Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Esophagogastric  Junction

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Volume: Barrett's Esophagus
Chapter: Pathophysiology

Is gastric secretion different in Barrett patients and in patients with reflux esophagitis?

M. Fein, K.H. Fuchs, S.M. Freys (Würzburg)

Patients with Barrett’s esophagus have the highest prevalence of an incompetent lower esophageal sphincter and frequently an esophageal motility disorder [1, 2]. As a consequence, these patients have a higher esophageal exposure to acid and to duodenal juice when compared to other patients with gastroesophageal reflux disease (GERD) [3, 4]. Beside the well known functional defects at the gastroesophageal junction it is unknown whether the increased esophageal exposure to acid or duodenal juice is also related to an increased gastric acid secretion or pathologic duodenogastric reflux. Additional gastric pathology may be particularly relevant for the treatment of patients with Barrett’s esophagus. The amount of gastric secretion in patients with Barrett’s esophagus is evaluated here.

Measurements of gastric secretion

In the first study on gastric acid secretion, 42 patients with Barrett's esophaguswere compared to 65normal subjects [5]. The results of this study are summarized in Table I. Gastric secretion (basal acid output) was significantly higher in patients withBarrett's esophagus. Ofnote, the male/female ratio

Table I. Gastric acid secretion in normal subjects and in patients with Barrett's esophagus.

and the age were different between the two groups. Furthermore, it was not mentioned if any of these patients had duodenal ulcer or Zollinger-Ellison (ZE) syndrome. Because all these parameters might have influenced the measurement, the second study on gastric acid secretion was conducted with 'appropriate controls' [6]. In this study, 30 patients with Barrett's esophagus were evaluated in comparison to matched controls with respect to age and sex as well as to conditions like duodenal ulcer, that may affect secretion independently. Moreover, cases were also matched for the presence of esophagitis so that the only difference between the groups was the presence and absence of Barrett's epithelium. The results are listed in Table II. In contrast to the first study, no differences in gastric acid secretion were found in any of the comparisons. Among the group with no

Table II. Gastric acid secretion in patients with gastroesophageal reflux disease with and without Barrett's esophagus.

duodenal ulcer, the (nonsignificant) numerical difference in basal acid outpout (BAO) would be further reduced by a correction for the 20% weight difference between the two groups. In summary, by matching the controls as closely as possible, no difference was found in basal or maximum acid secretion and in gastrin serum level. The discrepancy between the first and the second study arises mainly from the influence of background disease such as duodenal ulcer of ZE syndrome, which affects gastric secretion independent of the GERD. Furthermore, the control group were normal subjects in the first study and patients with reflux esophagitis in the second.

Gastric pH monitoring

The functional assessment of the patients with GERD in Würzburg includes gastric pH monitoring. One hundred eighty nine patients with documented reflux disease were evaluated and classified according to the endoscopic findings. Patients with gastric or duodenal ulcer or ZE syndrome had been excluded. The results are listed in Table III. In accordance to the second study on gastric acid secretion, there was no significant difference between the three groups of patients with GERD, indicating that the gastric acid secretion is comparable between patients with Barrett's esophagus and patients with reflux esophagitis.

Table III. Gastric pH monitoring in patients with gastroesophageal reflux disease.


In summary, gastric secretion was not different between patients with Barrett's esophagus and patients with reflux esophagitis. With regard to the possible role of acid in causing Barrett's esophagus, there is little convincing evidence that the amount of gastric acid secretion is related to the new development or the progression of Barrett's esophagus. The extent of Barrett's esophagus appears to be uninfluenced by either reducing acid exposure or failing to do so [7, 8]. Moreover, hypersecretion of acid per se is not a likely determinant of Barrett's, since the three cases of hypersecretion mentioned in the study of Hirschowitz were the only cases of Barrett's among over 100 patients who had extreme hypersecretion (BAO > 15 meq/hr) [6]. It is also unlikely that the amount of acid secretion in any way influences the process of carcinogenesis in Barrett's esophagus either in its initiation or progression. The new development or the progression of Barrett's seem to require esophageal reflux of duodenal juice [9, 10], which had been shown to act synergistically with the acid reflux [11]. Furthermore, the importance of gastroduodenal reflux for cancer development had been demonstrated especially in animal models [12, 13].


Present studies showed no significant difference in acid secretion between patients with Barrett's esophagus and patients with reflux esophagitis. Consequently, the pathophysiology of Barrett's esophagus could not be related to the gastric secretory status. The need for higher dosages for proton pump inhibitors (PPI) in some patients with reflux disease may be partially influenced by gastric acid secretion in these patients. Higher dosages are also driven by other factors such as reduced compliance, PPI resistance, or rapid PPI metabolism by the cytochrome P450 system [14]. Independent of the question about gastric acid secretion, the development of dysplasia and cancer complicating Barrett's esophagus may well be a separate problem requiring more than control of acid exposure.


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2. Stein HJ, Barlow AP, DeMeester TR, Hinder RA. Complications of gastroesophageal reflux disease:Role of the lower esophageal sphincter, esophageal acid and acid/alkaline exposure, and duodenogastric reflux. Ann Surg 1992;216:3543.

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5. Collen MJ, Johnson DA. Correlation between basal acid output and daily ranitidine dose required for therapy in Barrett's esophagus. Dig Dis Sci 1992;37:570-576.

6. Hirschowitz BI. Gastric acid and pepsin secretion in patients with Barrett's esophagus and appropriate controls. Dig Dis Sci 1996;41:1384-1391.

7. Sampliner RE, Hixson LJ, Fennerty MB, Garewal HS. Regression of Barrett's esophagus by laser ablation in an anacid environment. Dig Dis Sci 1993;38:365-368.

8. Williamson WA, Ellis FH, Gibb SP, Shahian DM, Aretz HT. Effect of antireflux operation on Barrett's mucosa. Ann Thorac Surg 1990;49:537-541.

9. Attwood SE, Smyrk TC, DeMeester TR, Mirvish SS, Stein HJ, Hinder RA. Duodenoesophageal reflux and the development of esophageal adenocarcinoma in rats. Surgery 1992;111:503-510.

10. Miwa K, Sahara H, Segawa M, Kinami S, Sato T, Miyazaki I, Hattori T. Reflux of duodenal or gastro-duodenal contents induces esophageal carcinoma in rats. Int J Cancer 1996;67:269-274.

11. Vaezi MF, Richter JE. Synergism of acid and duodenogastroesophageal reflux in complicated Barrett's esophagus. Surgery 1995;117:699-704.

12. Fein M, Peters JH, Baril N, McGarvey M, Chandrasoma P, Shibata D, Laird PW, Skinner KA. Loss of function of Trp53, but not Apc, leads to the development of adenocarcinoma in mice with jejunoesophageal reflux. J Surg Res 1999;83:4855.

13. Chen X, Ding YW, Yang G, Bondoc F, Lee MJ, Yang CS. Oxidative damage in an esophageal adenocarcinoma model with rats. Carcinogenesis 2000;21:257-263.

14. Fass R, Sampliner RE, Malagon IB, Hayden CW, Camargo L, Wendel CS, Garewal HS. Failure of oesophageal acid control in candidates for Barrett's oesophagus reversal on a very high dose of proton pump inhibitor. Aliment Pharmacol Ther 2000;14:597-602.

Publication date: August 2003 OESO©2015