These mediators also trigger a systemic inflammation besides local inflammation, which can in turn augment inflammation in both the upper and lower airways. This explains the link to asthma. The prevalence of asthma in AR patients has been reported to be from 10% up to 40%. Clinical studies have revealed that although AR patients may not have asthma, they can have eosinophilic infiltration in bronchial mucosa. Epidemiologic studies have reported that a significant proportion of the asthma patients have eosinophilic inflammation of nasal mucosa regardless of nasal symptoms. Cumulative evidence has shown that there is similarity of allergic inflammatory cells, inflammatory mediators
These mediators also trigger a systemic inflammation besides local inflammation, which can in turn augment inflammation in both the upper and lower airways. This explains the link to asthma. The prevalence of asthma in AR patients has been reported to be from 10% up to 40%. Clinical studies have revealed that although AR patients may not have asthma, they can have eosinophilic infiltration in bronchial mucosa. Epidemiologic studies have reported that a significant proportion of the asthma patients have eosinophilic inflammation of nasal mucosa regardless of nasal symptoms. Cumulative evidence has shown that there is similarity of allergic inflammatory cells, inflammatory mediators