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DOI: 10.1055/a-1313-7239
Gastric metaplasia of the duodenal mucosa in Crohn’s disease: novel histological and endoscopic findings
Abstract
Background and study aims Upper gastrointestinal endoscopy and biopsy are useful for differential diagnosis of Crohn’s disease (CD) of the large intestine and ulcerative colitis (UC). We aimed to identify novel histopathological and endoscopic findings in the upper gastrointestinal tract in patients with CD who did not have Helicobacter pylori infection.
Patients and methods Upper gastrointestinal endoscopy was performed on patients with CD and UC. Mucosal lesions detected were subsequently observed using magnifying endoscopy with narrow-band imaging (M-NBI), following which biopsy was performed. When no mucosal lesion was detected on conventional endoscopy, M-NBI and biopsy were performed on four sites: the gastric body, gastric antrum, duodenal bulb, and second portion of the duodenum.
Results The prevalences of gastric metaplasia (GM) were 48 % (24/50) and 16 % (8/50) in the CD and UC groups, showing a significant difference (P = 0.001). In 23 of 24 patients with histologically proven GM in the CD group, mucosal lesions were detected using conventional white-light imaging (C-WLI). In 22 of 24 patients with histologically proven GM in the CD group, disappearance of normal villous structure and the presence of curved marginal crypt epithelium were noted using magnifying endoscopic findings characteristic of GM (M-GM). A combination of C-WLI and M-NBI yielded a significantly increased specificity (P = 0.004) and accuracy (P = 0.039).
Conclusions The prevalence of GM in the duodenal mucosa was significantly higher in patients with CD than in controls. The identified endoscopic findings may be useful as novel indicators for the histological diagnosis of GM in the duodenum.
Publication History
Received: 01 July 2020
Accepted: 08 October 2020
Article published online:
25 January 2021
© 2021. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commecial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)
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References
- 1 Yao T, Iwashita A. Upper gastrointestinal involvements of Crohn’s disease. Stomach Intest (Tokyo) 1983; 18: 1323-1334 (in Japanese, with English abstract)
- 2 Yokota K, Saito Y, Einami K. et al. bamboo joint-like appearance of the gastric body and cardia: possible association with Crohn’s disease. Gastrointest Endosc 1997; 46: 268-272
- 3 Sakatani A, Fujiya M, Kashima S. et al. Upper-gastrointestinal Lesions in Patients with Inflammatory Bowel Diseases. Stomach Intest (Tokyo) 2013; 48: 636-644 (in Japanese, with English abstract)
- 4 Yoshiki N, Kentaro M, Mikihiro F. et al. The endoscopic findings of the upper gastrointestinal tract in patients with Crohn's disease. Clin J Gastoroenterol 2017; 10: 289-296
- 5 Iwashita A, Yamada Y, Yao T. et al. Pathology for Crohn’s disease. Stomach Intest (Tokyo) 1997; 32: 365-376 (in Japanese, with English abstract)
- 6 Oberhuber G. Focally enhanced gastritis: A frequent type gastritis in patients with Crohn’s disease. Gastroenterology 1997; 112: 698-706
- 7 Akemoto Y, Sakuraba H, Tanaka M. et al. Gastric focal neutrophil infiltration and wide duodenal gastric foveolar metaplasia are histologic discriminative markers for Crohn’s disease and Behcet’s disease. Digestion 2019; 100: 210-219
- 8 Kimura K, Takemoto T. An endoscopic recognition of the atrophic border and its significance in chronic gastritis. Endoscopy 1969; 1: 87-97
- 9 Saskaki N, Momma K, Egawa N. et al. The influence of Helicobacter pylori infection on the progression of gastric mucosal atrophy and occurrence of gastric cancer. Eur J Gastroenterol Hepatol (Suppl l) 1995; S59-62
- 10 Oken MM, Creec RH. et al. Toxicity and response criteria Of The Eastern Cooperative Oncology Group. Am J Clin Oncol 1982; 5: 649-655
- 11 Gormally SM, Kierce BM, Daly LE. et al. Gastric metaplasia and duodenal ulcer disease in children infected by Helicobacter pylori. Gut 1996; 38: 513-517
- 12 Voutilanen M, Juhola M, Farkkila M. et al. Gastric metaplasia and chronic inflammation at the duodenal bulb mucosa. DigestLiver Dis 2003; 35: 94-98
- 13 Landis JR, Koch GG. The measurement of observer agreement for categorical data. Biometrics 1977; 33: 159-174
- 14 Shirai T. The pathogenetic role of gastric metaplasia and Helicobacter Pylori duodenal ulcer. Gastroenterol Endosc 1991; 33: 2177-2182 (in Japanese, with English abstract)
- 15 Nakai H, koizumi I, Saionnji K. Relation to the background gastric mucosa and Helicobacter pylori infections. Gastroenterol Endosc 1995; 37: 529-539 (in Japanese, with English abstract)
- 16 De Matos V, Russo PA, Cohen AB. et al. Frequency and clinical correlations of granulomas in children with Crohn’s disease. J Pediatr Gastroenterol Nutr 2008; 46: 392-398
- 17 Rubio CA, Orrego A, Nesi G. et al. Frequency of epithelioid granulomas in colonoscopic biopsy specimens from paediatric and adult patients with Crohn’s colitis. J Clin Pathol 2007; 60: 1268-1272
- 18 Mutoh H, Hakamata Y, Sato K. et al. Conversion of gastric mucosa to intestinal metaplasia in Cdx2-expressing transgenic mice. Biochem Biophys Res Commun 2002; 294: 470-479
- 19 Rita AB, Alex B. Intestinal metaplasia: A premalignant lesion involved in gastric carcinogenesis. J Gastroenterol Hepatol 2009; 24: 193-201
- 20 Yao K, Doyama H, Gotoda T. et al. Diagnostic performance and limitations of magnifying narrow-band imaging in screening endoscopy of early gastric cancer: a prospective multicenter feasibility study. Gastric Cancer 2014; 17: 669-679