Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2017
Two inflammatory phenotypes of nasal polyps and comorbid asthma.
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Wu Dawei, Li Lun, Zhang Min, Wang Jianting, Wei Yongxiang
Аннотация
BACKGROUND: Nasal polyps and comorbid asthma (NPCA) is a common united airway disease. However, the inflammatory phenotyes of NPCA are not clear.
OBJECTIVE: To identify inflammatory phenotypes of NPCA.
METHODS: A total of 106 patients diagnosed with NPCA were recruited from rhinologic clinics. A combined method of biopsies from nasal polyps and fractional exhaled nitric oxide (FeNO) was used to explore inflammatory phenotyes of NPCA. Patients were evaluated with respect to clinical, functional, and inflammatory parameters. Clinical outcomes after medical treatment were also assessed.
RESULTS: Two distinct inflammatory phenotypes (eosinophilic [64.15%] and noneosinophilic phenotypes [35.85%]) were identified. Inflammatory patterns of upper and lower airways were consistent in NPCA. Patients with eosinophilic NPCA had a higher nasal polyps recurrence rate than did patients with noneosinophilic NPCA, a more severe asthma phenotype (P < .001), higher exhaled nitric oxide levels (P < .001), higher IgE levels (P < .001), higher Lund-Mackay scores (P < .05), and more blood eosinophilia (P < .001). In addition, eosinophilic NPCA was associated with worse pulmonary function and responded well to an 8-week course of medical treatment based on computed tomographic findings and the ratio of forced expiratory volume in 1 second to forced vital capacity. The total IgE concentration was a marker for eosinophilic NPCA (optimal cutoff, >55.5 kU/L; sensitivity, 86.2%; specificity, 85.4%).
CONCLUSION: Patients with NPCA had 2 inflammatory phenotypes with distinct clinical profiles. Total IgE is a marker of eosinophilic NPCA.
OBJECTIVE: To identify inflammatory phenotypes of NPCA.
METHODS: A total of 106 patients diagnosed with NPCA were recruited from rhinologic clinics. A combined method of biopsies from nasal polyps and fractional exhaled nitric oxide (FeNO) was used to explore inflammatory phenotyes of NPCA. Patients were evaluated with respect to clinical, functional, and inflammatory parameters. Clinical outcomes after medical treatment were also assessed.
RESULTS: Two distinct inflammatory phenotypes (eosinophilic [64.15%] and noneosinophilic phenotypes [35.85%]) were identified. Inflammatory patterns of upper and lower airways were consistent in NPCA. Patients with eosinophilic NPCA had a higher nasal polyps recurrence rate than did patients with noneosinophilic NPCA, a more severe asthma phenotype (P < .001), higher exhaled nitric oxide levels (P < .001), higher IgE levels (P < .001), higher Lund-Mackay scores (P < .05), and more blood eosinophilia (P < .001). In addition, eosinophilic NPCA was associated with worse pulmonary function and responded well to an 8-week course of medical treatment based on computed tomographic findings and the ratio of forced expiratory volume in 1 second to forced vital capacity. The total IgE concentration was a marker for eosinophilic NPCA (optimal cutoff, >55.5 kU/L; sensitivity, 86.2%; specificity, 85.4%).
CONCLUSION: Patients with NPCA had 2 inflammatory phenotypes with distinct clinical profiles. Total IgE is a marker of eosinophilic NPCA.