Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Mucosa
 The
 Esophagogastric  Junction
 Barrett's
 Esophagus

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OESO©2015
 
Volume: Barrett's Esophagus
Chapter: Pathophysiology
 

In patients with esophagitis, does gastric surgery increase the prevalence of Barrett's esophagus?

P. Parrilla, L.F. Martínez de Haro, A. Ortiz, R. Lirón, V. Munitiz (Murcia)

Although various clinical and experimental studies [1-13] suggest that duodenogastroesophageal reflux is involved in the pathogenesis of Barrett's esophagus and its related complications, there are still controversial aspects. One of these is to determine whether pancreatic-biliary reflux needs concomitant pathological acid reflux in order to exercise its harmful effects. Furthermore, it is a well known fact that patients who undergo gastric surgery that destroys or distorts the pylorus have abundant duodenogastric reflux [14-16], with the consequent presence of bile to flow to the esophagus. Moreover, such surgery, due to the vagotomy or antrectomy, causes a significant decrease in gastric secretion. Therefore, this is a very useful experimental model for seeing the harmful effect of pancreatic-biliary reflux to the esophagus in patients with decreased gastric secretion.

In order to compare the prevalence of Barrett's esophagus in patients with an intact stomach and in patients with an operated stomach, we made a retrospective study [17] in which 22,236 upper digestive endoscopy reports were reviewed and classified into two groups: intact stomach (n = 21,023) and operated stomach (n = 1,213). In turn, the latter was divided into five subgroups according to surgical techniques:
- bilateral truncal vagotomy plus pyloroplasty (n = 444);
- distal partial gastric resection with gastrojejunostomy (Billroth II) (n = 445);
- distal partial gastric resection with gastroduodenostomy (Billroth I) (n = 211);
- bilateral truncal vagotomy plus gastrojejunostomy (n = 59); -total gastrectomy with Roux-en-Y gastrojejunostomy (n = 54).

The number and percentage of cases of esophagitis in each of the groups (intact and operated stomach) were calculated. The number and percentage of cases of Barrett's esophagus (complicated or not) in relation to the number of patients with esophagitis were also calculated. The same calculations were made for the five operated-stomach subgroups. Comparisons were made between intact stomach and operated stomach overall and between intact stomach and each of the operated stomach subgroups. The parameters compared were: percentage of patient total with esophagitis, percentage of esophagitis patients with Barrett's esophagus, and percentage of Barrett's esophagus patients with complications. The ?2 test was used to compare ratios.

Our results showed that the percentage of esophagitis was significantly higher (p < 0.05) in patients with an intact stomach (19.5%) than in the operated stomach group (12.4%) considered overall. This difference may be related to the decrease in acid secretion and accelerated gastric emptying in patients with previous gastric surgery or to the fact that the percentage of patients in whom endoscopy was indicated for esophageal symptoms was higher (30%) in the intact stomach group than in the operated stomach group (15%). However, we believe that differences between the two groups with regard to indications for endoscopy do not necessarily influence the aim of the study, which was to assess the percentage of esophagitis patients with Barrett's esophagus. The results in comparing intact stomach with operated stomach according to surgical technique are shown in Table I.

Table I. Results in comparing intact stomach with operated stomach according to surgical technique.

When we compared the percentages of esophagitis patients with Barrett's esophagus, our results showed that this percentage was higher in the operated patients (3.3%) considered overall, than in the patients with an intact stomach (2.6%), although the differences were not statistically significant. In the same way, the percentage of total Barrett's esophagus cases with complications was also higher among patients with an operated stomach (80%) than among those with intact stomach (44.8%) but the differences were not statistically significant. Despite there being no differences, our results do not allow us to exclude the influence of bile and pancreatic juice on the genesis of Barrett's esophagus, because gastric surgery patients have, together with a greater amount of duodenal contents to flow to the esophagus, a smaller amount of gastric acid juice due to the vagotomy, antrectomy, or removal of the acid secreting portion. The duodenal contents may favour the appearance of Barrett's esophagus or its related complications, but may also need the acid juice that has been reduced in the gastric surgery patients.

In conclusion, our results suggest that previous gastric surgery, in spite of increasing the rate of duodenogastric reflux, with the duodenal contents in a position to flow toward the esophagus, does not modify the prevalence of Barrett's esophagus in pateints with esophagitis.

References

1. Gillen P, Keeling P, Byrne PJ, et al. Implication of duodenogastric reflux in the pathogenesis of Barrett' oesophagus. Br J Surg 1988;75:540-543.

2. Attwood SE, De Meester TR, Bremner CG, et al. Alkaline gatroesophageal reflux: implications in the development of complications in Barrett's columnar-lined lower esophagus. Surgery 1989;106:764-770.

3. Richter JE. Barrett's esophagus: too much acid, alkali, or both? Gastroenterology 1990;98:798.

4. Waring JP, Legrand J, Chinichian A, et al. Duodenogastric reflux in patients with Barrett's esophagus. Dig Dis Sci 1990;35:759-762.

5. Attwood SE, Ball CS, Barlow AP, et al. Role of intragastric and intraoesophageal alkalinization in the genesis of complications in Barrett's columnar-lined lower oesophagus. Gut 1993;34:11-15.

6. Iftikhar SY, Evans DF, Steele RJC, et al. Bile reflux in Barrett's oesophagus. Gut 1991;32:A554.

7. Champion G, Richter JE, Vaezi MF, et al. Duodenogastroesophageal reflux: relationship to pH and importance in Barrett's esophagus. Gastroenterology 1994;107:747-754.

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

9. Kauer WKH, Peters JH, De Meester TR, et al. Mixed reflux of gastric and duodenal juices is more harmful to the esophagus than gastric juice alone. The need for surgical therapy re-emphasized. Ann Surg 1995;222:525-533.

10. Caldwell MTP, Lawlor P, Byrne PJ, Walsh TN, Hennessy TPJ. Ambulatory oesophageal bile reflux monitoring in Barrett's oesophagus. Br J Surg 1995;82:657-660.

11. Gillen P, Keeling P, Byrne PJ, et al. Experimental columnar metaplasia in the canine oesophagus. Br J Surg 1988;75:113115.

12. Seto Y, Kobori O. The role of reflux oesophagitis and acid in the development of columnar epithelium in the rat oesophagus. Br J Surg 1993;80:467-470.

13. Pera M, Trastek VF, Carpenter HA, et al. Influence of pancreatic and biliary reflux on the development of esophageal carcinoma. Ann Thorac Surg 1993;55:1386-1392.

14. Robles R, Parrilla P, Luján JA, et al. Quantification of duodenogastric reflux in gastroduodenal peptic ulcer and in gastric operated patients using a 24-h gastric pH measurement as a quantification technique. Br J Surg 1990;77:428-431.

15. Parrilla P, Luján JA, Robles R, et al. Duodenogastric reflux quantification in peptic ulcer surgery: comparison between different surgical techniques. Surgery 1993;113:43-47.

16. Poxon V, Hogg B, Youngs D, et al. Incidence of bile reflux in gastric ulcer and after partial gastrectomy. Br J Surg 1986;73:295-297.

17. Parrilla P, Lirón R, Martínez de Haro LF, et al. Gastric surgery does not increase the risk of developing Barrett's esophagus. Am J Gastroenterol 1997;92:960-963.


Publication date: August 2003 OESO©2015