الفهرس 
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Abstract
This study was performed to study the effect of smoking and asthma on airways and study the interrelation between them and to compare between the effect of corticosteroid on asthmatic smokers and non-smokers. In order to achieve these goals, this study included 117 asthmatic patients (42 smokers, 30 ex-smokers and 45 non-smokers) randomly selected from patients attended at Chest Out-patient clinic in Assuit University Hospital. Features used in making the diagnosis of asthma according to GINA guidelines 2020. All patients were males with mean age of asthmatic smokers and non-smokers were significantly lower than ex-smokers (32.40 ± 8.22 and 28.93 ± 7.98 vs. 38.20 ± 7.76 years; P < 0.001, respectively). All patients were subjected to the following: Medical history, asthma control questionnaire (ACQ) score, clinical examination, spirometry, Sputum cytology and serum levels of periostin and eotaxin-2. The following results were observed: Based on asthma control questionnaire (ACQ); the majority of asthmatic smokers and ex-smokers were uncontrolled in comparison to asthmatic non-smokers. However, the majority of asthmatic non-smokers were well controlled. Moreover, Post-bronchodilators FEV1/FVC and post-bronchodilators FEV1 were significantly lower among asthmatic smokers and ex-smoker in comparison to non-smokers. Regarding inhaled corticosteroid (ICS) therapy use, it was significantly higher in asthmatic smokers and ex-smokers in comparison to non-smokers. Dose of inhaled corticosteroid was low in all asthmatic non-smokers received ICS, while the majority of asthmatic smokers and ex-smokers received medium to high dose. As Regards sputum cellularity, most asthmatic smokers and ex-smokers had higher cellularity in comparison to non-smokers. Asthmatic non-smokers had higher sputum eosinophils, while asthmatic smokers and ex-smokers had higher sputum neutrophils.
Serum periostin was significantly higher in non-smokers in comparison to smokers and ex-smokers. Moreover, serum periostin in all asthmatic patients and smokers had significant negative correlation with smoking index, and positive correlation with eosinophils count. However, serum eotaxin-2 was significantly higher among smokers in comparison to non-smokers and ex-smokers. Moreover, serum eotaxin-2 in all asthmatic patients and smokers had significant positive correlation with smoking index, eosinophilic and neutrophilic count in sputum. However, it had negative correlation with forced expiratory volume-1. As regard ICS response, asthmatic smokers who received ICS had poor response and had insignificant improvement in comparison to those didn’t receive ICS as regard ACQ, sputum cytology, pulmonary function test, eotaxin-2 and periostin. However, asthmatic ex-smokers who received ICS had partial response. As regard PFT they had significantly higher post-BD FEV1 and post-BD FVC in comparison to those didn’t receive ICS. Asthmatic non-smokers who received ICS showed the best response as they were significantly well controlled as regard ACQ in comparison to those didn’t receive ICS. Moreover, they had significantly higher post-BD FEV1/FVC, post-BD FEV1 and post-BD FEF25-75. Also, they had significantly lower sputum eosinophils and neutrophils. We can conclude that; Asthmatic smokers likely represent a distinct phenotype of the disease and have worse outcomes compared with non-smoking asthmatics. Smoking cessation improves several asthma outcomes. The respiratory health benefits of not starting smoking and smoking cessation among those who do smoke are of considerable benefit. Smokers with asthma have a lower response to the beneficial effects of inhaled corticosteroids (ICS). Smoking adversely affects the course and response to ICS therapy in asthma. There is currently no optimal drug therapy to effectively treat airway inflammation in smokers with asthma, however many potential targets for future therapies exist. Since the inflammatory phenotype seen in smokers with asthma showed neutrophilic inflammation with low eosinophils, increased serum eotaxin-2 and low serum periostin, this phenotype of asthma requires specific therapeutic intervention aimed at prevent and reduce the remodeling and the most promising therapies may need further studies.