Eformoterol

Eformoterol

Eformoterol

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Eformoterol in patients with asthma



Donald M. Newnham MRCP, Denis G. McDevitt DSc and Brian J. Lipworth MD

Department of Clinical Pharmacology, Ninewells Hospital and Medical School, Dundee, Scotland, United Kingdom.

Received 29 June 1993; accepted 15 December 1993. Available online 17 June 2004.

The aim of the present study was to evaluate in vivo and in vitro β2-adrenoceptor responsiveness after chronic inhaled therapy with the long-acting β2-agonist eformoterol or placebo, given twice daily, in patients with mild to moderate asthma.



Seven asthmatic patients, age 34 ± 5 years were evaluated. Mean forced expiratory volume in 1 second (FEV1) (%predicted) at entry was 58 ± 5%. After at least 2 weeks run-in without β2-agonist therapy, patients were randomized to receive regular treatment with eformoterol 24μg twice daily or placebo twice daily given by metered-dose inhaler for 4 weeks, in a double-blind, crossover design. Dose-response curves (DRC) to eformoterol (cumulative dose 6μg to 126μg) for airways and systemic β2-responses were constructed at the end of each treatment period. Responses were measured at baseline, 30 minutes after each dose, and for 6 hours after the last dose. In addition, in vitro parameters of lymphocyte β2-receptor function were evaluated prior to the DRC after each treatment period.



There was a nonsignificant trend towards higher baseline values after eformoterol compared with placebo for FEV1: 0.16 L (95% CI −0.04 to 0.36) and forced expiratory flow (FEF25–75): 0.27 L/sec (95% CI −0.08 to 0.62). The peak bronchodilator response from the DRC and response 6 hours after the last dose were both significantly (P <0.05) attenuated after chronic therapy with eformoterol compared with placebo. The mean differences between eformoterol and placebo for delta FEV1 were as follows: peak: 0.26 L (95% CI 0.09 to 0.43), and at 6 hours: 0.39 L (95% CI 0.20 to 0.58). Corresponding values for delta FEF25–75 were as follows: peak: 0.41 L/sec (95% CI 0.10 to 0.71), 6 hours 0.52 L/sec (95% CI 0.22 to 0.82). Systemic responses were likewise significantly blunted after eformoterol treatment compared with placebo. There was also subsensitivity of lymphocyte β2-adrenoceptor function after treatment with eformoterol compared with placebo.



Our results suggest that chronic therapy with eformoterol produces tachyphylaxis to its bronchodilator response, which was greatest at 6 hours after the last dose, tachyphylaxis of extrapulmonary β2-mediated responses, and subsensitivity of in vitro β2-adrenoceptor function.

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