Download PDF
CC BY-NC-ND 4.0 · Int Arch Otorhinolaryngol 2021; 25(01): e88-e91
DOI: 10.1055/s-0040-1702972
Original Research

Montelukast Has no Impact on the Systemic Production of TGFβ-1 in Patients with Nasal Polyposis Associated with Aspirin Intolerance

Rogério Pezato 
1   Department of Otorhinolaryngology – Head and Neck Surgery, Universidade Federal de São Paulo, São Paulo, Brazil
,
Luciano Lobato Gregório
1   Department of Otorhinolaryngology – Head and Neck Surgery, Universidade Federal de São Paulo, São Paulo, Brazil
,
Claudina Pérez-Novo
1   Department of Otorhinolaryngology – Head and Neck Surgery, Universidade Federal de São Paulo, São Paulo, Brazil
,
Thiago Ferreira Pinto Bezerra
2   Department of Otorhinolaryngology, Universidade Federal de Pernambuco, Recife, Pernambuco, Brazil
,
Eduardo Macoto Kosugi
1   Department of Otorhinolaryngology – Head and Neck Surgery, Universidade Federal de São Paulo, São Paulo, Brazil
› Author Affiliations
› Further Information
   Permissions and Reprints

Abstract

Introduction Nasal polyposis is a disease characterized by a mechanical dysfunction of the nasal mucosa, closely related to the unique makeup of its extracellular matrix, which develops as the result of an anomalous tissue remodeling process.

Transforming growth factor beta 1 (TGF-β1) is reduced not only in the nasal polypoid tissue, but also in the plasma of aspirin-intolerant patients. These patients exhibit an imbalance in the production of eicosanoids characterized by an increase in leukotrienes. Thus, it is important that the relationship between the production of leukotrienes and TGF-β1 be assessed.

Objective To evaluate the effects of the cysteinyl leukotriene (CysLT) receptor antagonist montelukast on the systemic production of TGF-β1 in patients with nasal polyposis, with or without concomitant aspirin intolerance.

Methods The sample comprised 48 individuals with diagnosis of nasal polyposis and 15 healthy controls for comparison of the baseline TGF-β1 levels in the peripheral blood and after treatment with CysLT receptor antagonist montelukast in the nasal-polyposis group.

Results There was no difference in the change in TGF-β1 levels after the treatment with montelukast in the subgroup of patients with polyposis and asthma (p = 0.82) and in the subgroup with polyposis, asthma, and aspirin intolerance (p = 0.51).

Conclusion we found no impact of the therapy with a leukotriene receptor blocker on the production of TGF-β1, making the antileukotriene therapy a highly questionable choice for the treatment of nasal polyposis, particularly from the standpoint of seeking to modify the remodeling process in this disease.

Keywords

rhinosinusitis - airway - nasal polyposis - inflammation - allergy


Publication History

Received: 02 July 2019

Accepted: 26 December 2019

Article published online:
27 April 2020

© 2020. Fundação Otorrinolaringologia. This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

Thieme Revinter Publicações Ltda.
Rua do Matoso 170, Rio de Janeiro, RJ, CEP 20270-135, Brazil

 

  • References

  • 1 Pezato R, Voegels RL, Pinto Bezerra TF, Perez-Novo C, Stamm AC, Gregorio LC. Mechanical disfunction in the mucosal oedema formation of patients with nasal polyps. Rhinology 2014; 52 (02) 162-166
    CrossrefPubMedGoogle Scholar
  • 2 Pezato R, Voegels RL, Stamm AC, Gregório LC. Why we should avoid using inferior turbinate tissue as control to Nasal Polyposis studies. Acta Otolaryngol 2016; 136 (09) 973-975
    CrossrefPubMedGoogle Scholar
  • 3 Pezato R, Voegels RL. Why do we not find polyps in the lungs? Bronchial mucosa as a model in the treatment of polyposis. Med Hypotheses 2012; 78 (04) 468-470
    CrossrefPubMedGoogle Scholar
  • 4 Gregório L, Pezato R, Felici RS, Kosugi EM. Fibrotic Tissue and Middle Turbinate Exhibit Similar Mechanical Properties. Is Fibrosis a Solution in Nasal Polyposis?. Int Arch Otorhinolaryngol 2017; 21 (02) 122-125
    Article in Thieme ConnectPubMedGoogle Scholar
  • 5 Pezato R, Voegels RL, Pignatari S. et al. Nasal Polyposis: More than a Chronic Inflammatory Disorder-A Disease of Mechanical Dysfunction-The São Paulo Position. Int Arch Otorhinolaryngol 2019; 23 (02) 241-249
    Article in Thieme ConnectPubMedGoogle Scholar
  • 6 Pezato R, Balsalobre L, Lima M. et al. Convergence of two major pathophysiologic mechanisms in nasal polyposis: immune response to Staphylococcus aureus and airway remodeling. J Otolaryngol Head Neck Surg 2013; 42 (01) 27
    CrossrefPubMedGoogle Scholar
  • 7 Figueiredo CR, Santos RP, Silva ID, Weckx LL. Microarray cDNA to identify inflammatory genes in nasal polyposis. Am J Rhinol 2007; 21 (02) 231-235
    CrossrefPubMedGoogle Scholar
  • 8 Watelet JB, Bachert C, Claeys C, Van Cauwenberge P. Matrix metalloproteinases MMP-7, MMP-9 and their tissue inhibitor TIMP-1: expression in chronic sinusitis vs nasal polyposis. Allergy 2004; 59 (01) 54-60
    CrossrefPubMedGoogle Scholar
  • 9 Balsalobre L, Pezato R, Perez-Novo C. et al. Epithelium and stroma from nasal polyp mucosa exhibits inverse expression of TGF-β1 as compared with healthy nasal mucosa. J Otolaryngol Head Neck Surg 2013; 42 (01) 29
    CrossrefPubMedGoogle Scholar
  • 10 Pezato P, Claeys C, Holtappels G, Bachert C, Pérez-Novo CA. LTD4 and TGF-β1 induce the expression of metalloproteinase-1 in chronic rhinosinusitis via a cysteinyl leukotriene receptor 1-related mechanism. Sinusitis 2016; 1 (01) 65-75
    CrossrefGoogle Scholar
  • 11 Pezato R, Świerczyńska-Krępa M, Niżankowska-Mogilnicka E. et al. Systemic expression of inflammatory mediators in patients with chronic rhinosinusitis and nasal polyps with and without Aspirin Exacerbated Respiratory Disease. Cytokine 2016; 77: 157-167
    CrossrefPubMedGoogle Scholar
  • 12 Pezato R, Świerczyńska-Krępa M, Niżankowska-Mogilnicka E, Derycke L, Bachert C, Pérez-Novo CA. Role of imbalance of eicosanoid pathways and staphylococcal superantigens in chronic rhinosinusitis. Allergy 2012; 67 (11) 1347-1356
    CrossrefPubMedGoogle Scholar
  • 13 Fokkens WJ, Lund VJ, Mullol J. , et al. European Position Paper on Rhinosinusitis and Nasal Polyps 2012. Rhinol. Suppl. 3 p preceding table of contents, 1-298 ( 2012
    PubMed
  • 14 Shevchenko I, Karakhanova S, Soltek S. et al. Low-dose gemcitabine depletes regulatory T cells and improves survival in the orthotopic Panc02 model of pancreatic cancer. Int J Cancer 2013; 133 (01) 98-107
    CrossrefPubMedGoogle Scholar
  • 15 Pérez-Novo CA, Claeys C, Van Cauwenberge P, Bachert C. Expression of eicosanoid receptors subtypes and eosinophilic inflammation: implication on chronic rhinosinusitis. Respir Res 2006; 7: 75
    CrossrefPubMedGoogle Scholar
  • 16 Pérez-Novo CA, Watelet JB, Claeys C, Van Cauwenberge P, Bachert C. Prostaglandin, leukotriene, and lipoxin balance in chronic rhinosinusitis with and without nasal polyposis. J Allergy Clin Immunol 2005; 115 (06) 1189-1196
    CrossrefPubMedGoogle Scholar