Preoperative Gastric Acid Secretion Defines a Subgroup of Patients with High-Risk to Develop Barrett’S Esophagus in the Esophageal Stump After Esophagectomy for End Stage Chagasic Achalasia
Julio R. Da Rocha*1, Ulysses Ribeiro1, SéRgio Szachnowicz1, Elisa R. Baba1,2, Adriana V. Safatle-Ribeiro1, Kiyoshi Iriya2, Ary Nasi1, Rubens Sallum1, Ivan Cecconello1
1Gastroenterology, University of São Paulo, São Paulo, Brazil; 2Pathology, University of São Paulo, São Paulo, Brazil
Subtotal esophagectomy and gastric pull-up with cervical anastomosis is the main treatment for end stage achalasia. This surgical technique has been associated to esophagitis and also Barrett’s epithelium in the esophageal stump following esophagectomy. The contributing factors to Barrett’s esophagus development in this situation are not completely known. Aim: To determine the involvement of preoperative conditions, regarding gastric secretory and hormonal response, in the appearance of Barrett’s esophagus in the esophageal stump, in patients who underwent subtotal esophagectomy for end stage chagasic achalasia. Methods: 101 patients submitted to esophagectomy and cervical gastric pull-up were followed-up prospectively for a mean of 10.5 + 8.8 years. All patients underwent clinical, endoscopic and histopathologic evaluation every two years. Thirty-six patients (35.6%) had developed columnar metaplasia during follow-up. Gastric acid secretion in basal condition and after pentagastrin stimulation, serum pepsinogen levels in basal condition and after betazole stimulation, and basal gastrin serum levels were measured preoperatively in 15 patients with end stage chagasic achalasia who have developed Barrett’s esophagus, and the results were compared to 25 chagasic achalasia patients who did not have Barrett’s esophagus. Results: In the Barrett’s group, the mean basal and pentagastrin stimulated gastric acid secretion was significantly higher than in the non Barrett’s group (basal: 1.52 vs. 1.04, p = 0.04, stimulated: 19.40 vs. 13.78, p = 0.03). Basal and stimulated pepsinogen were increased at the Barrett’s group compared to non Barrett’s group (Basal = 94.1 vs., 66.1, p = 0.03; stimulated = 139.3 vs. 101.4, p = 0.04). There was no difference in serum gastrin between the two groups. Moreover, gastritis was present during endoscopic examination in 60% of the Barrett’s group, while it was detected only in 16% of the non Barrett’s group, p = 0.006. Conclusions: 1. Barrett’s esophagus in the esophageal stump was associated to the preoperative levels of gastric acid secretion and serum pepsinogen; 2. The presence of gastritis in the transposed stomach, probably due to exposure to duodenogastric reflux, may indicate higher risk for developing Barrett in the esophageal stump.
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