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Re: Smoke sensitivity versus corticosteroid insensitivity in asthma

Dear Editor,

The study by Tomlinson and colleagues [1] stirs further debate in relation to patients with asthma who continue to smoke. There are several points in the study, which are pertinent to consider.

Firstly, the small but statistically significant difference of 25 l/min in morning peak expiratory flow (PEF) observed between smokers and non-smokers following 12 weeks of low dose inhaled corticosteroid (ICS) therapy may not be clinically relevant. Indeed, there was no difference demonstrated in pre-bronchodilator forced expiratory volume in one second (FEV1) following treatment with either low or high dose ICS therapy between smokers and non-smokers. Moreover, the relatively high baseline pre-bronchodilator FEV1 of more than 80% of predicted normal, further questions the relevance of such a small difference in PEF.

Secondly, the increased exacerbation rate observed in asthmatic smokers may be directly attributable to tobacco smoke itself rather than corticosteroid insensitivity. This is because even with high doses of ICS, a difference persisted in morning PEF between smokers and non-smokers, albeit of smaller magnitude with a statistically non-significant trend. One could therefore argue that high doses of ICS may actually mask the negative effects of smoking.

Finally, the comment that asthmatics who continue to smoke may require alternative or additional anti-inflammatory drug treatment should be treated with caution. This may give the wrong impression that the medical profession will automatically deal with tobacco addiction through alternative pharmacological intervention. Clinicians should never forget that the first line management of all asthmatic smokers must always be strong encouragement to quit.

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