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Article Abstract
Objectives: Halofuginone is a low-molecular weight quinazolinone alkaloid coccidiostat that inhibits collagen type I synthesis, extracellular matrix deposition, and angiogenesis. This study was conducted to assess its potential in preventing subglottic stenosis (SGS).
Methods: We induced SGS in 10 dogs randomly divided into 2 groups. Each group received treatment between 3 days before and 21 days after the induction of SGS. One group received oral halofuginone 40 microg/kg, and the other was given placebo. The area of the subglottic lumen was measured at baseline and 3 months later. In addition, human tracheal fibroblasts were cultured. The inhibitory effect of halofuginone was compared to the effect of mitomycin.
Results: All dogs survived throughout the study with no side effects. Three months after the operation, no halofuginone-treated dog had SGS, in contrast to a 66% to 80% stenosis rate (mean, 72%) in controls (p < .008). Thick fibrotic tissue was found in the placebo-treated larynges, whereas an almost normal architecture was observed in halofuginone-treated larynges. Halofuginone inhibited the growth of human tracheal fibroblasts by 75%, in comparison with 60% inhibition by mitomycin (no statistically significant difference).
Conclusions: This preliminary study shows that halofuginone is effective in preventing SGS caused by an acute injury. Halofuginone has a potential therapeutic role in preventing SGS in humans.
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| http://dx.doi.org/10.1177/000348940611500511 | DOI Listing |
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