Page 174 - ADULT-ONSET ASTHMA PREDICTORS OF CLINICAL COURSE AND SEVERITY

ADULT-ONSET ASTHMA – PREDICTORS OF CLINICAL COURSE AND SEVERITY
had persistent asthma. Perhaps treatment of a common underlying in ammatory mechanism (associated to eosinophilia) or avoidance of causa ve agents will lead to a be er outcomes of both diseases.
If complete asthma remission, including resolu on of pathophysiologic abnormali es, is possible, one could speculate that aggressive treatment of asthma in an early phase of the disease can alter the prognosis. Whether this will be possible in real life will depend on several factors that lead to the clinical expression of asthma: 1) Speci c asthma triggers like allergens, infec ons, pollutants, work related agents and smoke. 2) The extent and type of the present in ammatory pa erns caused by the asthma trigger(s) and its consistency. 3) Structural airway changes due to in amma on and triggers (also dependent on the dura on and con nua on of triggers). 4) Sensi vity to therapy with inhaled cor costeroids and B agonists (gene c predisposi on, epigene c changes). 5) The in uence of comorbid condi ons like obesity, GERD, atopy and sinonasal diseases. Taken together, the best approach for treatment of an adult asthma pa ent with the current knowledge, would be a full assessment and treatment of the above men oned associated factors.
FUTURE DIRECTIONS
Extensive data from the Adonis study is available to address a wide range of research ques ons:
– Evalua on of lung func on over the years, what factors are associated with an
accelerated decline in lung func on?
– How did asthma severity develop during 5 years? Do we nd the same predictors of
increased severity as a er two years? Or perhaps some pa ents have uctua ons in
severity? Can this be linked to uctua ons in in ammatory markers?
– Inves ga on of biological data (sputum supernatant, sputum cells, serum, are available
at baseline and 5 year follow-up):
– Looking at markers of oxida ve stress, one could hypothesize that the level of oxida ve
stress correlates to clinical decline or decline in lung func on.
– Markers of in amma on or in ammatory pathways might be interes ng: not
just eosinophils but perhaps cytokines or chemokines could teach us more about in ammatory phenotypes and the link to clinical phenotype.
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