الفهرس 
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Abstract
The natural history of chronic obstructive pulmonary disease is characterized by frequent exacerbations. Majority of the exacerbations are infectious and bacteria responsible for 30-50% of these cases. The purpose of this study was to assess the effect of COPD and smoking on the serum ADA level, it was found that serum ADA level decreased in COPD patients and healthy smoking group.
This study was carried out on 100 subjects (patients and controls). The Patients carried out from The Abbasyia Chest Hospital. subjects divided into 50 cases (control group) which contained 25 healthy smoker group and 25 healthy nonsmoker group, and 50 cases diagnosed as having COPD according the criteria of the global initiative for chronic obstructive lung disease (GOLD 2016), which contained 25 COPD patients were in stable state, 25 COPD patients were in acute exacerbation. Acute exacerbation was defined by the presence of an increase in at least two of the following symptoms:
1. Increased cough
2. Increased purulence and/or volume of expectorations
3. Increased severity of dyspnoea (Saikat et al., 2013)
All patients were subjected to Laboratory investigations: serum ADA.
The current study observed that ADA activity decreased in acute exacerbation of COPD, COPD in the stable state and the control healthy smoking group. These results were matching with Goodarzi et al. (2010) who studied the ADA activity in COPD patients and healthy subjects (smoker /nonsmoker) and found that serum ADA activity in acute exacerbation of COPD and smoker control groups was significantly lower than nonsmoker groups. Decrease in ADA activity in COPD patients and in healthy control groups might be related to COPD and/or smoking, as the ADA activity decreased in all COPD patients with (acute exacerbation and stable state) and all COPD patients were smokers.
from the present study it was concluded that:
1) ADA level was low in all studied COPD patients and in healthy smoker group
2) ADA level was normal in healthy non smoker group
3) ADA therapy(gene therapy) could play an important role in controlling the pulmonary inflammation
4) It was concluded that high formation of adenosine in the lung might cause profibrotic pathways and might result in pulmonary fibrosis.
5) CRP is the common marker to show the existence of infection in patients with COPD.
RECOMMENDATION
1) ADA gene therapy can play an important role in controlling the pulmonary inflammation.
2) ADA enzymatic therapy is a polyethylene glycol-conjugated adenosine deaminase (PEG-ADA)therapy, enzymatically active ADA continuously circulates to act as a metabolic sink, detoxifying the adenosine and deoxyadenosine metabolites that accumulate to high levels in the absence of ADA. It increases the absolute numbers of circulating T and B lymphocytes and NK cells.
3) Inflammatory markers as CRP is recommended to all patients with AECOPD as The level of this inflammatory marker increases during exacerbations
4) Influenza vaccines recommended to all patients with previous history of frequent exacerbation of COPD especially elderly patients
5) Sputum culture is mandatory for all patients with AE-COPD before use of empirical antibiotics
6) Atypical organism is one of the commonest cause for AE-COPD so early detection by serological techniques and choice of proper antibiotics for it is very important
7) Giving proper antibiotics according to culture results help to reduce development of multi-drug resistant organisms.