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T R DeMeester, Twenty-four hour pH score is still useful after 45 years, Diseases of the Esophagus, Volume 32, Issue 5, May 2019, doy134, https://doi.org/10.1093/dote/doy134
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Nearly a half century ago, 24-hour esophageal pH monitoring was introduced as a method to identify, in a near-physiologic setting, patients with increased esophageal acid exposure.1 It did so by measuring the frequency and duration of acid exposure to the mucosa of the esophagus. I felt a quiet sense of personal pleasure learning from the article by Neto, Herbella, Schlottmann, and Patti that 24-hour esophageal pH monitoring is still clinically useful from 44 years after its introduction in 1974. Its initial development was fostered by the disappointment in the correlation between the lower esophageal sphincter (LES) pressure and the presence of symptoms, endoscopic findings, and radiographic evidences of gastro-esophageal reflux disease (GERD). Consequently, practitioners were energized to quantify directly the amount of gastric acid that refluxed into the esophagus as a way of identifying patients with GERD. Achieving this goal was more arduous than thought.
It is important to emphasize that esophageal pH monitoring is not only a test to measure esophageal acid exposure, but also when and how that exposure occurred. To make this assessment required measuring the frequency and duration of esophageal reflux episodes below the pH of 4. This pH value was chosen on the basis of the landmark studies of Bernstein and Baker, and Tuttle and Grossman, both in 1958.2,3 Bernstein and Baker were the first to recognize the relationship between the presence of acid in the esophagus and symptoms of heartburn and regurgitation. They developed an acid perfusion test to reproduce the patient's esophageal symptoms by the instillation of 0.1 N HCl acid into the esophagus. Tuttle and Grossman attempted, with minimal success, to improve on the low specificity of the Bernstein test by directly measuring intraesophageal pH at rest and after the patient performed certain reflux provoking maneuvers. In 1961, Tuttle et al.4 showed that the onset of heartburn occurred when the intra-esophageal pH dropped to a value of <4. Four years later, in 1965, Piper and Fenton5 showed that the proteolytic enzyme pepsin was activated by an intraluminal esophageal pH of <4 and induced hemorrhagic erosive esophagitis. Together these studies identified that the critical determinant of GERD was exposure of the esophageal mucosa to a pH <4. Despite this discovery, it soon became apparent that just improving the ability to detect esophageal exposure to a pH <4 was of limited value in differentiating between normal subjects and patients with symptoms of GERD.
