Correlation between basal acid output and daily ranitidine dose required for therapy in Barrett's esophagus

Abstract

We prospectively evaluated basal gastric acid secretion in 42 consecutive patients with Barrett's esophagus to determine the optimal dose requirement for an H2-receptor antagonist in relation to the gastric acid secretory status of each patient. All patients with Barrett's esophagus had pyrosis and 31 of the 42 patients had erosive esophagitis. Mean extension of Barrett's epithelium was 6.9 cm (range 2-17 cm). Mean basal acid output for the patients with Barrett's esophagus was 8.0 +/- 5.2 meq/hr, which was significantly different compared to a group of 65 normal subjects with mean basal acid output of 3.0 +/- 2.7 meq/hr (P less than 0.001). There was no correlation between basal acid output and extension of Barrett's epithelium. All patients with Barrett's esophagus were treated with ranitidine, with 24 requiring standard-dose (300 mg/day) and 18 requiring increased doses (mean 1170 mg/day, range 600-2400 mg/day) for complete healing of esophagitis and disappearance of pyrosis. There was a significant correlation between basal acid output and daily ranitidine dose required for therapy (r = 0.52, P less than 0.001). Fifteen of the 42 patients with Barrett's esophagus (36%) had gastric acid hypersecretion. There was a significant association between gastric acid hypersecretion defined as a basal acid output of greater than 10.0 meq/hr and a requirement for increased daily ranitidine doses (greater than 300 mg/day) (P less than 0.0002). No side effects occurred with any of these high doses of ranitidine. We conclude that as a group, patients with Barrett's esophagus have significantly higher basal acid outputs than normal subjects and many require increased therapeutic doses of ranitidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Cisapride inhibits meal‐stimulated gastric acid secretion and post‐prandial gastric acidity in subjects with gastro‐oesophageal reflux disease

“…Although the inhibition of gastric acid secretion is known to decrease the time that the oesophageal pH < 4, 8,[36][37][38] gastric acidity has received limited attention with respect to its potential underlying role in oesophageal acid exposure in GERD. [39][40][41][42][43][44][45] The present finding that cisapride decreases post-prandial oesophageal acid exposure in subjects with GERD agrees with previous findings by others, [11][12][13][14][15] who have attributed this action of cisapride to its motility effects on the lower oesophageal sphincter pressure, oesophageal peristalsis and gastric emptying. [11][12][13][14][15] Our present results, however, indicate that the decrease in oesophageal acidity can be explained by a cisapride-induced decrease in gastric acidity.…”

Time series analysis of gastric acid secretion over a 20-year period in normal Japanese men

“…Previous studies reported that the gastric acid secretion level in erosive esophagitis patients is higher than that in controls [2][3][4][5], although one study did not agree with this [6]. In particular, a study successfully demonstrated that gastric acid secretion is associated with erosive esophagitis independent of other well-recognized contributors for GERD, esophageal motility dysfunction such as disorders of the lower esophageal sphincter, or esophageal peristalsis [7].…”

Esophageal motility and gastric acid secretion in patients with Barrett's esophagus

“…There have been some reports with regard to gastric acid secretion in patients with BE [18,19]. Collen and Johnson [18] have reported that basal acid output in patients with BE was signifi cantly higher than that of normal subjects; however, in that study the male/female ratio and age differed between the groups.…”