Today's treatment of airway obstruction ... and tomorrow's?
Airflow limitation results from loss of elastic recoil (as in emphysema), or narrowing of large and small airways from smooth muscle contraction, mucosal swelling and/or oedema, mucous plugging (as in asthma), and loss of small airways (as in COPD). Bronchodilator regimes in asthma include inhaled beta 2-agonists, but these do not reduce bronchial hyper-reactivity but act quickly and synergise with oral slow-release theophyllines (serum level 10-20 micrograms/ml), without potentiating tremor which occurs with oral beta 2-agonists. Airway inflammation as the mechanism of asthma, although fashionable, remains unproven, and clearly requires to be specified for asthma. Inhaled steroids slowly improve FEV1 in asthma and in 10-20% of COPD, and reduce hyper-reactivity. Nedocromil has yet to reveal similar potency. Clinical trial of effective anti-PAF drugs or anti-leukotriene agents are awaited, but understanding the specific asthmatic inflammation is still needed for rational therapy. In COPD combining inhaled beta 2-agonists with ipratropium--both given by a reservoir device--can be effective, along with oral slow-release theophylline and possibly inhaled steroids. New inhalation devices (i.e. modified dry powder inhalers) will be needed as the freon propellents in MDI may soon cease manufacture due to potential environmental hazards.
Flenley
D C
DC
Department of Respiratory Medicine, University of Edinburgh, UK.
D000280:Administration, Inhalation; D000318:Adrenergic beta-Agonists / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy*; D001991:Bronchitis / Q000188:drug therapy*; D001993:Bronchodilator Agents / Q000627:therapeutic use*; D006801:Humans; D011656:Pulmonary Emphysema / Q000188:drug therapy*
D000318:Adrenergic beta-Agonists; D001993:Bronchodilator Agents