To the Editor:
We read with interest the article by Rossi et al,1 in the January 2006 issue of Annals of Surgery. The work profoundly adds to our knowledge on the management of gastroesophageal reflux disease (GERD).2 The importance and actuality of the paper for clinical routine are 2-fold: the data indicate that surgery is more potent than medical therapy for regression of low-grade dysplasia, thus “reducing” the risk to develop adenocarcinoma of the esophagus.3,4 Second, although dysplasia regresses, individuals will still have to undergo surveillance since biopsy sampling error (due to patchy distribution of dysplastic areas within columnar lined esophagus) and relapse of dysplasia can never be ruled out.1,3,4
The advantage of antireflux surgery is inhibition of both acidic and nonacidic reflux.2,4 In contrast, treatment with proton pump inhibitor only affects the pH, but not the volume of reflux. This has been recently demonstrated by use of multichannel intraluminal impedance technology.5,6 In keeping with recent clinical studies,2–4 Rossi et al1 provide additional evidence in favor of the notion that development of esophageal columnar metaplasia and dysplasia is in fact triggered by a mechanism involving both acid and bile, and that bile may be more carcinogenic (at less acidic pH). However, concerning interpretation of the data, it should be considered that Rossi et al1 compared fundoplication versus administration of 20 mg omeprazole twice daily. For example, 80% inhibition of gastric acid secretion is achieved after administration of 40 mg of esomeprazole twice daily, when compared with 73% inhibition with 20 mg twice daily.5 Successful antireflux surgery represents the most effective therapy against gastroesophageal reflux; 20 mg omeprazole does not represent maximal medical treatment available. Therefore, future studies should compare fundoplication versus maximal effective proton pump inhibitor doses (ie, 40 mg twice daily). Only then we will provide “fair” data for those, who still do not believe that successful antireflux surgery is more effective than medical treatment in reducing the oncologic risks of GERD.1–4
Johannes Lenglinger, MD
Margit Eisler, MD
Martin Riegler, MD
Manometry Lab & Department of General Surgery
University Clinic of Surgery
Medical University Vienna
Vienna, Austria
franz.riegler@meduniwien.ac.at
REFERENCES
- 1.Rossi M, Barreca M, de Bortoli N, et al. Efficacy of Nissen fundoplication versus medical therapy in the regression of low grade dysplasia in patients with Barrett esophagus. Ann Surg. 2006;243:58–63. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Wykypiel H, Gadenstätter M, Granderath FA, et al. Pathophysiology of gastroesophageal reflux disease (GERD) with respect to reflux induced carcinogenesis. Eur Surg. 2002;34:296–302. [Google Scholar]
- 3.Öberg S, Wenner J, Johansson J, et al. Barrett esophagus: risk factors for progression to dysplasia and adenocarcinoma. Ann Surg. 2005;242:49–54. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Csendes A, Bragetho I, Burdiles P, et al. Regression of intestinal metaplasia to cardiac or fundic mucosa in patients with Barrett's esophagus submitted to vagotomy, partial gastrectomy and duodenal diversion: a prospective study of 78 patients with more than 5 years of follow up. Surgery. 2006;139:46–53. [DOI] [PubMed] [Google Scholar]
- 5.Tamhankar AP, Peters JH, Portale G, et al. Omeprazole does not reduce gastroesophageal reflux: new insights using multichannel intraluminal impedance technology. J Gastrointest Surg. 2004;8:890–897. [DOI] [PubMed] [Google Scholar]
- 6.Kahrilas PJ. Is stringent control of gastric pH useful and practical in GERD? Aliment Pharmacol Ther. 2004;20(suppl 5):89–94. [DOI] [PubMed] [Google Scholar]