BACKGROUND: No current methods exist to determine meal-stimulated gastric acid secretion in humans under conditions that approximate those of daily living with the ingestion of breakfast, lunch and dinner. METHODS:Gastric and oesophageal pH were measured in 26 healthy subjects and in 59 subjects with gastro-oesophageal reflux disease. Meal-stimulated gastric acid secretion was calculated from the buffer capacity of the meals determined in vitro and from the time required for the gastric pH to decrease to pH 2 in vivo following ingestion of the meal. RESULTS: There was a significant correlation between gastric secretion with each meal and the corresponding post-prandial integrated gastric acidity. There was also a significant correlation between meal-stimulated gastric secretion and integrated gastric acidity from 09.00 to 22.00 h in both subjects with gastro-oesophageal reflux disease and controls. In subjects with gastro-oesophageal reflux disease, gastric secretion and integrated gastric acidity from 09.00 to 22.00 h were significantly higher than those in controls. There was a significant correlation between oesophageal acidity and integrated gastric acidity from 09.00 to 22.00 h in subjects with gastro-oesophageal reflux disease. CONCLUSIONS: As post-prandial gastric acidity is increased in subjects with gastro-oesophageal reflux disease, it seems likely that increased gastric acidity is an important aetiological factor in this disease.
RCT Entities:
BACKGROUND: No current methods exist to determine meal-stimulated gastric acid secretion in humans under conditions that approximate those of daily living with the ingestion of breakfast, lunch and dinner. METHODS: Gastric and oesophageal pH were measured in 26 healthy subjects and in 59 subjects with gastro-oesophageal reflux disease. Meal-stimulated gastric acid secretion was calculated from the buffer capacity of the meals determined in vitro and from the time required for the gastric pH to decrease to pH 2 in vivo following ingestion of the meal. RESULTS: There was a significant correlation between gastric secretion with each meal and the corresponding post-prandial integrated gastric acidity. There was also a significant correlation between meal-stimulated gastric secretion and integrated gastric acidity from 09.00 to 22.00 h in both subjects with gastro-oesophageal reflux disease and controls. In subjects with gastro-oesophageal reflux disease, gastric secretion and integrated gastric acidity from 09.00 to 22.00 h were significantly higher than those in controls. There was a significant correlation between oesophageal acidity and integrated gastric acidity from 09.00 to 22.00 h in subjects with gastro-oesophageal reflux disease. CONCLUSIONS: As post-prandial gastric acidity is increased in subjects with gastro-oesophageal reflux disease, it seems likely that increased gastric acidity is an important aetiological factor in this disease.
Authors: D H Weinstein; S deRijke; C C Chow; L Foruraghi; X Zhao; E C Wright; M Whatley; R Maass-Moreno; C C Chen; S A Wank Journal: Aliment Pharmacol Ther Date: 2013-05-03 Impact factor: 8.171
Authors: Lauren B Gerson; George Triadafilopoulos; Peyman Sahbaie; Winston Young; Sheldon Sloan; Malcolm Robinson; Philip B Miner; Jerry D Gardner Journal: BMC Gastroenterol Date: 2008-05-23 Impact factor: 3.067