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Barrett's esophagus can develop after antireflux surgery

Barrett-Ösophagus nach Antireflux-Chirurgie

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Zusammenfassung

GRUNDLAGEN: Antireflux-Chirurgie stellt eine gute Alternative zur medikamentösen Therapie der gastroösophagealen Refluxkrankheit (GERD) ohne Barrett-Ösophagus (BE) dar, bei denen sie die Entstehung eines BE verhindern soll. Diese Studie untersuchte die Entstehung von BE nach Antireflux-Chirurgie. METHODIK: Von 115 Personen ohne BE vor der Operation haben 12 (10,4 %) eine intestinale Metaplasie entwickelt und wurden mittels Endoskopie, Histologie und Funktionsdiagnostik untersucht. ERGEBNISSE: Die 12 Personen hatten durchschnittlich 5 Endoskopien mit Biopsien. Symptome bestanden bei 10 (83 %) Patienten 80 Monate nach der OP. Die Nachsorge betrug im Mittel 135 Monate. Vier Personen hatten keinen Reflux beim pH und Bilitec Monitoring; 8 Patienten hatten pathologischen Reflux. Es gab keinen Unterschied zwischen jenen mit normaler und pathologischer Refluxaktivität bezüglich Endoskopie, Histologie und Manometrie. Eine intestinale Metaplasie entstand in 58–90 Monaten ausgehend von cardiac oder oxyntocardiac mucosa. Vier Personen hatten eine Regression von intestinaler Metaplasie zu cardaic mucosa nach intensiver medikamentöser Therapie. SCHLUSSFOLGERUNGEN: Antireflux-Chirurgie kann die Entstehung eines BE in 10 % der Fälle nicht verhindern, wobei 1/3 der Personen pathologischen Reflux hatten. Mittels Histopathologie kann eine Progression von oxyntocardiac und cardaic mucosa zur intestinalen Metaplasie bzw. Dysplasie und Karzinom bzw. Regression vom BE zur cardiac und odyntocardiac mucosa monitiert und mit der Funktionsdiagnostik korreliert werden.

Summary

BACKGROUND: Surgical treatment in patients with gastroesophageal reflux disease (GERD) without Barrett's esophagus (BE) is an excellent alternative therapy to medical treatment, preventing the development of complications and the appearance of BE. PURPOSE: To determine the newly developed BE in a group of patients without BE prior to surgery, the patients were submitted to a late subjective and objective follow-up. METHODS: From 115 non-BE patients submitted to surgery and followed up for a long period, 12 (10.4%) developed intestinal metaplasia after operation. They were submitted to endoscopic, histologic, manometric and functional studies (24-h pH and Bilitec). RESULTS: The 12 patients had an average of 5 endoscopies after surgery with several biopsy samples. Symptoms of recurrent reflux were present in only 10 patients (83%) at a mean of 80 months after surgery. The mean follow-up was 135 months. Four patients showed the absence of pathologic reflux measured by 24-h pH and Bilitec monitoring, while 8 had the presence of abnormal acid reflux. There were no significant differences between endoscopic, histologic and functional studies comparing patients with the presence or absence of pathologic reflux. The time of appearance to intestinal metaplasia from cardiac or oxynto–Cardiac mucosa was 58–90 months. Four patients showed regression of intestinal metaplasia to cardiac mucosa after intensive medical treatment. CONCLUSIONS: Antireflux surgery in patients without BE does not prevent the late appearance of BE in near 10% of the cases, provided that a long-term follow-up is performed and several endoscopic and histologic evaluations are repeated. Near 2/3 of these patients showed the presence of acid reflux, while 1/3 showed no abnormal reflux. With this method of follow-up, metaplastic changes from cardiac to intestinal metaplasia and from intestinal metaplasia to low-grade dysplasia can be documented, as well as regression from intestinal metaplasia to cardiac mucosa.

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Authors and Affiliations

  1. Departments of Surgery and Pathology, University Hospital, Santiago de Chile, Chile

    A. Csendes, G. Smok, P. Burdiles, I. Braghetto & A. Henriquez

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  1. A. Csendes
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  2. G. Smok
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  3. P. Burdiles
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  4. I. Braghetto
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  5. A. Henriquez
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Correspondence to A. Csendes.

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Csendes, A., Smok, G., Burdiles, P. et al. Barrett's esophagus can develop after antireflux surgery. Eur Surg 40, 245–252 (2008). https://doi.org/10.1007/s10353-008-0426-9

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  • DOI: https://doi.org/10.1007/s10353-008-0426-9

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