Meal-stimulated gastric acid secretion and integrated gastric acidity in gastro-oesophageal reflux disease J. D. GARDNER*, S. SLOAN  , P. B. MINER JR à & M. ROBINSON à *Science for Organizations, Inc., Chatham, NJ, USA;  Janssen Pharmaceutica Inc., Titusville, NJ, USA; àOklahoma Foundation for Digestive Research, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA Accepted for publication 21 January 2003 SUMMARY 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 gas- tric 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 integ- rated 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 import- ant aetiological factor in this disease. INTRODUCTION Although the inhibition of gastric acid secretion by histamine-2 receptor antagonists and proton pump inhibitors decreases oesophageal acid exposure, 1, 2 gastric acidity has received limited attention with respect to its pathophysiological potential in influencing oesophageal acid exposure in gastro-oesophageal reflux disease (GERD). 3–12 Hirschowitz reported that basal and pentagastrin-stimulated gastric acid secretion in sub- jects with oesophagitis was comparable with that in subjects with unspecified medical conditions without oesophagitis. 3, 10, 11 Others, however, have reported increased basal, peak and maximal gastric acid secre- tion in subjects with GERD when compared with those in healthy subjects. 4–6, 12 Initially, the measurement of meal-stimulated gastric acid secretion involved manual intragastric titration whereby, after a meal, NaHCO 3 or NaOH was repeatedly infused into the stomach in amounts sufficient to maintain the gastric pH at a pre-determined, constant value. 13–15 Subsequently, we developed a technique to measure meal-stimulated gastric acid secretion based on the buffer capacity of the meal determined in vitro and the time required for the gastric pH to decrease to pH 2 in vivo following ingestion of the meal. 16, 17 These studies, however, involved a single meal ingested by subjects who were restricted to a bed or a chair in a study unit. 16, 17 Correspondence to: Dr J. D. Gardner, Science for Organizations, Inc., 156 Terrace Drive, Chatham, NJ 07928, USA. E-mail: gardnerj@bellatlantic.net Aliment Pharmacol Ther 2003; 17: 945–953. doi: 10.1046/j.0269-2813.2003.01533.x Ó 2003 Blackwell Publishing Ltd 945