GINA guidelines suggest that optimal asthma control can be gained by regular monitoring of symptoms, rescue medication use, airways obstruction and variability upon time of airways flows. Our aim was to check if therapy according to GINA rules is able to lower airways inflammation, measured by the level of IL4 in expired breath condensate (EBC). One hundred patients affected by bronchial asthma in different levels were recruited as they come to the ambulatory ward. They were cured according to GINA guidelines for one year, using inhaled fluthicasone as inhaled steroid. Symptoms were monitored by asthma control test score (ACT), airways obstruction by FEV1, bronchial reactivity by PD20, airways inflammation by IL4 in EBC. ACT showed complete control in the first three GINA levels, improving incompletely in the GINA level 4 (from 20±2 to 21±12; from 17±2 to 22±2; from 14±4 to 18±3; from 10±3 to 14±3 units respectively in the first to fourth levels of asthma). FEV1 improved, but both baseline and after therapy levels were worst in severe persistent asthma (from 96±5 to 96±4; from 92±6 to 93±3; from 74±6 to 83±8; from 45±10 to 60±5% of normal standards respectively from the 1st to 4th level). PD20 and IL4 were fairly normalized by therapy in the s and third levels, improved in the last one (PD20 from 437±329 to 460±269, from 364±308 to >1600, from 436±252 to 890±220; from 45±25 to 60±40 mcg respectively, IL4 in EBC from 60±6 to 40±12, from 65±10 to 41±9, from 72±8 to 45±6, from 78±20 to 52±5 respectively). IL4 and PD20 were significantly related. Experimental data allowed the assessment of the correlation of inflammation with bronchial reactivity and the relevance of addressing therapy upon IL4. Severe persistent asthma behave as a different entity with worst baseline inflammation, partially refractory asthma and persistent inflammation, needing specific immunologic weapons. Bronchial inflammation was fairly reduced but not normalized after one year of therapy.
bronchial asthma, Il4 , GINA , expired breath condensate, bronchial hyperreactivity, EBC, TD20.