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Helicobacter pylori infection, not gastroesophageal reflux, is the major cause of inflammation and intestinal metaplasia of gastric cardiac mucosa.
Am J Gastroenterol 2002; 97(2):302-11AJ

Abstract

OBJECTIVE

The etiology of inflammation below the normal Z-line is an area of intense debate. Some suggest this is the earliest change of chronic gastroesophageal reflux disease (GERD), whereas others indict Helicobacter pylori (H. pylori) as the main cause. The aim of this study was to evaluate the relationship among inflammation of gastric cardiac mucosa (carditis), H. pylori infection, and intestinal metaplasia in patients with GERD and Barrett's esophagus compared with age-matched controls.

METHODS

Patients with GERD and Barrett's esophagus were compared with controls undergoing endoscopy for a variety of other conditions. Endoscopic biopsy specimens from the gastric cardia (obtained on retroflexed view), fundus, and antrum were evaluated for inflammation, H. pylori infection, and intestinal metaplasia.

RESULTS

The prevalence of H. pylori infection did not significantly differ among the study populations: controls (42%), GERD (33%), and Barrett's esophagus (27%) (p = 0.20). However, the prevalence of carditis significantly decreased from the control group (30%) to those with GERD (23%) and Barrett's esophagus (11%) (p = 0.03). Overall, 42 of 51 (82%) patients with carditis had H. pylori; all had pangastritis. The prevalence of cardia intestinal metaplasia also significantly decreased from the control group (15%) to those with GERD (4%) and Barrett's esophagus (0%) (p = 0.003). Of 13 patients with cardia intestinal metaplasia, 12 had carditis, 10 had H. pylori infection, and seven had intestinal metaplasia elsewhere in the stomach.

CONCLUSIONS

Inflammation of gastric cardiac mucosa decreases in prevalence from controls to patients with GERD and Barrett's esophagus and correlates strongly with H. pylori infection. Cardia intestinal metaplasia is associated with H. pylori-related cardiac inflammation and intestinal metaplasia elsewhere in the stomach.

Authors+Show Affiliations

Center for Swallowing and Esophageal Disorders and Department of Anatomic Pathology, Cleveland Clinic Foundation, Ohio 44195, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

11866266

Citation

Goldblum, John R., et al. "Helicobacter Pylori Infection, Not Gastroesophageal Reflux, Is the Major Cause of Inflammation and Intestinal Metaplasia of Gastric Cardiac Mucosa." The American Journal of Gastroenterology, vol. 97, no. 2, 2002, pp. 302-11.
Goldblum JR, Richter JE, Vaezi M, et al. Helicobacter pylori infection, not gastroesophageal reflux, is the major cause of inflammation and intestinal metaplasia of gastric cardiac mucosa. Am J Gastroenterol. 2002;97(2):302-11.
Goldblum, J. R., Richter, J. E., Vaezi, M., Falk, G. W., Rice, T. W., & Peek, R. M. (2002). Helicobacter pylori infection, not gastroesophageal reflux, is the major cause of inflammation and intestinal metaplasia of gastric cardiac mucosa. The American Journal of Gastroenterology, 97(2), pp. 302-11.
Goldblum JR, et al. Helicobacter Pylori Infection, Not Gastroesophageal Reflux, Is the Major Cause of Inflammation and Intestinal Metaplasia of Gastric Cardiac Mucosa. Am J Gastroenterol. 2002;97(2):302-11. PubMed PMID: 11866266.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Helicobacter pylori infection, not gastroesophageal reflux, is the major cause of inflammation and intestinal metaplasia of gastric cardiac mucosa. AU - Goldblum,John R, AU - Richter,Joel E, AU - Vaezi,Michael, AU - Falk,Gary W, AU - Rice,Thomas W, AU - Peek,Richard M, PY - 2002/2/28/pubmed PY - 2002/3/15/medline PY - 2002/2/28/entrez SP - 302 EP - 11 JF - The American journal of gastroenterology JO - Am. J. Gastroenterol. VL - 97 IS - 2 N2 - OBJECTIVE: The etiology of inflammation below the normal Z-line is an area of intense debate. Some suggest this is the earliest change of chronic gastroesophageal reflux disease (GERD), whereas others indict Helicobacter pylori (H. pylori) as the main cause. The aim of this study was to evaluate the relationship among inflammation of gastric cardiac mucosa (carditis), H. pylori infection, and intestinal metaplasia in patients with GERD and Barrett's esophagus compared with age-matched controls. METHODS: Patients with GERD and Barrett's esophagus were compared with controls undergoing endoscopy for a variety of other conditions. Endoscopic biopsy specimens from the gastric cardia (obtained on retroflexed view), fundus, and antrum were evaluated for inflammation, H. pylori infection, and intestinal metaplasia. RESULTS: The prevalence of H. pylori infection did not significantly differ among the study populations: controls (42%), GERD (33%), and Barrett's esophagus (27%) (p = 0.20). However, the prevalence of carditis significantly decreased from the control group (30%) to those with GERD (23%) and Barrett's esophagus (11%) (p = 0.03). Overall, 42 of 51 (82%) patients with carditis had H. pylori; all had pangastritis. The prevalence of cardia intestinal metaplasia also significantly decreased from the control group (15%) to those with GERD (4%) and Barrett's esophagus (0%) (p = 0.003). Of 13 patients with cardia intestinal metaplasia, 12 had carditis, 10 had H. pylori infection, and seven had intestinal metaplasia elsewhere in the stomach. CONCLUSIONS: Inflammation of gastric cardiac mucosa decreases in prevalence from controls to patients with GERD and Barrett's esophagus and correlates strongly with H. pylori infection. Cardia intestinal metaplasia is associated with H. pylori-related cardiac inflammation and intestinal metaplasia elsewhere in the stomach. SN - 0002-9270 UR - https://www.unboundmedicine.com/medline/citation/11866266/Helicobacter_pylori_infection_not_gastroesophageal_reflux_is_the_major_cause_of_inflammation_and_intestinal_metaplasia_of_gastric_cardiac_mucosa_ L2 - http://Insights.ovid.com/pubmed?pmid=11866266 DB - PRIME DP - Unbound Medicine ER -