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Vol. 43. Issue 6.
Pages 340-345 (January 2007)
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Vol. 43. Issue 6.
Pages 340-345 (January 2007)
Review Article
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Asthma and Smoking: An Unfortunate Combination
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Jesús Bellido Casado
Corresponding author
jbellido@santpau.es

Correspondence: Dr. J. Bellido Casado. Departamento de Neumología, Hospital de la Santa Creu i Sant Pau. Sant Antoni M. Claret, 167. 08025 Barcelona. España
Departamento de Neumología, Hospital de la Santa Creu i Sant Pau, Facultad de Medicina, Universidad Autónoma de Barcelona, Barcelona, Spain
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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.

Key words:
Asthma
Smoking
Inflammation
Eosinophils
Neutrophils
Prevention

El asma es una enfermedad inflamatoria de las vías aéreas en la que desempeñan un papel primordial determinadas células y mediadores (linfocitos T helper -2, mastocitos, eosinófilos, interleucinas-4 y 5). En algunas situaciones la inflamación predominante está mediada por linfocitos T helper -1, macrófagos y neutrófilos, como en el asma por irritantes, el síndrome de disfunción reactiva de las vías aéreas, el asma por diisocianato de tolueno (TDI), etc. Por otra parte, también el tabaco produce inflamación bronquial, fundamentalmente mediada por macrófagos y neutrófilos, aunque en algunos fumadores se observa también un predominio de eosinófilos (respuesta inmunoalérgica a determinados antígenos). El remodelado bronquial que acompaña a la cascada inflamatoria crónica puede modificar la respuesta celular y confundir sobre el predominio de uno u otro tipo de infiltrado inflamatorio. La asociación de asma y tabaco constituye una realidad en nuestro medio, a la vez que modifica sustancialmente los mecanismos patogénicos, produce una clínica más florida y se observa resistencia a ciertos tratamientos habituales en el asma (corticoides), lo que ha propiciado la utilización de otros fármacos (antileucotrienos). Una de las medidas preventivas que deben utilizarse con más energía es propiciar el abandono del hábito tabáquico, prestando especial atención a los asmáticos fumadores.

Palabras clave:
Asma
Tabaco
Inflamación
Eosinófilos
Neutrófilos
Prevención
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Copyright © 2007. Sociedad Española de Neumología y Cirugía Torácica (SEPAR)
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