European journal of gastroenterology & hepatology · 2003
Inflammation at the cardio-oesophageal junction: relationship to acid and bile exposure.
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Bowrey David J, Williams Geraint T, Carey P Declan, Clark Geoffrey W
Аннотация
BACKGROUND: The aetiology of inflammation in cardiac mucosa at the gastro-oesophageal junction (carditis) is unclear, although gastro-oesophageal reflux has been suggested.
OBJECTIVES: To correlate histological features of carditis with oesophageal acid exposure (gastro-oesophageal reflux) and proximal gastric bile exposure (duodenogastric reflux) in patients with symptoms of gastro-oesophageal reflux disease (GORD).
METHODS: Sixty-six patients with reflux symptoms underwent endoscopy with biopsy, oesophageal manometry, 24-h oesophageal pH testing and 24-h proximal gastric Bilitec 2000 testing. Inflammation in glandular mucosa was assessed using the updated Sydney System. Fifteen healthy volunteers underwent pH and Bilitec 2000 testing and served as controls.
RESULTS: There was no correlation between either the presence or histological grade of carditis and oesophageal acid exposure or proximal gastric bilirubin exposure. Patients with reflux symptoms had as much duodenogastric reflux into the proximal stomach as did control subjects.
CONCLUSIONS: We were unable to establish either gastro-oesophageal or duodenogastric reflux as the predominant cause of inflammation in cardiac mucosa.
OBJECTIVES: To correlate histological features of carditis with oesophageal acid exposure (gastro-oesophageal reflux) and proximal gastric bile exposure (duodenogastric reflux) in patients with symptoms of gastro-oesophageal reflux disease (GORD).
METHODS: Sixty-six patients with reflux symptoms underwent endoscopy with biopsy, oesophageal manometry, 24-h oesophageal pH testing and 24-h proximal gastric Bilitec 2000 testing. Inflammation in glandular mucosa was assessed using the updated Sydney System. Fifteen healthy volunteers underwent pH and Bilitec 2000 testing and served as controls.
RESULTS: There was no correlation between either the presence or histological grade of carditis and oesophageal acid exposure or proximal gastric bilirubin exposure. Patients with reflux symptoms had as much duodenogastric reflux into the proximal stomach as did control subjects.
CONCLUSIONS: We were unable to establish either gastro-oesophageal or duodenogastric reflux as the predominant cause of inflammation in cardiac mucosa.