Patterns of gastritis in patients with gastro-oesophageal reflux disease

Abstract

Background-The cause of inflammation in cardiac mucosa at the gastrooesophageal 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 noncolonised 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. (Gut 1999;45:798-803)

Gastritis and Carditis

“…Its prevalence in patients with GERD has been estimated variously to be between 34 and 100% (117,122,(127)(128)(129). In contrast to H. pylori-associated carditis, GERD carditis is not associated with inflammation elsewhere in the stomach (121).…”

“…In a proportion of individuals, the cardiac-fundic mucosal interface comprises glands with a mixed cell population. Carditis has at least two causes: an isolated carditis associated with reflux and a pangastritis associated with H. pylori (118,127,129). Further work on the gastric cardia would greatly benefit from use of standardized nomenclature, with strict attention paid to the exact site of the endoscopic biopsy in relation to anatomical landmarks (131).…”

There is no difference in the disease severity of gastro‐oesophageal reflux disease between patients infected and not infected with Helicobacter pylori

“…However, given that we found no difference between the H. pylori-infected and noninfected GERD patients, the findings would likely not have altered our conclusions. Furthermore, Bowrey et al 39 examined gastric patterns in GERD patients and found gastritis of the cardia commonly regardless of whether patients were infected or not with H. pylori.…”

Optimizing Symptom Relief and Preventing Complications in Adults with Gastro-Oesophageal Reflux Disease

“…As a consequence, it has been speculated that H. pylori may protect against the development of mucosal oesophageal lesions: the improvement of gastritis in the oxyntic mucosa promoted by H. pylori eradication could result in an increase in the production of acid, which could backwash into the oesophagus. However, Bowrey et al [8]and our group [9]have clearly shown corpus gastritis to be significantly less common than antral gastritis in GORD patients infected with H. pylori . Moreover, in patients with GORD, corpus atrophy is mild and is present only in a minority, regardless of H. pylori status [10].…”