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Frequency analyses of gastric pH in control and gastro‐oesophageal reflux disease subjects treated with a proton‐pump inhibitor
Author(s) -
Gardner J. D.,
Sloan S.,
Robinson M.,
Miner Jr P. B.
Publication year - 2004
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.2004.02279.x
Subject(s) - gastro , medicine , reflux , proton pump inhibitor , gastroenterology , proton pump , disease , esophageal disease , esophagus , biochemistry , chemistry , atpase , enzyme
Summary Background : We are unaware of any solid theoretical or pathophysiological basis for selecting pH 4 or any other pH value to assess gastric acidity. Aim : To examine the frequency of different gastric pH values in control and GERD subjects. Methods : Gastric pH was measured for 24 h in 26 control subjects, 26 gastro‐oesophageal reflux disease subjects at baseline and the same 26 gastro‐oesophageal reflux disease subjects during treatment with a proton‐pump inhibitor. Histograms were constructed using the 21 600 values generated from each recording and bins of 0.25 pH units. Results : The distribution of gastric pH values in gastro‐oesophageal reflux disease subjects was significantly different from that in controls and in some instances the distributions detected significant differences that were not detected by integrated acidity. Proton‐pump inhibitor treatment significantly altered the distribution of gastric pH values and the nature of this alteration during the postprandial period was different from that during the nocturnal period. Using time pH≤4 can significantly underestimate the magnitude of inhibition of gastric acidity caused by a proton‐pump inhibitor. Conclusions : The distribution of gastric pH values provides a rationale for selecting a particular pH value to assess gastric acidity. In some instances, the distribution of gastric pH values detects significant differences between gastro‐oesophageal reflux disease and normal subjects that are not detected by integrated acidity.