Maximum Time of the Effect of Antileukotriene - Zileuton in Treatment of Patients with Bronchial Asthma.

Abstract

Objective:Maximum time of the effect of antileukotriene substances - Zileuton in the treatment of patients with bronchial asthma and increased bronchial reactivity and of the salbutamol as agonist of the beta2 adrenergic receptor studied in this work.Methods:Parameters of the lung function are determined with Body plethysmography. Raw and ITGV were registered and specific resistance (SRaw) was calculated. Zileuton (Zyflo, tbl. 600 mg), producer Cornerstone Therapeutics, USA was used in the research.Results:Results of this research, in patients with bronchial asthma, indicate that antileukotriene substances–Zileuton administered in a dose of 600 mg first day (oral route of administration 4 × 1 tbl.) has not caused significant decrease of the specific resistance of the airways (SRaw) (p value 0.1 > Alpha 0.05), whereas Zileuton administered two days in a row, in a dose of 600 mg (4 × 1 tbl. a day), has caused significant decrease of the specific resistance of the airways (SRaw) (P value 0.03 < Alpha 0.05). Effect of the control with salbutamol (beta2-adrenergic receptor agonist) is efficient in the removal of the increased bronchomotor tone, causing significant decrease of the resistance (Raw), respectively of the specific resistance (SRaw), (p value 0.05 = Alpha 0.05).Conclusion:Formation of leukotrienes depends on the lypoxygenation of the arachidonic acid by 5-lypoxygenase. Zileuton is an active and powerful inhibitor of the activity of 5- lypoxygenase and as such inhibits generation of its products. Consequently, besides inhibition of cys-LTs’, zileuton also inhibits the formation of leukotriene B4 (LTB4), which is a powerful chemotactic of other eicosanoids too, which depend on the synthesis of lekotriene A4 (LTA4). This suggests that the effect of antileukotrienes (Zileuton) is not immediate after oral administration, but the powerful effect of the Zileuton seen only after two days of inhibition of cys-LTs’, and inhibition of leukotriene B4 (LTB4) and A4 (LTA4).