Metaplastic Columnar Mucosa in the Cervical Esophagus After Esophagectomy

Abstract

ObjectiveTo evaluate the pathogenesis of metaplastic processes within the esophagus using a human model in which the exact duration of reflux was known. Summary Background DataThe pathogenesis of Barrett's esophagus (BE) is incompletely understood. Patients undergoing esophagectomy and gastric tube reconstruction represent a good model for studying the pathophysiology of columnar cell metaplasia of the human esophagus because the cervical esophagus is rarely or never exposed to gastric contents before the surgical procedure. MethodsThirty-two patients underwent manometry, simultaneous 24-hour pH and bilirubin monitoring, and endoscopy with biopsy 3 to 10.4 years after esophagectomy. The presence of columnar mucosa in the cervical esophagus was confirmed on histologic examination. The findings on endoscopy and histology were related to clinical data and the results of pH and bilirubin monitoring 1 cm proximal to the esophagogastrostomy. ResultsFifteen (46.9%) of the 32 patients had metaplastic columnar mucosa within their cervical esophagus. Metaplasia was significantly more common in patients with a preoperative diagnosis of BE. The length of metaplastic mucosa correlated significantly with the degree of esophageal acid exposure, but the presence of abnormal bilirubin exposure was unrelated to the presence of metaplasia. The prevalence of metaplasia did not change with increasing time. Intestinal metaplasia was found within the columnar-lined segment in three patients 8.5, 9.5, and 10.4 years after esophagectomy. All patients with intestinal metaplasia had abnormal exposure of both acid and bilirubin, but the presence of combined reflux was not significantly higher in these patients compared with patients with nonintestinalized segments of columnar mucosa. ConclusionsEsophageal columnar metaplasia is a common complication after gastric pull-up esophagectomy. Metaplasia is more likely to develop in patients with previous BE than other patients. Metaplasia develops in response to squamous epithelial injury in predisposed individuals.The clinical significance of Barrett's esophagus (BE) lies in its association with esophageal adenocarcinoma. The risk for this lethal malignancy has been reported to be 40 to 125 times greater in patients with BE compared with the normal population.1-3 The pathogenesis of BE is incompletely understood, but the condition is commonly believed to be the result of damaged squamous epithelium being replaced by cardiac-or junctional-type mucosa within which, over time and with persistent inflammation, intestinal metaplasia develops. 4-9Patients who have undergone esophagectomy and gastric tube reconstruction have an anastomosis between the cervical esophagus and the stomach in which the normal squamous epithelium of the esophagus is interposed to the acid-secreting mucosa of the gastric body. The reconstruction allows acid and duodenal juice to reflux from the gastric conduit to the remaining proximal esophagus, acting as model of gastroesophageal reflux. Both experimental and clinical stud...

Barrett’s Esophagus and Cardiac Intestinal Metaplasia: Two Conditions within the Same Spectrum

“…El-Serag et al (33) and Goldblum et al (34) suggest that gastroesophageal reflux disease is not a risk factor for CIM. On the other hand, Oberg et al (35) reported the development of cardiac mucosa (with some proceeding to IM) in the proximal esophagus after esophagectomy, suggesting that this is an acquired condition related to acid exposure. Interestingly, Sharma et al (16) found that there was a higher prevalence and incidence of dysplasia in their short segment BE group than in their CIM group (11.3% versus 4.6%, respectively).…”

Non-conventional surgical approach to achalasia: mucosectomy and endomuscular pull-through

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Early Diagnostic Biomarkers for Esophageal Adenocarcinoma—The Current State of Play

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