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Chapter 10 - Histology of Gastroesophageal Reflux Disease and Barrett’s Oesophagus

Published online by Cambridge University Press:  06 June 2020

By
Naziheh Assarzadegan  and
Maryam Kherad Pezhouh
Edited by
Roger M. Feakins
Roger M. Feakins
Affiliation:
Royal Free London NHS Foundation Trust, London, UK
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Summary

The upper gastrointestinal tract consists of oesophagus, stomach, and duodenum. These are distinct from one another histologically. The lining of the oesophagus consists mainly of non-keratinising stratified squamous epithelium, and there is a variable amount of columnar epithelium distally. The stomach has three main histological regions, which from proximal to distal are the cardia, the body/fundus, and the antrum. All of these regions include surface epithelial cells that extend downwards into foveolae. Beneath the foveolae are a short isthmic zone and a deeper glandular layer. In the body/fundus, the glandular layer is thicker and the glands are more closely packed than in the antrum. Parietal cells and chief cells are the main component of the body/fundus glands while in the antrum they are sparse. The gastric cardia is a short segment that usually lacks parietal and chief cells. In the normal state, columnar mucosa extends from the stomach upwards into the distal oesophagus for a variable length. In contrast, Barrett’s oesophagus is pathological replacement of the distal oesophageal mucosa by metaplastic columnar mucosa that may be gastric or intestinal. The duodenal mucosa includes villi and crypts, both lined by columnar absorptive cells. Other epithelial cell types include goblet cells and Paneth cells. Endocrine cells are present at all sites but are difficult to identify and sparse in the oesophagus.

Keywords

histologyanatomyoesophagusgastro-oesophageal junctionstomachduodenumepitheliuminflammatory cell
Type
Chapter
Information
Non-Neoplastic Pathology of the Gastrointestinal Tract
A Practical Guide to Biopsy Diagnosis
 , pp. 157 - 168
Publisher: Cambridge University Press
Print publication year: 2020

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References

Badillo, R, Francis, D. Diagnosis and treatment of gastroesophageal reflux disease. World J Gastrointest Pharmacol Ther. 2014;5(3):105–12.Google Scholar
Wilson, JL, Pruett, KL. Gastroesophageal reflux disease: treating wisely. N C Med J. 2016;77(3):202–5.Google ScholarPubMed
Nwokediuko, SC. Current trends in the management of gastroesophageal reflux disease: a review. ISRN Gastroenterol. 2012;2012:391631.CrossRefGoogle ScholarPubMed
Booth, CL, Thompson, KS. Barrett’s esophagus: a review of diagnostic criteria, clinical surveillance practices and new developments. J Gastrointest Oncol. 2012;3(3):232–42.Google ScholarPubMed
Fitzgerald, RC, di Pietro, M, Ragunath, K, et al. British Society of Gastroenterology guidelines on the diagnosis and management of Barrett’s oesophagus. Gut. 2014;63(1):7–42.Google Scholar
Ismail-Beigi, F, Horton, PF, Pope, CE, 2nd. Histological consequences of gastroesophageal reflux in man. Gastroenterology. 1970;58(2):163–74.CrossRefGoogle ScholarPubMed
Fiocca, R, Mastracci, L, Riddell, R, et al. Development of consensus guidelines for the histologic recognition of microscopic esophagitis in patients with gastroesophageal reflux disease: the Esohisto project. Hum Pathol. 2010;41(2):223–31.CrossRefGoogle ScholarPubMed
Martin, IW, Atkinson, AE, Liu, X, Suriawinata, AA, Lefferts, JA, Lisovsky, M. Mucosal inflammation in Candida esophagitis has distinctive features that may be helpful diagnostically. Mod Pathol. 2018;31(11):1653–60.Google Scholar
Chandrasoma, PT. Histologic definition of gastro-esophageal reflux disease. Curr Opin Gastroenterol. 2013;29(4):460–7.Google Scholar
Chandrasoma, PT, Der, R, Ma, Y, Peters, J, Demeester, T. Histologic classification of patients based on mapping biopsies of the gastroesophageal junction. Am J Surg Pathol. 2003;27(7):929–36.Google Scholar
Kilgore, SP, Ormsby, AH, Gramlich, TL, et al. The gastric cardia: fact or fiction? Am J Gastroenterol. 2000;95(4):921–4.Google Scholar
Runge, TM, Abrams, JA, Shaheen, NJ. Epidemiology of Barrett’s esophagus and esophageal adenocarcinoma. Gastroenterol Clin North Am. 2015;44(2):203–31.Google Scholar
Barrett, NR. Chronic peptic ulcer of the oesophagus and ‘oesophagitis’. Br J Surg. 1950;38(150):175–82.Google Scholar
Naini, BV, Souza, RF, Odze, RD. Barrett’s esophagus: a comprehensive and contemporary review for pathologists. Am J Surg Pathol. 2016;40(5):e45–66.CrossRefGoogle ScholarPubMed
Ronkainen, J, Aro, P, Storskrubb, T, et al. Prevalence of Barrett’s esophagus in the general population: an endoscopic study. Gastroenterology. 2005;129(6):1825–31.Google Scholar
Zagari, RM, Fuccio, L, Wallander, MA, et al. Gastro-oesophageal reflux symptoms, oesophagitis and Barrett’s oesophagus in the general population: the Loiano-Monghidoro study. Gut. 2008;57(10):1354–9.Google Scholar
Hayeck, TJ, Kong, CY, Spechler, SJ, Gazelle, GS, Hur, C. The prevalence of Barrett’s esophagus in the US: estimates from a simulation model confirmed by SEER data. Dis Esophagus. 2010;23(6):451–7.CrossRefGoogle ScholarPubMed
Leggett, CL, Nelsen, EM, Tian, J, et al. Metabolic syndrome as a risk factor for Barrett esophagus: a population-based case-control study. Mayo Clin Proc. 2013;88(2):157–65.Google Scholar
Leggett, CL, Gorospe, EC, Calvin, AD, et al. Obstructive sleep apnea is a risk factor for Barrett’s esophagus. Clin Gastroenterol Hepatol. 2014;12(4):583–8.Google Scholar
Iyer, PG, Borah, BJ, Heien, HC, Das, A, Cooper, GS, Chak, A. Association of Barrett’s esophagus with type II diabetes mellitus: results from a large population-based case-control study. Clin Gastroenterol Hepatol. 2013;11(9):1108–14.Google Scholar
Bhat, S, Coleman, HG, Yousef, F, et al. Risk of malignant progression in Barrett’s esophagus patients: results from a large population-based study. J Natl Cancer Inst. 2011;103(13):1049–57.Google Scholar
Shaheen, NJ, Falk, GW, Iyer, PG, Gerson, LB, American College of Gastroenterology. ACG clinical guideline: diagnosis and management of Barrett’s esophagus. Am J Gastroenterol. 2016;111(1):30–50; quiz 1.Google Scholar
Voltaggio, L, Montgomery, EA, Lam-Himlin, D. A clinical and histopathologic focus on Barrett esophagus and Barrett-related dysplasia. Arch Pathol Lab Med. 2011;135(10):1249–60.Google Scholar
Wang, KK, Sampliner, RE, Practice Parameters Committee of the American College of Gastroenterology. Updated guidelines 2008 for the diagnosis, surveillance and therapy of Barrett’s esophagus. Am J Gastroenterol. 2008;103(3):788–97.CrossRefGoogle ScholarPubMed
Weusten, B, Bisschops, R, Coron, E, et al. Endoscopic management of Barrett’s esophagus: European Society of Gastrointestinal Endoscopy (ESGE) Position Statement. Endoscopy. 2017;49(2):191–8.Google ScholarPubMed
Chandrasoma, P, Wijetunge, S, DeMeester, S, et al. Columnar-lined esophagus without intestinal metaplasia has no proven risk of adenocarcinoma. Am J Surg Pathol. 2012;36(1):1–7.Google Scholar
Bandla, S, Peters, JH, Ruff, D, et al. Comparison of cancer-associated genetic abnormalities in columnar-lined esophagus tissues with and without goblet cells. Ann Surg. 2014;260(1):72–80.Google Scholar
Kelty, CJ, Gough, MD, Van Wyk, Q, Stephenson, TJ, Ackroyd, R. Barrett’s oesophagus: intestinal metaplasia is not essential for cancer risk. Scand J Gastroenterol. 2007;42(11):1271–4.CrossRefGoogle Scholar
Takubo, K, Aida, J, Naomoto, Y, et al. Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma. Hum Pathol. 2009;40(1):65–74.CrossRefGoogle ScholarPubMed
Tan, WK, di Pietro, M, Fitzgerald, RC. Past, present and future of Barrett’s oesophagus. Eur J Surg Oncol. 2017;43(7):1148–60.Google Scholar
Bennett, C, Moayyedi, P, Corley, DA, et al. BOB CAT: a large-scale review and Delphi consensus for management of Barrett’s esophagus with no dysplasia, indefinite for, or low-grade dysplasia. Am J Gastroenterol. 2015;110(5):662–82; quiz 83.Google Scholar
Glickman, JN, Chen, YY, Wang, HH, Antonioli, DA, Odze, RD. Phenotypic characteristics of a distinctive multilayered epithelium suggests that it is a precursor in the development of Barrett’s esophagus. Am J Surg Pathol. 2001;25(5):569–78.Google Scholar
American Gastroenterological Association, Spechler, SJ, Sharma, P, Souza, RF, Inadomi, JM, Shaheen, NJ. American Gastroenterological Association medical position statement on the management of Barrett’s esophagus. Gastroenterology. 2011;140(3):1084–91.Google Scholar
Kerkhof, M, van Dekken, H, Steyerberg, EW, et al. Grading of dysplasia in Barrett’s oesophagus: substantial interobserver variation between general and gastrointestinal pathologists. Histopathology. 2007;50(7):920–7.Google Scholar
Kaye, PV, Haider, SA, Ilyas, M, et al. Barrett’s dysplasia and the Vienna classification: reproducibility, prediction of progression and impact of consensus reporting and p53 immunohistochemistry. Histopathology. 2009;54(6):699–712.CrossRefGoogle ScholarPubMed
Waters, KM, Salimian, KJ, Voltaggio, L, Montgomery, EA. Refined criteria for separating low-grade dysplasia and nondysplastic Barrett esophagus reduce equivocal diagnoses and improve prediction of patient outcome: a 10-year review. Am J Surg Pathol. 2018;42(12):1723–9.CrossRefGoogle Scholar
Goldblum, JR. Barrett’s esophagus and Barrett’s-related dysplasia. Mod Pathol. 2003;16(4):316–24.CrossRefGoogle ScholarPubMed
Taylor, PR, Abnet, CC, Dawsey, SM. Squamous dysplasia–the precursor lesion for esophageal squamous cell carcinoma. Cancer Epidemiol Biomarkers Prev. 2013;22(4):540–52.Google Scholar
Qiu, SL, Yang, GR. Precursor lesions of esophageal cancer in high-risk populations in Henan Province, China. Cancer. 1988;62(3):551–7.Google Scholar
Dawsey, SM, Lewin, KJ, Wang, GQ, et al. Squamous esophageal histology and subsequent risk of squamous cell carcinoma of the esophagus: a prospective follow-up study from Linxian, China. Cancer. 1994;74(6):1686–92.Google Scholar
Weinstein, WM, Bogoch, ER, Bowes, KL. The normal human esophageal mucosa: a histological reappraisal. Gastroenterology. 1975;68(1):40–4.Google Scholar
Singhi, AD, Arnold, CA, Crowder, CD, Lam-Himlin, DM, Voltaggio, L, Montgomery, EA. Esophageal leukoplakia or epidermoid metaplasia: a clinicopathological study of 18 patients. Mod Pathol. 2014;27(1):38–43.Google Scholar
Taggart, MW, Rashid, A, Ross, WA, Abraham, SC. Oesophageal hyperkeratosis: clinicopathological associations. Histopathology. 2013;63(4):463–73.CrossRefGoogle ScholarPubMed
Singhi, AD, Arnold, CA, Lam-Himlin, DM, et al. Targeted next-generation sequencing supports epidermoid metaplasia of the esophagus as a precursor to esophageal squamous neoplasia. Mod Pathol. 2017;30(11):1613–21.CrossRefGoogle ScholarPubMed
Hu, N, Huang, J, Emmert-Buck, MR, et al. Frequent inactivation of the TP53 gene in esophageal squamous cell carcinoma from a high-risk population in China. Clin Cancer Res. 2001;7(4):883–91.Google ScholarPubMed
Abedi-Ardekani, B, Kamangar, F, Sotoudeh, M, et al. Extremely high Tp53 mutation load in esophageal squamous cell carcinoma in Golestan Province, Iran. PLoS One. 2011;6(12):e29488.Google Scholar
Xing, EP, Nie, Y, Wang, LD, Yang, GY, Yang, CS. Aberrant methylation of p16INK4a and deletion of p15INK4b are frequent events in human esophageal cancer in Linxian, China. Carcinogenesis. 1999;20(1):77–84.Google Scholar
Su, H, Hu, N, Yang, HH, et al. Global gene expression profiling and validation in esophageal squamous cell carcinoma and its association with clinical phenotypes. Clin Cancer Res. 2011;17(9):2955–66.CrossRefGoogle ScholarPubMed
Agrawal, N, Jiao, Y, Bettegowda, C, et al. Comparative genomic analysis of esophageal adenocarcinoma and squamous cell carcinoma. Cancer Discov. 2012;2(10):899–905.Google Scholar
Wang, LD, Hong, JY, Qiu, SL, Gao, H, Yang, CS. Accumulation of p53 protein in human esophageal precancerous lesions: a possible early biomarker for carcinogenesis. Cancer Res. 1993;53(8):1783–7.Google Scholar
Roye, GD, Myers, RB, Brown, D, Poczatek, R, Beenken, SW, Grizzle, WE. CD44 expression in dysplastic epithelium and squamous-cell carcinoma of the esophagus. Int J Cancer. 1996;69(4):254–8.Google Scholar
Zhou, Q, Dong Wang, L, Du, F, t al. Changes of TGFbeta1 and TGFbetaRII expression in esophageal precancerous and cancerous lesions: a study of a high-risk population in Henan, northern China. Dis Esophagus. 2002;15(1):74–9.CrossRefGoogle ScholarPubMed
Chen, H, Wang, LD, Guo, M, et al. Alterations of p53 and PCNA in cancer and adjacent tissues from concurrent carcinomas of the esophagus and gastric cardia in the same patient in Linzhou, a high incidence area for esophageal cancer in northern China. World J Gastroenterol. 2003;9(1):16–21.Google Scholar
Kimos, MC, Wang, S, Borkowski, A, et al. Esophagin and proliferating cell nuclear antigen (PCNA) are biomarkers of human esophageal neoplastic progression. Int J Cancer. 2004;111(3):415–7.Google Scholar
Bai, P, Xiao, X, Zou, J, et al. Expression of p14(ARF), p15(INK4b), p16(INK4a) and skp2 increases during esophageal squamous cell cancer progression. Exp Ther Med. 2012;3(6):1026–32.Google Scholar
Xue, LY, Hu, N, Song, YM, et al. Tissue microarray analysis reveals a tight correlation between protein expression pattern and progression of esophageal squamous cell carcinoma. BMC Cancer. 2006;6:296.Google Scholar
Shimada, M, Yanagisawa, A, Kato, Y, et al. Genetic mechanisms in esophageal carcinogenesis: frequent deletion of 3p and 17p in premalignant lesions. Genes Chromosomes Cancer. 1996;15(3):165–9.Google Scholar
Roth, MJ, Hu, N, Emmert-Buck, MR, et al. Genetic progression and heterogeneity associated with the development of esophageal squamous cell carcinoma. Cancer Res. 2001;61(10):4098–104.Google ScholarPubMed
Nie, Y, Liao, J, Zhao, X, et al. Detection of multiple gene hypermethylation in the development of esophageal squamous cell carcinoma. Carcinogenesis. 2002;23(10):1713–20.Google Scholar
Roth, MJ, Abnet, CC, Hu, N, et al. p16, MGMT, RARbeta2, CLDN3, CRBP and MT1G gene methylation in esophageal squamous cell carcinoma and its precursor lesions. Oncol Rep. 2006;15(6):1591–7.Google ScholarPubMed
Ishii, T, Murakami, J, Notohara, K, et al. Oesophageal squamous cell carcinoma may develop within a background of accumulating DNA methylation in normal and dysplastic mucosa. Gut. 2007;56(1):13–9.Google Scholar
Adams, L, Roth, MJ, Abnet, CC, et al. Promoter methylation in cytology specimens as an early detection marker for esophageal squamous dysplasia and early esophageal squamous cell carcinoma. Cancer Prev Res (Phila). 2008;1(5):357–61.Google Scholar

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