The Role of Systemic Steroids in Postintubation Tracheal Stenosis: A Randomized Clinical Trial

Shadmehr, Mohammad Behgam; Abbasidezfouli, Azizollah; Farzanegan, R; Pejhan, Saviz; Kakhaki, Abolghasem Daneshvar; Sheikhy, Kambiz; Saghebi, Seyed Reza; Sadeghbeigee, Farahnaz; Gharedaghi, Abasad; Jahanshahi, N; Zangi, Mahdi

doi:10.1016/j.athoracsur.2016.05.063

Cited by 33 publications

(23 citation statements)

References 21 publications

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“…However, the molecular mechanisms of TS have not been elucidated. And the diagnosis of TS is usually made after discharge, affecting the therapeutic effect (Shadmehr et al, 2017). Therefore, it is important to find the pathogenesis of TS for the early diagnosis and targeted therapy.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis and verification of gene targets for benign tracheal stenosis

Wang

Qiu

et al. 2020

Molec Gen & Gen Med

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Background Tracheal injury could cause intratracheal scar hyperplasia which in turn causes benign tracheal stenosis (TS). With the increasing use of mechanical ventilation and ventilator, the incidence of TS is increasing. However, the molecular mechanisms of TS have not been elucidated. It is significant to further explore the molecular mechanisms of TS. Methods The repeatability of public data was verified. Differently expressed genes (DEGs) and most significant genes were identified between TS and normal samples. Enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were analyzed. The comparative toxicogenomics database were analyzed. TS patients were recruited and RT‐qPCR were performed to verify the most significant genes. Results There exist strong correlations among samples of TS and normal group. There was a total of 194 DEGs, including 61 downregulated DEGs and 133 upregulated DEGs. GO were significantly enriched in mitotic nuclear division, cell cycle, and cell division. Analysis of KEGG indicated that the top pathways were cell cycle, and p53 pathway. MKI67(OMIM:176741), CCNB1(OMIM:123836), and CCNB2(OMIM:602755) were identified as the most significant genes of TS, and validated by the clinical samples. Conclusion Bioinformatics methods might be useful method to explore the mechanisms of TS. In addition, MKI67, CCNB1, and CCNB2 might be the most significant genes of TS.

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Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis and verification of gene targets for benign tracheal stenosis

Wang

Qiu

et al. 2020

Molec Gen & Gen Med

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“…As adjuncts to the surgical interventions, primarily mitomycin C has been used in the treatment of TS, followed by several other pharmacological agents including the steroids, antibiotics, anti‐reflux medications, halofuginone, 5‐FU (fluorouracil), and carnitine . These treatment options were used in order to be effective on one or more stages of wound healing, including inflammation, proliferation, maturation, and remodeling …”

Section: Discussionmentioning

confidence: 99%

“…14,22 These treatment options were used in order to be effective on one or more stages of wound healing, including inflammation, proliferation, maturation, and remodeling. 2 The corticosteroids and antibiotics are effective during the stages of inflammation and proliferation; mitomycin C, the combination of 5-FU and triamcinolone acetate, and carnitine are effective during the proliferation stage; and halofuginone, β-aminopropionitrile, colchicine, penicillamine, and N-acetyl-L-cysteine are effective during the maturation stage. Provided by its mechanism of action, pirfenidone is effective during all three stages of wound healing.…”

Section: Discussionmentioning

confidence: 99%

“…Tracheal stenosis (TS) is the most common complication after tracheostomy and tracheal tube placement. Due to the pressure applied by the tracheal tube cuff, ischemia, edema, inflammation, and eventually fibrosis develops, playing an important role in the pathogenesis of tracheal stenosis, which occurs with an incidence of 0.6% to 21% …”

Section: Introductionmentioning

confidence: 99%

“…Due to the pressure applied by the tracheal tube cuff, ischemia, edema, inflammation, and eventually fibrosis develops, playing an important role in the pathogenesis of tracheal stenosis, which occurs with an incidence of 0.6% to 21% . 1,2 Current methods used in the treatment of tracheal stenosis include balloon dilatation, endoscopic laser surgery, tracheal resection, and end-to-end anastomoses. 3 However, the increased risk of restenosis after these treatment methods paved the way to search for innovative pharmacologic agents inhibiting the fibrosis, which is the main leading cause in the pathogenesis of fibrosis.…”

Section: Introductionmentioning

confidence: 99%

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Prevention of tracheal stenosis with pirfenidone after tracheotomy: An experimental study

Türkmen

Pata

2018

The Laryngoscope

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Objectives In this study, pirfenidone's role about reducing tracheal stenosis by suppressing fibrosis and inflammation was examined. Methods Tracheotomy was performed on 14 rats, and their cannulas were fixed to tracheotomy area by stoma suture. Two working groups were established. Rats in the first group were given 15 mg/kg/day (1 mL pirfenidone solution) pirfenidone intraperitoneally for 10 days. In the second group as a control group, 1 mL saline solution was applied intraperitoneally. Ten days later, rats were decanulated and kept alive for 3 more weeks. Anesthetized rats were sacrificed on day 30. All rat tracheas were resected between the first and seventh rings. Epithelial damage, inflammation, and fibrosis were determined histopathologically; diameters of intratracheal lumen and their mucosal thickness parameters were determined histomorphometrically; and TGFβ‐1 (the growth factor beta), TNFα (tumor necrosis factor alpha), and IL‐1β (Interleukin‐1 beta) values were determined immunohistochemically. Results According to the parameters of the control group, fibrosis; diameters of intratracheal lumen; and values of TGFβ‐1, TNFα, and IL‐1β were found to be statistically significant. Conclusion In our study, it was found that pirfenidone reduces fibrosis and narrowing of intratracheal lumen diameter significantly. Level of Evidence NA Laryngoscope, 129:E178–E186, 2019

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Antifibrotic Role of Nintedanib in Tracheal Stenosis After a Tracheal Wound

Fan

Fang

et al. 2021

The Laryngoscope

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Objectives/Hypothesis Tracheal stenosis is an obstructive disease of the upper airway that commonly develops as a result of abnormal wound healing. We evaluated the anti‐inflammatory and antifibrotic properties of nintedanib on tracheal stenosis both in vitro and in vivo. Study Design Prospective controlled animal study and in vitro comparative study of human cells. Methods An animal model of tracheal stenosis was induced via tracheal trauma. Postsurgical rats were orally administered with nintedanib (10 or 20 mg/kg/d) or saline (negative control) for 2 weeks, and tracheal specimens were harvested after 3 weeks. Degree of stenosis, collagen deposition, fibrotic surrogate markers expression, and T‐lymphocytic infiltration were evaluated. Human fetal lung fibroblast‐1 (HFL‐1) cells were cultured to determine the effects of nintedanib on changes of cellular biological function induced by transforming growth factor‐β1 (TGF‐β1). Results Rat tracheal stenotic tissues exhibited thickened lamina propria with irregular epithelium, characterized by significantly increased collagen deposition and elevated TGF‐β1, collagen I, α‐SMA and fibronectin expressions. Nintedanib markedly attenuated the tracheal stenotic lesions, reduced the collagen deposition and the expression of fibrotic marker proteins, and mitigated CD4+ T‐lymphocyte infiltration. Additionally, cellular proliferation and migration were decreased dose‐dependently in TGF‐β1‐stimulated HFL‐1 cells when treated with nintedanib. Furthermore, nintedanib inhibited TGF‐β1‐induced HFL‐1 differentiation and reduced the mRNA levels of the profibrotic genes. TGF‐β1‐activated phosphorylation of the TGF‐β/Smad2/3 and ERK1/2 pathways were also blocked by nintedanib. Conclusion Nintedanib effectively prevented tracheal stenosis in rats by inhibiting fibrosis and inflammation. The antifibrotic effect of nintedanib may be achieved by inhibiting fibroblasts' proliferation, migration and differentiation and suppressing the TGF‐β1/Smad2/3 and ERK1/2 signaling pathways. Level of Evidence NA Laryngoscope, 131:E2496–E2505, 2021

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The Role of Systemic Steroids in Postintubation Tracheal Stenosis: A Randomized Clinical Trial

Abstract: Early low-dose systemic corticosteroids can be beneficial in postintubation tracheal stenosis management.

Cited by 33 publications

References 21 publications

Bioinformatics analysis and verification of gene targets for benign tracheal stenosis

Bioinformatics analysis and verification of gene targets for benign tracheal stenosis

Prevention of tracheal stenosis with pirfenidone after tracheotomy: An experimental study

Antifibrotic Role of Nintedanib in Tracheal Stenosis After a Tracheal Wound

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