Evaluation of substance P and bradykinin levels in nasal secretions of patients with nasal polyposis with and without sensitivity to non‐steroidal anti‐inflammatory drugs

Abstract

Objective: The role of neurogenic inflammation in pathogenesis of chronic rhinitis is well known. However, very little is known about its importance in pathogenesis of nasal polyposis (NP), especially in form of NP which appears as a part of aspirinexacerbated respiratory disease (AERD). The aim of this study was to examine the concentrations of neuropeptides substance P (SP) and bradykinin (BK) in nasal secretions of patients with NP.Methods: Fourteen patients with NP as a part of AERD with mild persistent asthma, 14 patients with NP without aspirin sensitivity, and 14 control subjects without nasal inflammation (C) entered this cross-sectional study. Clinical parameters (symptoms, endoscopic, and radiological findings) were assessed. The concentrations of SP and BK were measured in the nasal secretion samples using commercial human enzyme immunoassay kits. Results:The concentration of SP in nasal secretions was significantly higher in NP patients without aspirin sensitivity and AERD patients compared to controls (p = .022; p < .0001, respectively), but higher in AERD than in non-AERD patients (p = .018). The level of BK in nasal fluid was higher in non-AERD and AERD NP patients than in controls (p < .0001; p < .0001, respectively), but also higher in AERD than in non-AERD patients (p < .0001). We found high positive correlations between BK in nasal fluid and Lund-Mackay computed tomography (CT) score in both non-AERD and AERD groups of NP patients. Conclusion:Our results suggest more intense release of SP and BK from the nasal mucosa in patients with AERD than in patients with NP who do not have aspirin sensitivity. The strong correlation between concentration of BK in nasal secretions and CT score suggests that BK in nasal fluid could be used as a marker for disease severity as measured by the Lund-Mackay score.

Angiogenesis and eosinophilia in the nasal mucosa of patients with different clinical phenotypes of chronic rhinosinusitis

“…Within the NP form, we distinguish a special clinical phenotype in which CRSwNP is associated with hypersensitivity to non-steroidal anti-inflammatory drugs (NSAIDs) and non-allergic asthma. This aspirin-exacerbated respiratory disease (AERD) was caused as a result of disturbances in the metabolism of arachidonic acid and is characterized by a particularly severe clinical feature with rapid disease progression and frequent relapses, relatively soon after endoscopic surgical treatment [1][2][3][4][5].…”