Abstract
Background and Aims
The causes for the occurrence of goblet cells at the gastroesophageal junction (GEJ-GC) are unknown. The aim of our study was to compare the concurrent histologic changes of the stomach in (1) patients with GEJ-GC, but without Barrett’s esophagus (BE) to those in (2) patients with BE and in (3) controls without GEJ-GC or BE.
Methods
We used an electronic database of histopathologic records from 1.3 million individual patients, who underwent esophago-gastro-duodenoscopy (EGD) in 2009–2018. We compared the prevalence of Helicobacter pylori-positive gastritis (HpG), gastric intestinal metaplasia (G-IM), chronic inactive gastritis (CIG), and reactive gastropathy (RG) among the 3 patient groups, using odds ratios and their 95% confidence intervals.
Results
Of all EGD patients, 4.0% harbored BE and 2.4% GEJ-GC. The average age of patients with GEJ-GC (60 ± 14) was significantly younger than the age of patients with BE (63 ± 12) and significantly older than the age of controls (55 ± 17). Female subjects were more common among GEJ-GC (54%) than BE (37%), but less common than among controls (63%). The 3 gastric histopathology changes associated with H. pylori were significantly more common in GEJ-GC than BE (for HpG 2.42, 2.29–2.56; for G-IM 1.82, 1.73–1.92; for CIG 1.31, 1.22–1.41). The corresponding differences between GEJ-GC and controls were less striking (for HpG 0.97, 0.93–1.01; for G-IM 1.15, 1.11–1.19; for CIG 0.90, 0.85–0.95). RG was slightly less common in GEJ-GC than BE (0.89, 0.86–0.92) and controls (0.94, 0.91–0.96).
Conclusions
With respect to its demographic and histopathologic features, GEJ-GC likely represents gastric intestinal metaplasia as opposed to BE and should prompt gastric intestinal metaplasia screening and management.
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References
Gupta S, Li D, El Serag HB, et al. AGA clinical practice guidelines on management of gastric intestinal metaplasia. Gastroenterology. 2020;158:693–702.
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;111:30–50.
Spechler SJ. Cardiac metaplasia: follow, treat, or ignore? Dig Dis Sci. 2018;63:2052–2058.
Genta RM, Huberman RM, Graham DY. The gastric cardia in Helicobacter pylori infection. Hum Pathol. 1994;25:915–919.
Goldblum JR, Vicari JJ, Falk GW, et al. Inflammation and intestinal metaplasia of the gastric cardia: the role of gastroesophageal reflux and H. pylori infection. Gastroenterology. 1998;114:633–639.
Oberg S, Peters JH, DeMeester TR, et al. Inflammation and specialized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease. Ann Surg. 1997;226:522–530.
McColl KE, Derakhshan MH, Mitchell DR. Short-segment and intrasphincteric gastroesophageal reflux. Curr Opin Gastroenterol. 2016;32:332–337.
Sonnenberg A, Lash RH, Genta RM. A national study of H. pylori infection in gastric biopsy specimens. Gastroenterology. 2010;139:1894–1901.
Sonnenberg A, Genta RM. Geographic distributions of microscopic colitis and inflammatory bowel disease in the United States. Inflamm Bowel Dis. 2012;18:2288–2293.
Lebwohl B, Blaser MJ, Ludvigsson JF, et al. Decreased risk of celiac disease in patients with Helicobacter pylori colonization. Am J Epidemiol. 2013;178:1721–1730.
Jensen ET, Shah ND, Hoffman K, Sonnenberg A, Genta RM, Dellon ES. Seasonal variation in detection of esophageal eosinophilia and eosinophilic esophagitis. Aliment Pharmacol Ther. 2015;42:461–469.
Sonnenberg A, Genta RM. Low prevalence of colon polyps in chronic inflammatory conditions of the colon. Am J Gastroenterol. 2015;110:1056–1061.
Turner KO, Genta RM, Sonnenberg A. Lesions of all types exist in colon polyps of all sizes. Am J Gastroenterol. 2018;113:303–306.
Srivastava A, Odze RD, Lauwers GY, Redston M, Antonioli DA, Glickman JN. Morphologic features are useful in distinguishing Barrett esophagus from carditis with intestinal metaplasia. Am J Surg Pathol. 2007;31:1733–1741.
Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis: the updated Sydney system. Am J Surg Pathol. 1996;120:1161–1181.
Genta RM. Differential diagnosis of reactive gastropathy. Semin Diagn Pathol. 2005;22:273–283.
Byrne JP, Bhatnagar S, Hamid B, Armstrong GR, Attwood SE. Comparative study of intestinal metaplasia and mucin staining at the cardia and esophagogastric junction in 225 symptomatic patients presenting for diagnostic open-access gastroscopy. Am J Gastroenterol. 1999;92:98–103.
Zaninotto G, Avellini C, Barbazza R, et al. Prevalence of intestinal metaplasia in the distal oesophagus, oesophagogastric junction and gastric cardia in symptomatic patients in north-east Italy: a prospective, descriptive survey. The Italian Ulcer Study Group “GISU”. Dig Liver Dis. 2001;33:316–321.
Srivastava A, Appelman H, Goldsmith JD, Davison JM, Hart J, Krasinskas AM. The use of ancillary stains in the diagnosis of Barrett esophagus and Barrett esophagus—associated dysplasia: recommendations from the Rodger C. Haggitt Gastrointestinal Pathology Society. Am J Surg Pathol. 2017;41:e8–e21.
Genta RM, Turner KO, Lash RH. Upfront Alcian Blue-periodic acid Schiff stain for the assessment of upper gastrointestinal disorders. Dig Liver Dis. 2018;50:417–418.
El-Serag HB, Mason AC, Petersen N, Key CR. Epidemiological differences between adenocarcinoma of the oesophagus and adenocarcinoma of the gastric cardia in the USA. Gut. 2002;50:368–372.
Erőss B, Farkas N, Vincze Á, et al. Helicobacter pylori infection reduces the risk of Barrett’s esophagus: a meta-analysis and systematic review. Helicobacter. 2018;23:e12504.
Banks M, Graham D, Jansen M, et al. British Society of Gastroenterology guidelines on the diagnosis and management of patients at risk of gastric adenocarcinoma. Gut. 2019;68:1545–1575.
Harewood GC, Holub JL, Lieberman DA. Biopsy specimen acquisition in patients with newly diagnosed peptic ulcer disease as determined from a national endoscopic database. Gastrointest Endosc. 2004;59:664–669.
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RMG and AS conceived and designed the study; AS, RMG, and KOT analyzed the data and wrote the manuscript.
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Kevin O. Turner and Robert M. Genta are employed by Inform Diagnostics, Irving, TX. Amnon Sonnenberg has no conflict of interest to declare.
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Turner, K.O., Genta, R.M. & Sonnenberg, A. The Meaning of Incidental Goblet Cells at the Gastroesophageal Junction. Dig Dis Sci 66, 1588–1592 (2021). https://doi.org/10.1007/s10620-020-06357-5
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DOI: https://doi.org/10.1007/s10620-020-06357-5