Gastric cardia inflammation: Role of Helicobacter pylori infection and symptoms of gastroesophageal reflux disease

Citation
S. Morini et al., Gastric cardia inflammation: Role of Helicobacter pylori infection and symptoms of gastroesophageal reflux disease, AM J GASTRO, 96(8), 2001, pp. 2337-2340
Citations number
31
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
AMERICAN JOURNAL OF GASTROENTEROLOGY
ISSN journal
00029270 → ACNP
Volume
96
Issue
8
Year of publication
2001
Pages
2337 - 2340
Database
ISI
SICI code
0002-9270(200108)96:8<2337:GCIROH>2.0.ZU;2-I
Abstract
OBJECTIVE: Although high prevalences of both chronic inflammation (carditis ) and intestinal metaplasia at the gastric cardia have been reported, the p athogenesis is still unclear. This study assesses the role of Helicobacter pylori (H. pylori) infection and symptoms of gastroesophageal reflux diseas e (GERD) in these histological alterations. METHODS: Consecutive patients who underwent upper endoscopy were enrolled i n the study, irrespective of their symptoms. Patients previously treated fo r It. pylori infection and those using proton pump inhibitors were excluded . Two biopsies were performed in the antrum, two in the gastric body, and t wo at the gastric cardia. All biopsies were used to look for H. pylori and for histological assessment. RESULTS: A total of 133 patients were enrolled. Carditis and intestinal met aplasia at the cardia were detected in 100 (75.2%) and in 18 (13.5%) patien ts, respectively. The H. pylori infection rate was significantly higher in patients with carditis than in those without it (87/100 vs 7/33; p < 0.0001 ), and was higher in those with intestinal metaplasia at the cardia than in those without it ( 17/94 vs 1/39: p = 0.03). Conversely, the prevalence of GERD symptoms was not significantly different between patients with and wi thout carditis (34/100 vs 16/33: p = NS), and between those with and withou t intestinal metaplasia (5150 vs 1.3/83: P = NS). Interestingly, the preval ence of both H. pylori (64/94 vs 39/94; p = 0.0005) and intestinal metaplas ia (18/133 vs 4/133; p = 0.0042) in the gastric cardia was significantly hi gher than that in gastric body. CONCLUSION: According to our study data, the gastric cardia is frequently i nfected with H. pylori with consequent development of both carditis and int estinal metaplasia, whereas GERD does not seem to be involved in these hist ological changes. (C) 2001 by Am. Coll. of Gastroenterology.