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Newly developed Barrett's esophagus after subtotal esophagectomy.

par Franchimont, Denis ;Covas, A;Brasseur, Camille ;Van Laethem, Jean-Luc ;El Nakadi, Issam ;Devière, Jacques
Référence Endoscopy, 35, 10, page (850-853)
Publication Publié, 2003-10

Article révisé par les pairs

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Résumé :

BACKGROUND AND STUDY AIMS: More detailed information regarding the early mucosal events that lead to intestinal metaplasia would be very beneficial for understanding the pathogenesis of Barrett's esophagus (BE). Gastroesophageal reflux and duodenogastroesophageal reflux play a major role in the pathogenesis of Barrett's esophagus. The aim of this study was to investigate the prevalence of newly developed BE in patients who had previously undergone a subtotal esophagectomy - a clinical condition characterized by the absence of a lower esophageal sphincter and massive gastroesophageal reflux. PATIENTS AND METHODS: A retrospective examination was carried out on all patients who underwent subtotal esophagectomy (n = 87) listed in our institution's computer files from 1995 to 2000. Twenty-one patients were excluded due to missing data or no upper gastrointestinal endoscopy after surgery. RESULTS: Based on the Savary-Miller classification, 47 patients developed either type I (n = 2), II (n = 8), III (n = 11) or IV (n = 26) esophagitis after surgery. Newly developed BE was observed in nine patients (13.5 %) after subtotal esophagectomy (median time to diagnosis: 489 days, range 43 - 1172). None of the patients had persistent BE immediately after surgery, and two of the patients with newly developed BE had had no history of BE before surgery or at the time of surgery. Proton-pump inhibitor therapy after surgery and neoadjuvant chemotherapy did not appear to influence the development of BE after subtotal esophagectomy. CONCLUSIONS: Newly developed BE after subtotal esophagectomy may provide further insights into the early mucosal events that lead to intestinal metaplasia and into the roles of gastroesophageal and duodenoesophageal reflux in the pathogenesis of BE.