used to measure the expression of a panel of 9 genes that has been shown to differentiate BE from other foregut mucosa (Cox2, Cdx1, Cdx2, VEGF, TSP1, Survivin, TIMP1, Bcl2, CTNNB1). Next, cluster analysis using linear discriminant analysis of logged expression data was used to classify samples into groups based solely on similarity of gene expression. Cluster analysis was performed for 3 groups (CIM vs BE vs GIM) and 2 groups (CIM+BE vs GIM).
Results: Median BE length was 4.5 cm. There was no difference in H. pylori infection among groups (p = 0.68). Three group clustering had a misclassification rate of 0.39 (p = 0.001); most errors occurred between CIM and BE (Table 1). Two group clustering had a misclassification rate of 0.18 (p<0.001) (Table 2):[figure 1]
Conclusions: The gene expression profiles of CIM and BE were similar in 91% of patients and differed significantly from that of GIM. Those with misclassification of CIM as GIM may have an alternate etiology such as H. pylori. The similar gene expression profile of CIM and BE suggests a shared reflux etiology in the majority of patients and calls into question the perception that CIM is an innocuous process.© The American College of Gastroenterology 2005. All Rights Reserved.