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Published on: November 1, 2024
'Cardiac-type' (mucinous) mucosa and carditis are both associated with Helicobacter pylori-related gastritis
Christian Gulmann1, Omar Rathore, Antoinette Grace
1Department of Pathology, Beaumont Hospital, Dublin, Ireland. cgulmann@rcsi.ie
Insights
Helicobacter pylori gastritis is linked to carditis and mucinous cardiac mucosa, suggesting metaplasia that may play a role in gastro-oesophageal junction cancer development.
Area of Science:
- Gastroenterology
- Pathology
- Oncology
Background:
- Adenocarcinoma of the gastro-oesophageal junction incidence is rising, prompting research into precursor lesions.
- The etiology of gastric cardia inflammation (carditis) and the nature of cardiac mucosa are debated.
Purpose of the Study:
- To explore the association between cardiac mucosa type, carditis, and histological/clinical factors.
- To investigate the role of Helicobacter pylori in these changes.
Main Methods:
- Prospective collection of 98 gastric biopsy sets from patients with upper GI symptoms.
- Scoring of inflammation, H. pylori density, intestinal metaplasia, and atrophy using the Sydney classification.
- Recording of cardiac mucosa type (oxyntic vs. mucinous) and presence/absence of oesophagitis.
Main Results:
- Carditis and mucinous cardiac mucosa were significantly associated with H. pylori-related gastritis (P < 0.001).
- No significant association was found between carditis/mucinous mucosa and gastro-oesophageal reflux.
- Mucinous mucosa in the cardia was observed in only 17% of biopsies.
Conclusions:
- H. pylori gastritis is associated with both carditis and mucinous-type cardiac mucosa.
- This suggests metaplasia of oxyntic to mucinous mucosa in H. pylori gastritis.
- This metaplasia may contribute to the carcinogenesis of the gastro-oesophageal junction.
Background:
Adenocarcinoma of the gastro-oesophageal junction is rapidly increasing in incidence and there is much interest in precursor lesions. The aetiology of inflammation of the gastric cardia (carditis) and the concept of the cardia as a native zone of mucinous gastric glands are disputed.
Aims:
To investigate the relationship between the type of cardiac mucosa and carditis with various histological and clinical parameters.
Methods:
Ninety-eight sets of gastric biopsies (cardia, corpus, incisura and antrum) were obtained prospectively in young patients (median age 40 years) who presented to the outpatient clinic with symptoms of gastro-oesophageal reflux (n = 25) or other upper gastrointestinal symptoms. Patients with neoplasia or Barrett's oesophagus were excluded. The presence (n = 19) or absence of oesophagitis at endoscopy was recorded. The degree of inflammation, Helicobacter pylori density, intestinal metaplasia and atrophy were scored according to the Sydney classification and the type of cardiac mucosa (oxyntic or mucinous) was noted.
Results:
We found that carditis and mucinous-type cardiac mucosa were strongly associated with H. pylori-related gastritis (P = 0.00019 and P = 0.006, respectively) but not with clinical or endoscopic gastro-oesophageal reflux. Mucinous mucosa in the cardia was only seen in 17% of biopsies.
Conclusion:
H. pylori-related gastritis is associated with mucinous-type cardiac mucosa as well as with carditis. The former strongly points to expansion of mucinous cardiac mucosa in H. pylori gastritis. This probably represents metaplasia of oxyntic to mucinous mucosa and raises the possibility of a role in carcinogenesis of the gastro-oesophageal junction.
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