Duodenogastric reflux in patients with gastric ulcer disease.
We studied reflux of duodenal contents into the stomach in patients with gastric ulcers, patients with duodenal ulcers, and normal subjects. Duodenogastric reflux was assessed in the fasting state and after cholecystokinin octapeptide administration (0.02 micrograms/kg intravenously). Slight reflux was observed in the fasting state in all three groups. However, after cholecystokinin octapeptide administration, reflux was significantly greater in gastric ulcer patients than in control patients for pancreatic phospholipase A2 (p less than 0.01) and lysophosphatidylcholine (p less than 0.001). Also in gastric ulcer patients, the gastric contents were significantly more alkaline (pH 5.26 +/- 0.58, p less than 0.001) during duodenogastric reflux than in normal subjects (pH 3.65 +/- 0.50) or duodenal ulcer patients (pH 2.67 +/- 0.63). Our results suggest that reflux of both pancreatic and biliary secretions might contribute to the gastric mucosal injury in gastric ulcer patients and we postulate that pancreatic phospholipase A2 might have a greater role in this process than has been previously acknowledged.
D000328:Adult; D000368:Aged; D001647:Bile Acids and Salts / Q000378:metabolism; D002766:Cholecystokinin / Q000378:metabolism; D004383:Duodenogastric Reflux / Q000209:etiology*; D005260:Female; D005750:Gastric Juice / Q000502:physiology; D006461:Hemolysis; D006801:Humans; D008244:Lysophosphatidylcholines / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010741:Phospholipases A / Q000378:metabolism; D054467:Phospholipases A2; D013276:Stomach Ulcer / Q000150:complications* / Q000503:physiopathology
D001647:Bile Acids and Salts; D008244:Lysophosphatidylcholines; D002766:Cholecystokinin; D010741:Phospholipases A; D054467:Phospholipases A2