[New developments in asthma therapy: how do individual leukotriene antagonists work?].
Today it is generally acknowledged that bronchial asthma is a chronic inflammatory airway disease which is marked by recurrent bronchial obstructions and hyperreactivity of the airways. The best anti-inflammatory characteristics are shown by corticosteroids. However these can have considerable side-effects in long-term, systemic use. The search for alternative forms of therapy has for some time concentrated on the development and testing of leukotriene antagonists. These can limit the effect of leukotrienes via receptor antagonism or synthesis inhibition. The leukotrienes B4, C4, and D4 count as important key mediators in bronchial asthma. They are released by numerous inflammatory cells, have a bronchoconstricting effect and chemotactic characteristics, promote vessel permeability and increase mucous secretion. In addition, they probably increase bronchial hyperreactivity. Among biosynthesis restrictors, the 5-lipoxygenase restrictors have shown an anti-inflammatory effect in both experimental asthma models and in clinical use. In mild to moderate asthma, lung function improved and the use of a concomitant beta-agonist medication was reduced. While the older leukotriene receptor antagonists were rather disappointing, the newer substances display a significantly improved effect, are generally well tolerated and can also be given orally. In experimental asthma models, receptor antagonists, after antigen provocation, led to a marked reduction in bronchoconstriction and a decrease in the number of inflammatory cells (lymphocytes and eosinophils) in bronchial alveolar fluid. In clinical studies, this new class of drugs showed a reduction in clinical symptoms and an improvement in lung function in mild to moderate asthma. In addition, a bronchodilatatory effect was shown. The option of oral administration and good tolerance should improve compliance. The potential and long-term efficacy in severe asthma remains unclear. Further studies are required to elucidate the scope of their role and define their place in the treatment of asthma.
Wagener
M
M
Abteilung Chirurgie I, Kantonsspital Nidwalden.
D018927:Anti-Asthmatic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000502:physiology; D020024:Leukotriene Antagonists; D015289:Leukotrienes / Q000502:physiology; D016859:Lipoxygenase Inhibitors / Q000009:adverse effects / Q000627:therapeutic use; D018077:Receptors, Leukotriene / Q000502:physiology; D016896:Treatment Outcome
D018927:Anti-Asthmatic Agents; D018836:Inflammation Mediators; D020024:Leukotriene Antagonists; D015289:Leukotrienes; D016859:Lipoxygenase Inhibitors; D018077:Receptors, Leukotriene
Neue Entwicklungen in der Asthmatherapie: Wie wirken die einzelnen Leukotrienantagonisten?