Resection and advancement of esophageal mucosa. A potential therapy for Barrett's esophagus.

BACKGROUND: Barrett's esophagus affects 5-10% of patients with gastroesophageal reflux disease (GERD) and is associated with a 40-fold increased risk of malignant transformation. Ablative therapies may lead to esophageal perforation or stricture formation if applied too liberally and residual glandular tissue and persistent cancer risk if utilized too sparingly.
METHODS: Ten pigs underwent gastrotomy. Mucosa below the gastroesophageal (GE) junction was elevated by saline injections, circumferentially incised, and secured to an orogastric tube. By traction, the distal esophageal mucosa was inverted 10 cm proximally, then returned to the gastric lumen. In group A (n = 4), the mucosa (5 cm) was resected and the remnant was allowed to retract. In group B (n = 4), the mucosa was simply sutured back into its native position. In group C (n = 2), the mucosa (5 cm) was resected and the proximal segment was advanced and sutured to the gastric mucosa. At 6 weeks, or sooner if stricture developed, the animals were killed. Stricture formation was determined by ex vivo barium esophagram and gross assessment. The extent of fibrosis and epithelial healing were established histologically.
RESULTS: Group A (mucosa resected) developed weight loss and anorexia within 4 weeks. Pathology revealed dense fibrotic stricture without reepithelialization. Group B (mucosa elevated/replaced) gained weight after the operation. Histology demonstrated mucosal healing without significant stricture or fibrosis. Group C (mucosa resected/advanced) also thrived postoperatively. Histology confirmed mucosal healing without evidence of retraction or dense stricture.
CONCLUSIONS: Exposure of submucosal tissues causes esophageal stricture. Mucosal coverage minimizes submucosal fibrosis after injury. Mucosal resection and advancement allows healing without stricture and may have therapeutic potential for patients with Barrett's esophagus.