Abstract

Objective:The aim of this study is to observe the effects of asthma and aspirin asthma on chronic rhinosinusitis and to explore the corresponding clinical value. Method: Eighty-six patients with CRS and asthma who were treated in the outpatient clinic during March 2015 to January 2018 were divided into asthma group(52 cases) and aspirin asthma group(34 cases) according to asthma and aspirin asthma. The clinical symptoms of the two groups were analyzed by symptomatic VAS score, Lund-Mackay score of sinus CT, and Lund-Kennedy score by nasal endoscopy.The scores of the two groups were compared under different lung function. Enzyme-linked immunosorbent assay the levels of inflammatory markers IL-5,IL-17,IFN-γ and TNF-α in the sinus secretions of the two groups were detected.Result:There were no significant differences in age, gender, smoking history, allergy history, surgical history and course of disease between the two groups(P<0.05), suggesting that the data were comparable. The sinus CT results showed that compared with the aspirin asthma group, the asthmatic group had irregular turbinates and a large turbinate,as shown in Figure 1. There were significant differences between the two groups in VAS score,Lund-Mackay score of sinus CT and Lund-Kennedy score by nasal endoscopy.The difference was statistically significant(P<0.05). And the forehead and/or facial pain or pain in the symptomatic VAS score(P<0.05), the Lund-Mackay score of the sinus CT(P<0.05),and intranasal.The difference in the Lund-Kennedy score(P<0.05) was statistically significant.There were significant differences in the distribution of lung function levels between the two groups of patients with mild airway obstructive respiratory dysfunction and pulmonary ventilation obstructive disorder(P<0.05).The average levels of IL-5,IL-17,IFN-γ and TNF-α in the aspirin asthma group were significantly lower than those in the asthma group(P<0.05).Conclusion:Aspirin-induced CRS produces asthma symptoms more severely than traditional asthma symptoms, but the induced local inflammatory response is relatively weak, and the mechanism may be closely related to IL-5,IL-17,IFN-γ and TNF-α levels.

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