Asma y tabaco: una unión inconveniente

Asthma is an inflammatory disease of the airways in which a key role is played by certain cells and mediators (T-helper 2 cells, mast cells, eosinophils, interleukin 4 and 5). In certain disorders such as irritant-induced asthma, reactive airways dysfunction syndrome, and asthma due to toluene diisocyanate, inflammation is mediated predominantly by T-helper 1 cells, macrophages and neutrophils. Smoking also produces bronchial inflammation, in this case mediated primarily by macrophages and neutrophils although eosinophil predominance has also been observed in some smokers (an allergic response to certain antigens). The remodeling of the airway wall that accompanies the chronic inflammatory cascade may alter the cell response profile making it difficult to determine which type of inflammatory infiltrate is predominant. The association of asthma and smoking is a reality in our society, and it is a combination that substantially modifies pathogenic mechanisms and gives rise to a more severe clinical picture. Resistance to some of the pharmacotherapies used routinely in the treatment of asthma (corticosteroids) has also been observed and this has favored the use of other drugs (antileukotrienes). One of the preventative measures that should be used more energetically is to encourage patients to stop smoking, paying particular attention to asthmatic smokers.