β2-agonists in asthma

Britton, John; Pavord, Ian; Wong, C. S.; Tattersfield, AE; Persson, C. G. A.; Morley, John E.

doi:10.1016/0140-6736(91)90912-9

Cited by 7 publications

(1 citation statement)

References 6 publications

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“…Inhaled salbutamol is a potent inhibitor of mast cell degranulation and abolishes the early, but not the late, bronchoconstrictor response to allergen (Cockcroft et al 1987;Howarth et al 1985). However, the protective effect of salmeterol against the late allergen response (Twentyman et al 1990) may simply reflect the longer duration of bronchial smooth muscle relaxation, as opposed to any true anti-inflammatory properties (Britton et al 1991;Rogers et al 1991). This hypothesis is also supported by data showing that there is no difference between inhaled salmeterol and salbutamol 4h after allergen challenge in terms of suppression of in vivo inflammatory mediator release, despite more prolonged protection against allergen-induced bronchoconstriction with salmeterol (O'Shaughnessy et al 1991).…”

Section: Novel {J2-agonistsmentioning

confidence: 97%

Risks Versus Benefits of Inhaled ??2-Agonists in the Management of Asthma

Lipworth

1992

Drug Safety

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The therapeutic goal for the treatment of asthma should be to suppress bronchial mucosal inflammation with preventive drugs such as inhaled corticosteroids, and to relieve symptoms of wheezing and breathlessness with bronchodilator drugs. The lower recommended doses of inhaled beta 2-agonists produce rapid effective bronchodilatation without systemic adverse effects; higher doses may produce substantial improvements in airway response which may help patients with more severe airflow obstruction. Higher doses of inhaled beta 2-agonists also cause dose-related systemic adverse beta 2 effects including tremor, tachycardia, hypokalaemia and associated electrocardiographic sequelae. In this respect, although fenoterol appears to cause greater extrapulmonary beta 2-mediated adverse effects at higher doses, there is no evidence to suggest that it is any less beta 2-selective. There is also some evidence to suggest that use of regular inhaled beta 2-agonists may cause increased bronchial hyperreactivity and possibly deterioration in disease control. Patients who require such regular use should therefore be given additional anti-inflammatory therapy with inhaled corticosteroids. The recent availability of novel, longer-acting inhaled beta 2-agonists such as salmeterol and formoterol will also make necessary a careful reappraisal of their long term use in patients with asthma.

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Section: Novel {J2-agonistsmentioning

confidence: 97%