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

T. M. Farrell, S. B. Archer, R. E. Metreveli, C. D. Smith, John Hunter

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)937-941
Number of pages5
JournalSurgical Endoscopy and Other Interventional Techniques
Volume15
Issue number9
DOIs
StatePublished - 2001
Externally publishedYes

Fingerprint

Barrett Esophagus
Mucous Membrane
Pathologic Constriction
Esophageal Stenosis
Fibrosis
Therapeutics
Histology
Esophageal Perforation
Esophagogastric Junction
Traction
Anorexia
Barium
Gastroesophageal Reflux
Gastric Mucosa
Esophageal Mucosa
Weight Loss
Stomach
Swine
Pathology
Weights and Measures

Keywords

  • Barrett's esophagus
  • Esophageal mucosa
  • Fibrosis
  • Gastroesophageal reflux disease
  • Metaplasia
  • Mucosal resection
  • Porcine model
  • Stricture

ASJC Scopus subject areas

  • Surgery

Cite this

Resection and advancement of esophageal mucosa : A potential therapy for Barrett's esophagus. / Farrell, T. M.; Archer, S. B.; Metreveli, R. E.; Smith, C. D.; Hunter, John.

In: Surgical Endoscopy and Other Interventional Techniques, Vol. 15, No. 9, 2001, p. 937-941.

Research output: Contribution to journalArticle

Farrell, T. M. ; Archer, S. B. ; Metreveli, R. E. ; Smith, C. D. ; Hunter, John. / Resection and advancement of esophageal mucosa : A potential therapy for Barrett's esophagus. In: Surgical Endoscopy and Other Interventional Techniques. 2001 ; Vol. 15, No. 9. pp. 937-941.
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AU - Archer, S. B.

AU - Metreveli, R. E.

AU - Smith, C. D.

AU - Hunter, John

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AB - 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.

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KW - Stricture

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