الفهرس 
TitleOnly 14 pages are availabe for public view
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Abstract
Asthma and COPD are common chronic inflammatory diseases of the airways and/or the lung with different inflammatory mechanisms and clinical phenotypes. A considerable percentage of patients with chronic airway disease have characteristics of both asthma and COPD. This condition is currently recognized as Asthma-COPD Overlap (ACO). There is a growing research interest to define ACO and characterise its pathophysiological features including the pattern of airway inflammation, the structural and functional characteristics of this understudied population.
Interleukin-17 (IL-17) is a key cytokine of the Th17 cells that has been suggested to orchestrate the neutrophilic airway inflammation. Thus, IL-17 has been suggested to play a role in the pathophysiology of severe asthma and COPD.
The aim of the present work was to study the pathophysiological features of ACO including the pattern of airflow limitation, airway inflammation and remodeling and the possible role of IL-17 in these pathophysiological mechanisms. To achieve this aim, the present study was conducted on 20 control subjects and 60 patients with chronic respiratory symptoms; 20 with asthma, 20 with COPD and 20 with ACO. Patients were identified using GINA and GOLD guidelines. All the patients withheld their bronchodilator medications for appropriate time before the study. Full medical history and routine physical examination were performed to all the patients. The following investigations were carried out:
1. All the subjects performed baseline pulmonary function tests using computerized spirometer (Erich Jaeger GmbH D-97204).
2. Bronchodilator reversibility testing was performed to all the patients using 800 μg Salbutamol inhaler.
3. Chest High Resolution Computerized Tomography (HRCT) was performed to all patients using a 16-slice spiral CT scanner (Siemens) to determine airway wall dimensions and the extent of emphysema.
4. Sputum cell count was performed to all subjects; Total cell count (TCC) was performed manually using a haemocytometer and Differential cell count (DCC) was performed using Leishman stain.
5. Sputum IL-17 level was measured in all subjects using Enzyme Linked Immunosorbant Assay (ELISA) technique.
6. Data were calculated and analysed using SPSS (version 20).
Our study revealed that ACO patients had similar clinical, physiological and radiological features to patients with COPD. Patients with ACO and COPD had similar lung functions except for bronchodilator responsiveness. Patients with ACO had greater flow response than patients with COPD, which was similar to asthma. In addition, ACO patients had a characteristic volume response after bronchodilatation, which distinguished them from patients with either asthma or COPD with cut off values for ΔFVC> 340 ml and %change FVC >18.44%.
Summary, Conclusion and Recommendations
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HRCT measurement demonstrated that ACO patients had similar airway dimensions to patients with either asthma or COPD. The extent of emphysema was similar in patients with ACO and COPD and both were higher than patients with asthma. In patients with ACO, FEV1/FVC was negatively correlated with the extent of emphysema. Nevertheless, bronchial wall thickness (WA/BSA) was negatively correlated with BDR in FEV1.
The percentages of sputum cells were similar among our patients group. Meanwhile, in our patients, sputum neutrophil% had a strong positive association with HRCT detected structural changes, including bronchial wall thickening, luminal airway narrowing and the extent of emphysema. Sputum neutrophil number was negatively associated with BDR in FEV1 in either the total patients or patients with ACO and post-bronchodilator FEV1 in ACO patients only.
As regards sputum IL-17, its levels were similar among our studied groups. However, sputum IL-17 levels were correlated positively with BDR in FEV1 and negatively with sputum neutrophils in patients with ACO. Accordingly, we suggest that IL-17 may have a physiological role in the protection against the adverse effects of sputum neutrophilia in patients with ACO.