الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Chronic obstructive pulmonary disease (COPD) is one of the most important respiratory causes of chronic morbidity and mortality throughout the world. Currently, COPD ranks fourth as a cause of death in the United States, behind heart disease, cancer, and stroke and further increases in its prevalence and mortality are expected in the near future.
It is defined as preventable and treatable disease, characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients.
Chronic tobacco smoking is the major risk factor for the development of COPD. Only a relatively small proportion of smokers Actually develop airway obstruction. Genetic factors are related to this Susceptibility and include nicotinic acetylcholine receptors genes(nAChRs) SNP rs1051730.
The aim of our study was to evaluate the association between single nucleotide polymorphism (SNP) of Nicotinic acetylcholine receptors (nAChRs) rs1051730 and clinical and pathological feature of COPD, smoking index and cigarette consumption per day and to clarify the role of smoking in (nAChRs) rs1051730 gene polymorphism.
The current study was carried out on 65 patients with COPD diagnosed and classified according to GOLD 2015, referred to Chest Department, Faculty of Medicine, Menoufia University hospitals and 35 healthy smoker controls.
Full history, general examination, local chest examination and spirometric measurements were made to every subject. Laboratory investigations were also carried out to all individuals including: complete blood picture ,serum lipid profile, and SNP assay for genotyping of (nAChRs) rs1051730 gene .
Subjects were divided into:- group I: include 65 smokers‘ subjects with COPD diagnosed spirometrically as forced expiratory volume in the first second (FEV1) < 80% of predicted values and forced vital capacity (FVC) <70%.
This group was sub classified according to severity by Global Initiative for chronic Obstructive Lung Disease (GOLD) strategy, as follows. Stage 1 (mild): FEV1 < 80% predicted; stage 2 (moderate): FEV1 50–79% pred; stage 3 (severe): FEV1 30–49% pred; and stage 4 (very severe): FEV1 <30% pred. group II: include 35 apparently healthy smokers‘ subjects with no COPD. Who had no history of lung or cardiovascular diseases served as a control group.
The current study showed:
A statistically significant decrease in pulmonary function test (FEV1%, FVC% and FEV1/FVC), Red blood cell count, Hemoglobin level and significant increase in white blood cells in patients group compared to the controls. While, there was none statistically significant difference among the two studied groups regarding age and cigarette smoking per day, smoking index and lipid profile.
There was a significant increased frequency of the AA genotype and A allele of the nicotinic acetylcholine receptors (nAChRs) SNP rs1051730 in patients group comparing to controls. AA genotypes increase the risk of COPD by 5.9 fold and A allele increases the risk by 2.6 fold.
AA genotype has significantly higher smoking index and more cigarette smoking per day than both AG and GG (p<0.05).
AA genotypes increase the risk of heavy smoking as indicator of nicotine dependence by 24.0 fold and A allele increases the risk by 3.36 fold.
Suggesting that nicotinic acetylcholine receptor (nAChRs) SNP rs1051730 has a role in COPD and of nicotine dependence.