Meal-stimulated gastric acid secretion and integrated gastric acidity in gastro-oesophageal reflux disease

被引:30
作者
Gardner, JD
Sloan, S
Miner, PB
Robinson, M
机构
[1] Sci Org Inc, Chatham, NJ 07928 USA
[2] Janssen Pharmaceut Inc, Titusville, NJ USA
[3] Univ Oklahoma, Hlth Sci Ctr, Oklahoma Fdn Digest Res, Oklahoma City, OK USA
关键词
D O I
10.1046/j.1365-2036.2003.01533.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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.
引用
收藏
页码:945 / 953
页数:9
相关论文
共 18 条
[1]   APPROPRIATE ACID SUPPRESSION FOR THE MANAGEMENT OF GASTROESOPHAGEAL REFLUX DISEASE [J].
BELL, NJV ;
BURGET, D ;
HOWDEN, CW ;
WILKINSON, J ;
HUNT, RH .
DIGESTION, 1992, 51 :59-67
[2]   CONCENTRATION OF REFLUXED ACID AND ESOPHAGEAL MUCOSAL INJURY [J].
BREMNER, RM ;
CROOKES, PF ;
DEMEESTER, TR ;
PETERS, JH ;
STEIN, HJ .
AMERICAN JOURNAL OF SURGERY, 1992, 164 (05) :522-527
[3]   GASTRIC-ACID HYPERSECRETION IN REFRACTORY GASTROESOPHAGEAL REFLUX DISEASE [J].
COLLEN, MJ ;
LEWIS, JH ;
BENJAMIN, SB .
GASTROENTEROLOGY, 1990, 98 (03) :654-661
[4]   CORRELATION BETWEEN BASAL ACID OUTPUT AND DAILY RANITIDINE DOSE REQUIRED FOR THERAPY IN BARRETTS-ESOPHAGUS [J].
COLLEN, MJ ;
JOHNSON, DA .
DIGESTIVE DISEASES AND SCIENCES, 1992, 37 (04) :570-576
[5]   Gastro-oesophageal reflux disease [J].
Dent, J .
DIGESTION, 1998, 59 (05) :433-445
[6]   Influence of H-pylori infection on meal-stimulated gastric acid secretion and gastroesophageal acid reflux [J].
Feldman, M ;
Cryer, B ;
Sammer, D ;
Lee, E ;
Spechler, SJ .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 1999, 277 (06) :G1159-G1164
[7]   TOTAL 24-HOUR GASTRIC-ACID SECRETION IN PATIENTS WITH DUODENAL-ULCER - COMPARISON WITH NORMAL SUBJECTS AND EFFECTS OF CIMETIDINE AND PARIETAL-CELL VAGOTOMY [J].
FELDMAN, M ;
RICHARDSON, CT .
GASTROENTEROLOGY, 1986, 90 (03) :540-544
[8]   GASTRIC-ACID SECRETION RATE AND BUFFER CONTENT OF STOMACH AFTER EATING - RESULTS IN NORMAL SUBJECTS AND IN PATIENTS WITH DUODENAL-ULCER [J].
FORDTRAN, JS ;
WALSH, JH .
JOURNAL OF CLINICAL INVESTIGATION, 1973, 52 (03) :645-657
[9]   Cisapride inhibits meal-stimulated gastric acid secretion and post-prandial gastric acidity in subjects with gastro-oesophageal reflux disease [J].
Gardner, JD ;
Rodriguez-Stanley, S ;
Robinson, M ;
Miner, PB .
ALIMENTARY PHARMACOLOGY & THERAPEUTICS, 2002, 16 (10) :1819-1829
[10]   Measurement of meal-stimulated gastric acid secretion by in vivo gastric autotitration [J].
Gardner, JD ;
Ciociola, AA ;
Robinson, M .
JOURNAL OF APPLIED PHYSIOLOGY, 2002, 92 (02) :427-434