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Patterns of gastritis in patients with gastro-oesophageal reflux disease.
Gut 1999; 45(6):798-803Gut

Abstract

BACKGROUND

The cause of inflammation in cardiac mucosa at the gastro-oesophageal junction (GOJ) is unclear, both gastro-oesophageal reflux disease (GORD) and Helicobacter pylori having been implicated.

AIMS

To describe patterns of gastritis in patients with symptomatic GORD.

METHODS

In 150 patients (126 normally located Z-line, 24 Barrett's oesophagus) with symptoms of GORD, biopsies were taken of the GOJ, corpus, and antrum. Inflammation was assessed using the updated Sydney System.

RESULTS

For the 126 patients with a normally located Z-line, biopsies of the GOJ revealed cardiac mucosa in 96, fundic mucosa in 29, and squamous mucosa in one. Inflammation in glandular mucosa at the GOJ was present in 99/125 specimens (79%), including 87/96 (91%) with cardiac mucosa and 12/29 (41%) with fundic mucosa. Inflammation in fundic mucosa was closely related to H pylori and active inflammation was only seen in its presence. Inflammation in cardiac mucosa was less closely linked to H pylori. When H pylori was present in cardiac mucosa (28/96, 29%) active inflammation was usually present (25/28, 89%). However, active inflammation was also found in 34/68 (50%) cardiac mucosa specimens without H pylori. Overall, 28/87 (32%) biopsies with carditis were colonised with H pylori and 59/87 (68%) were not. In H pylori colonised patients, inflammation was seen throughout the stomach, while in non-colonised patients, it was confined to cardiac mucosa.

CONCLUSIONS

Patients with symptomatic GORD had a high prevalence of carditis. This was of two types, H pylori associated and unassociated. Except on Giemsa staining, the two were morphologically identical, suggesting mediation by a similar immunological mechanism.

Authors+Show Affiliations

University Department of Surgery, University of Wales College of Medicine, Cardiff, UK.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10562575

Citation

Bowrey, D J., et al. "Patterns of Gastritis in Patients With Gastro-oesophageal Reflux Disease." Gut, vol. 45, no. 6, 1999, pp. 798-803.
Bowrey DJ, Clark GW, Williams GT. Patterns of gastritis in patients with gastro-oesophageal reflux disease. Gut. 1999;45(6):798-803.
Bowrey, D. J., Clark, G. W., & Williams, G. T. (1999). Patterns of gastritis in patients with gastro-oesophageal reflux disease. Gut, 45(6), pp. 798-803.
Bowrey DJ, Clark GW, Williams GT. Patterns of Gastritis in Patients With Gastro-oesophageal Reflux Disease. Gut. 1999;45(6):798-803. PubMed PMID: 10562575.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Patterns of gastritis in patients with gastro-oesophageal reflux disease. AU - Bowrey,D J, AU - Clark,G W, AU - Williams,G T, PY - 1999/11/24/pubmed PY - 1999/11/24/medline PY - 1999/11/24/entrez SP - 798 EP - 803 JF - Gut JO - Gut VL - 45 IS - 6 N2 - BACKGROUND: The cause of inflammation in cardiac mucosa at the gastro-oesophageal junction (GOJ) is unclear, both gastro-oesophageal reflux disease (GORD) and Helicobacter pylori having been implicated. AIMS: To describe patterns of gastritis in patients with symptomatic GORD. METHODS: In 150 patients (126 normally located Z-line, 24 Barrett's oesophagus) with symptoms of GORD, biopsies were taken of the GOJ, corpus, and antrum. Inflammation was assessed using the updated Sydney System. RESULTS: For the 126 patients with a normally located Z-line, biopsies of the GOJ revealed cardiac mucosa in 96, fundic mucosa in 29, and squamous mucosa in one. Inflammation in glandular mucosa at the GOJ was present in 99/125 specimens (79%), including 87/96 (91%) with cardiac mucosa and 12/29 (41%) with fundic mucosa. Inflammation in fundic mucosa was closely related to H pylori and active inflammation was only seen in its presence. Inflammation in cardiac mucosa was less closely linked to H pylori. When H pylori was present in cardiac mucosa (28/96, 29%) active inflammation was usually present (25/28, 89%). However, active inflammation was also found in 34/68 (50%) cardiac mucosa specimens without H pylori. Overall, 28/87 (32%) biopsies with carditis were colonised with H pylori and 59/87 (68%) were not. In H pylori colonised patients, inflammation was seen throughout the stomach, while in non-colonised patients, it was confined to cardiac mucosa. CONCLUSIONS: Patients with symptomatic GORD had a high prevalence of carditis. This was of two types, H pylori associated and unassociated. Except on Giemsa staining, the two were morphologically identical, suggesting mediation by a similar immunological mechanism. SN - 0017-5749 UR - https://www.unboundmedicine.com/medline/citation/10562575/Patterns_of_gastritis_in_patients_with_gastro_oesophageal_reflux_disease_ L2 - http://gut.bmj.com/cgi/pmidlookup?view=long&pmid=10562575 DB - PRIME DP - Unbound Medicine ER -