Page 115 - ADULT-ONSET ASTHMA PREDICTORS OF CLINICAL COURSE AND SEVERITY

CLINICAL PREDICTORS OF REMISSION AND PERSISTENCE OF ADULT-ONSET ASTHMA
is cigare e smoke. Cigare e smoking has been shown to be a risk factor for development of chronic airways disease.44 In our study, the group of pa ents with persistent asthma and nasal polyps consisted of smokers and ex-smokers for more than 70%. A common mechanism could include cigare e smoke-induced in amma on in the airways, associated with nasal polyp forma on and insensi vity to cor costeroids,45 leading to an increased severity and persistence of nasal polyps and asthma.16
Almost two-thirds of the pa ents with polyps in our cohort had already undergone surgical treatment for nasal polyposis before the onset of asthma, sugges ng that in these pa ents nasal polyposis had preceded the onset of asthma. However, despite this treatment, progression to persistent asthma had s ll occurred. Apparently, early treatment of nasal polyposis does not prevent asthma to develop or become chronic. Although adequate medical treatment of rhini s has been shown to improve asthma control46 our data suggest that surgical treatment of nasal polyposis is insu cient to prevent the development of persistent asthma.
The strength of our study was the prospec ve follow-up design and the extensive baseline characterisa on of the pa ents. In addi on, stringent criteria for asthma were used, consis ng of physician’s diagnosis con rmed by lung func on measurements.15
A poten al limita on of the study could be our de ni on of asthma remission. Clinical remission might not re ect pathophysiological remission, which includes normal airway responsiveness, and absence of airway in amma on. Previous studies have demonstrated on- going eosinophilic airway in amma on, airway hyperresponsiveness and airway remodelling in adolescents in clinical remission of atopic asthma.47 Thus, subclinical asthma might have overes mated remission rates in our pa ents with adult-onset asthma. Another poten al limita on of our study is that data from only 170 of 200 pa ents were available a er 5 years. This could have introduced a selec on bias, for example if the pa ents who were lost to follow-up had been the ones with an extensive smoking history. (Ex)smoking has been shown to worsen the prognosis of adult onset asthma,16 and might thereby also in uence the chance of asthma remission. However, by comparing pa ents who were lost to follow-up with the rest of the cohort, we did not observe di erences in smoking history.
Finally, the majority of pa ents were assessed at yearly intervals, which might have in uenced the results of our study. However, we do not believe that this was the case, because these interval assessments were done by study inves gators who were not linked to the health care providers of the pa ents. The results of these assessments were not communicated to the health care providers, and did not lead to changes in treatment.
Our study has several clinical implica ons. Firstly, it provides useful indicators to iden fy pa ents with newly diagnosed asthma who are at risk of persistent disease. This new insight
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