Prevention of esophageal strictures in a caustic burn model using halofuginone, an inhibitor of collagen type I synthesis

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Prevention of esophageal strictures in a caustic burn model using halofuginone, an inhibitor of collagen type I synthesis

Year: 

2005

Source of publication :

Laryngoscope

Authors :

Genina, Olga

;

Pines, Mark

.

Volume :

115

Co-Authors: 

Arbell, D., Department of Pediatric Surgery, Hadassah University Hospital, Jerusalem, Israel, Department of Pediatric Surgery, Hadassah University Hospital, Kyriat Hadassah, PO Box 12000, 91120 Jerusalem, Israel
Udassin, R., Department of Pediatric Surgery, Hadassah University Hospital, Jerusalem, Israel
Koplewitz, B.Z., Department of Radiology, Hadassah University Hospital, Jerusalem, Israel
Ohana, M., Department of Liver Research, Hadassah University Hospital, Jerusalem, Israel
Genina, O., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel
Pines, M., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel
Nagler, A., Department of Hematology and Bone Marrow Transplantation, Chaim Sheba Medical Center, Tel Hashomer, Israel

From page: 

1632

To page: 

1635

(

Total pages: 

4

)

Link :

Prevention of esophageal strictures in a caustic burn model using halofuginone, an inhibitor of collagen type I synthesis

Abstract: 

Objective: Esophageal strictures caused by caustic injury continue to be a plaguing problem. Halofuginone (HF) has been proven to inhibit the formation of fibrosis in various animal models and human diseases. Its mechanism appears to be through the suppression of the production of collagen α1(I) and transforming growth factor-β signaling pathway. We tried to assess whether HF would have an effect on the formation of strictures after inducing caustic esophageal. Materials and Methods: Esophageal injury was caused by injecting 25% NaOH to an isolated esophageal segment. Study group rats were treated with HF orally for 3 consecutive days before the injury and afterward. Control group rats received regular chow. The results were evaluated by upper gastrointestinal series (UGI) and through pathologic studies. Results: HF treatment resulted in marked improvement in the esophageal strictures. The UGI series showed esophageal patency of 73% (45%-100%) in the treated animals (n = 7) as compared with almost no patency, 11% (5-16%), in the controls (n = 4) (P = .018). The histologic examination showed significantly less stricture and scarring in the treated group. Whereas the ratio between the esophageal wall thickness to mucosal thickness was 2.34 ± 0.23 in the study group, the control group had a ratio of 9.56 ± 0.69 (P = .0044). Finally, whereas 86% of the study group survived, all the rats in the control group died by day 20. Conclusions: HF modulated the wound healing reaction caused by caustic injury of the esophagus in a rat model, resulting in increased esophageal patency, reduction in esophageal wall thickness, and increased survival. © 2005 The American Laryngological, Rhinological and Otological Society, Inc.