Abstract
Smoking in asthmatics is responsible for the worsening of asthma symptoms, more frequent asthma exacerbations and hospitalizations and lowered quality of life. In smoking asthmatics the designated doses of the inhaled corticosteroid treatment are usually insufficient to accomplish total asthma control. Out of 54 screened adult patients up to 50 years old with mild asthma, 38 were involved in the study. They were divided in two groups: smokers and non-smokers. They received a total daily dosage of 500 µg of inhaled fluticasone propionate. A rescue medication, a short-acting ß2 agonist (salbutamol) in a dosage of 0.1 mg/per inhaled dose, was used when needed. Asthma was diagnosed by a positive metacholine provocation test and/or a positive bronchodilatator response. An asthma control test i.e. the ACT-TM questionnaire was performed before the beginning of the study and 6 weeks after the treatment with fluticasone propionate of the previous corticosteroid-naive patients. A statistically positive response (p<0.05) was reached in favor of non-smoking asthmatics. It can be concluded that ACT is a reliable tool to assess the effect of the topical corticosteroid treatment in non-smoking and smoking asthmatics. An achievement of better asthma control could be expected among both of the examined groups, but the effect of the intervention in the therapy is estimated to be more expressed within the group of asthmatic non-smokers. In smoking asthmatics there is a need for other therapeutic modalities such as increasing the dosage of inhaled corticosteroids, usage of combination therapy and/or adding low doses of aminophylline.
Highlights
The prevalence of smokers in the USA is 16.7% among men and 13.6% among women (CDC, USA, 2015)
It can be concluded that asthma control test (ACT) is a reliable tool to assess the effect of the topical corticosteroid treatment in non-smoking and smoking asthmatics
An achievement of better asthma control could be expected among both of the examined groups, but the effect of the intervention in the therapy is estimated to be more expressed within the group of asthmatic non-smokers
Summary
The prevalence of smokers in the USA is 16.7% among men and 13.6% among women (CDC, USA, 2015). It is well known that the exposure to tobacco smoke can cause bronchoconstriction and acute asthma attack, worsening of asthma symptoms and decline in FEV1, more frequent asthma exacerbations, more frequent hospitalizations, lowered quality of life, as well as altered or insufficient therapeutic response to the standard therapy, envisaged in the global guidelines for asthma treatment around the world (Thomson et al, 2005; Thomson et al 2013). Tobacco smoke has an effect on the immune system, modifying the inflammation associated with asthma; it causes oxidative stress, changes in the remodeling of the respiratory airways and possible emphasis of the allergenic sensitivity. Modified inflammation among smokers with asthma is not very investigated, because most of the studies for asthmatics on which the effects of anti-inflammatory therapy are followed are executed on a group of examinees with asthma that are non-smokers. A cause for this phenomenon could be a possible corticosteroid resistance among smokers with asthma, but the reason for this is still insufficiently researched. The anticipated doses are insufficient for achieving full asthma control within smoking asthmatics and there is an inadequate improvement of the respiratory function
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