Chronic rhinosinusitis and the coagulation system

Dong Young Kim, Seong H. Cho, Tetsuji Takabayashi, Robert P. Schleimer*

*Corresponding author for this work

Research output: Contribution to journalReview article

13 Scopus citations

Abstract

Chronic rhinosinusitis (CRS) is one of the most common chronic diseases in adults and severely affects quality of life in patients. Although various etiologic and pathogenic mechanisms of CRS have been proposed, the causes of CRS remain uncertain. Abnormalities in the coagulation cascade may play an etiologic role in many diseases, such as asthma and other inflammatory conditions. While studies on the relationship between asthma and dysregulated coagulation have been reported, the role of the coagulation system in the pathogenesis of CRS has only been considered following recent reports. Excessive fibrin deposition is seen in nasal polyp (NP) tissue from patients with chronic rhinosinusitis with nasal polyp (CRSwNP) and is associated with activation of thrombin, reduction of tissue plasminogen activator (t-PA) and upregulation of coagulation factor XIII-A (FXIII-A), all events that can contribute to fibrin deposition and crosslinking. These findings were reproduced in a murine model of NP that was recently established. Elucidation of the mechanisms of fibrin deposition may enhance our understanding of tissue remodeling in the pathophysiology of NP and provide new targets for the treatment of CRSwNP.

Original languageEnglish (US)
Pages (from-to)421-430
Number of pages10
JournalAllergy, Asthma and Immunology Research
Volume7
Issue number5
DOIs
StatePublished - 2015

Keywords

  • Coagulation
  • Factor XIIIa
  • Fibrinolysis
  • Nasal polyps
  • Rhinosinusitis
  • Tissue plasminogen activator

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Pulmonary and Respiratory Medicine

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