Особенности локального воспаления слизистой оболочки носа у детей с бронхиальной астмой

Abstract

Bronchial asthma (BA) is often associated with chronic inflammatory processes in the nasal mucosa; these processes give rise to allergic rhinitis (AR), chronic rhinosinusitis, adenoiditis and polypous rhinosinusitis. Due to their multiple symptoms, these diseases of the upper respiratory tract, especially allergic rhinitis, are often difficult to verify in patients with asthma. The aim of the study was to assess the features of local inflammation of the nasal mucosa in patients with BA and AR. Patients and methods. 93 children with BA were examined. General clinical, allergological, functional examination, measurement of endonasal temperature and determination of IgE and IL4 content in nasal secretions were performed. Results. Children with BA have lower values of endonasal temperature than healthy ones. There was a tendency to decrease endonasal temperature as the symptoms of AR increased. In the acute stage of AR, the temperature values were lower than in the remission stage, р = 0,02. The addition of infectious inflammation of the nasal mucosa in children with AD was accompanied by an increase in endonasal temperature, р = 0,04. The increase of the content of nasal IgE in acute AR – 115,6 (49,9; 181,2) ME/mg, compared to the remission period to 24,9 (6,2; 43,7) ME/mg. Exacerbation of AR was associated with increased IL4 to 109,7 (54,2; 165,2) PG/mg, in the period of remission – 34,4 (12,0; 56,8) PG/mg. The increase of these biomarkers of allergic inflammation have a correlative relationship, R = 0,44, p = 0,002. The relationship of IL4 content with endonasal temperature, R = 0,44 р = 0,02 was established. Conclusion. Patients with BA and AR showed a decrease in endonasal temperature compared to healthy ones. Exacerbation of AR in children with BA characterized by an increase in the content of nasal IgE and IL4 and a decrease in endonasal temperature, which allows us to consider these indicators as biomarkers of activation of allergic inflammation.