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首页> 外文期刊>Surgical Endoscopy >Resection and advancement of esophageal mucosa. A potential therapy for Barrett's esophagus.
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Resection and advancement of esophageal mucosa. A potential therapy for Barrett's esophagus.

机译：食管粘膜的切除和发展。巴雷特食管的一种潜在疗法。

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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.
机译：背景：巴雷特食管会影响5-10％的胃食管反流病（GERD）患者，并使其恶性转化的风险增加40倍。如果过于宽松地使用消融疗法，可能会导致食管穿孔或狭窄，而如果过于谨慎地使用，则可能会残留腺体组织并持续致癌。方法：十只猪接受了胃切除术。食管（GE）交界处下方的粘膜通过盐水注射而升高，沿周向切开，并固定在口胃管上。通过牵引，食管远端粘膜向近端倒置10 cm，然后返回胃腔。在A组（n = 4）中，切除粘膜（5 cm），并让残余物缩回。在B组（n = 4）中，仅将粘膜缝合回到其原始位置。在C组（n = 2）中，切除粘膜（5 cm）并将近端切入并缝合至胃粘膜。在6周或更短的时间（如果出现狭窄）处死动物。通过离体钡食管造影和肉眼评估确定狭窄的形成。组织学确定纤维化程度和上皮愈合。结果：A组（切除粘膜）在4周内出现体重减轻和厌食症。病理显示密集的纤维化狭窄，没有再上皮化。手术后B组（粘膜升高/置换）增重。组织学显示粘膜愈合无明显狭窄或纤维化。术后C组（粘膜切除/进展）也很旺盛。组织学证实粘膜愈合，没有缩回或密集狭窄的迹象。结论：粘膜下组织暴露可引起食管狭窄。粘膜覆盖可使损伤后的粘膜下层纤维化最小化。粘膜切除和进展可使愈合而无狭窄，对巴雷特食管患者可能具有治疗潜力。

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