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Feasibility study of corticosteroid treatment for esophageal ulcer after EMR in a canine model

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Abstract

Background

Intralesional or systemic steroid administration is a promising strategy for the prevention of esophageal stricture after endoscopic therapy. The aim of this study was to evaluate the influence of steroid therapy on the process of healing of defects in the esophageal mucosa after endoscopic mucosal resection (EMR).

Methods

Nine beagle dogs were divided into three equal groups: group A, intralesional injection (n = 3), group B, peroral administration (n = 3), and group C, untreated control (n = 3). In group A, triamcinolone acetonide 1 ml (10 mg) was injected directly into the exposed submucosal layer immediately after EMR, and again on postoperative day (POD) 7. In group B, dogs were administered prednisolone 0.5 mg/kg/day orally for 14 days after EMR. In group C, 1 ml normal saline was injected by the same method as that used for group A. On POD 28, histological examination was performed to evaluate epithelialization, inflammation, angiogenesis, and atrophy of the muscularis propria.

Results

In groups A, B, and C, the mean ulcer area was 50.1, 22.7, and 7.4 mm2, respectively. The difference between groups A and C was significant (p < 0.01). Inflammatory cells were significantly more evident in the lesions of group A than in those of group C (p < 0.05). In all groups, atrophy of the muscularis propria was evident. However, transmural destruction and fibrosis were observed only in group A.

Conclusion

It was speculated that the esophageal ulcer causes the fibrosis of the submucosa and atrophy of the muscularis propria during process of healing. Intralesional steroid injection deepened the esophageal ulcers and delayed epithelialization, whereas systemic administration did not clearly improve the lesion healing process.

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Correspondence to Tatsuo Nakamura.

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Honda, M., Nakamura, T., Hori, Y. et al. Feasibility study of corticosteroid treatment for esophageal ulcer after EMR in a canine model. J Gastroenterol 46, 866–872 (2011). https://doi.org/10.1007/s00535-011-0400-3

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  • DOI: https://doi.org/10.1007/s00535-011-0400-3

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