Lipid mediator pathways in the lung: leukotrienes as a new target for the treatment of asthma

Authors
Citation
Se. Dahlen, Lipid mediator pathways in the lung: leukotrienes as a new target for the treatment of asthma, CLIN EXP AL, 28, 1998, pp. 141-146
Citations number
43
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
CLINICAL AND EXPERIMENTAL ALLERGY
ISSN journal
09547894 → ACNP
Volume
28
Year of publication
1998
Supplement
5
Pages
141 - 146
Database
ISI
SICI code
0954-7894(199811)28:<141:LMPITL>2.0.ZU;2-6
Abstract
This article summarizes recent evidence supporting that antileukotriene dru gs represent a new treatment of asthma which may be particularly effective when combined with drugs that have complementary effects on airway obstruct ion and inflammation. Firstly, it has been documented that glucocorticosteroids do not inhibit in vivo production of leukotrienes in asthmatics. In line with such findings, addition of antileukotriene drugs to a group of aspirin-intolerant asthmat ics maintained on conventional therapy was found to result in an improvemen t of the asthma over and above the effect of the baseline treatment with in haled and/or oral glucocorticosteroids. Likewise, in a 6-week trial in a gr oup of severe asthmatics, the asthma deterioration caused by a reduction of the dose of inhaled steroids by half, was prevented by addition of a leuko triene antagonist to the lowered dose of glucocorticosteroids. Current evid ence therefore supports that antileukotriene drugs treat components of the pathophysiology which are left unaffected by treatment with glucocorticoste roid. Secondly, in experimental studies as well as in a recent allergen bronchopr ovocation study in asthmatics, it has been found that the combination of an tihistaminics with antileukotriene drugs will result in a profound inhibiti on of both the early and the late phase of allergen-induced airway obstruct ion. It is hypothesized that such a combination may be useful against bronc hoconstriction induced by other asthma trigger factors as well as in the tr eatment of asthma and rhinitits.