الفهرس 
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Abstract
Chronic obstructive pulmonary disease (COPD) is a multicomponent disease characterized by airflow limitation that is not fully reversible and is often treated with bronchodilators. Its pathology includes abnormal airway inflammation, airway remodeling, alveolar destruction and enlargement of airspaces (emphysema), leading to poor gas exchange and clinical symptoms from dyspnea and cough. Smoking cigarettes as environmental factor significantly increases the risk of developing COPD. Passive exposure to cigarette smoke known as environmental tobacco smoke (ETS) contributes to respiratory symptoms and COPD. Over 300 million people worldwide have COPD. The WHO predicts that by 2020, COPD will be the third leading cause of mortality and the fifth leading cause of morbidity throughout the world.
Environmental tobacco smoke (ETS) is a complicated mix of substances and chemicals found in the indoor air as a direct result of tobacco smoking. Active exposure to tobacco smoke that comes from directly smoking tobacco is now known to be very harmful to health and increased risk of cancer, respiratory and cardiovascular disease. Oxidative imbalance has been considered a major feature of COPD for some time.
In this regard, the present study aimed to evaluate the important role of biochemical investigations and shed light on smoking as environmental factors on the chronic obstructive pulmonary disease patients and passive smokers compared to control group.
All subjects in this study were subjected to full history taking, thorough clinical examination, chest X-ray, spirometry, routine laboratory investigations and new biochemical markers (fibrinogen level, serum alpha one antitrypsin, serum C-reactive protein, serum nitric oxide and sputum nitric oxide).
Results of the present study showed that pulmonary function tests (FEV1&FEV1/FVC) significantly lower in COPD patients than in passive smokers and controls. ABG analysis (Pco2) showed significantly higher in COPD patients than in passive smokers and controls whereas (Po2) showed significantly lower in COPD patients than in passive smokers and controls. The mean serum levels of A1AT, NO and ALB significantly lower in COPD patients than in passive smokers and controls. Mean levels of plasma fibrinogen, serum CRP, NO in sputum and other liver function tests (ALT & AST) showed significantly higher in COPD patients than in passive smokers and controls. Kidney function tests (BUN & Creatinine) showed significantly higher in COPD patients than in passive smokers and controls. Also ESR, WBC and NE% showed significantly higher in COPD patients than in passive smokers and controls. While Hb and PLT showed significantly lower in COPD patients than in passive smokers and controls.
Plasma Fibrinogen level, Serum C-reactive protein and sputum nitric oxide are significantly raised in COPD patients and passive smokers, indicating that they may be used as biomarkers for exacerbation. Also serum alpha one antitrypsin and nitric oxide are significantly reduced in COPD patients and passive smokers. Their levels were correlated with pulmonary functions (FEV1 & FEV1/FVC) and arterial blood gases.
Biochemical markers used to asses COPD patient activity and detect exacerbation of the disease.