الفهرس 
CHRONIC OBSTRUCTIVE PULMONARY DISEASEOnly 14 pages are availabe for public view
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Abstract
hronic 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 of dyspnea and cough. Tobacco smoking is the primary cause and major risk factor for the development of COPD and, in most industrialized countries, the disease has an increasing prevalence. Today, 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.
Early detection of COPD is clinically relevant because adequate treatment reduce exacerbations and improve quality of life. Nonetheless, diagnosing COPD is difficult, as a single gold standard is not yet available. Currently, diagnosis is based on assessment of symptoms, signs and spirometry results; namely the forced expiratory volume in one second (FEV1) and the forced vital capacity (FVC). For COPD diagnosis, spirometric airflow obstruction is a prerequisite, defined as a lowered ratio of the FEV1 to the FVC (FEV1/FVC ratio), persisting after bronchodilation. However, a controversy around the optimum FEV1/FVC threshold for COPD exists, which renders spirometry an insufficient diagnostic tool. Moreover, spirometry abnormalities can be subtle in the early phase.
Finding a biomarker that is specific for COPD has been challenging. The recent biomarker discovery has thus, focused on proteins synthesized predominantly in the lungs. Of these, surfactant protein (SP)-D has been the most studied.
Surfactant protein-D is a large, multimeric, collagen-containing, calcium-dependent collectin (C-type lectin), expressed predominantly in the endoplasmic reticulum of type 2 pneumocytes and in the secretory granules of Clara or nonciliated bronchiolar cells. The highest expression of SP-D in human tissues is observed in the distal airways and alveoli (mostly in type 2 pneumocytes). It is normally responsible for surfactant lipid homeostasis and pulmonary host defenses against microorganisms by promoting opsonization, neutralization, agglutination, complement activation and enhanced phagocytosis.
In this regard, our study aimed to investigate the clinical utility of serum surfactant protein D (SP-D) as a lung-specific marker in different stages of COPD, and to compare its levels between patients with stable disease and those on acute exacerbation, and also to correlate it with pulmonary function tests, measured by spirometry, namely; the forced expiratory volume in one second (FEV1) and the forced vital capacity (FVC), expressed as FEV1/FVC ratio.
This study was conducted at the Department of Chest at Ain Shams University Hospitals on 50 COPD patients (Group I) who were classified clinically into SCOPD (Group Ia) which included 30 patients, and AECOPD (Group Ib) which included 20 patients, and 30 controls (Group II) who were classified into 15 control non-smokers (Group IIa) and 15 control smokers (Group IIb). Patients in group (Ia) were reclassified according to FEV1% pred. into mild, moderate, severe and very severe SCOPD (subgroup Ia1, Ia2, Ia3 and Ia4 respectively).
All patients in this study were subjected to full history taking, thorough clinical examination, radiological investigations including chest X-ray, spirometry, routine laboratory investigations and serum SP-D assay which was carried-out using ELISA technique.
Results of the present study showed that there was a highly significant increase in serum level of SP-D in both SCOPD and AECOPD patients when compared to control groups (p<0.001, respectively) with the highest levels observed in the AECOPD group. Also, serum SP-D levels were significantly higher in AECOPD than in SCOPD or controls (p<0.001, respectively). However, no significant difference was observed between SCOPD subgroups.
Our results also demonstrated that serum SP-D is affected by smoking, where a highly significant increase in SP-D levels was demonstrated in smokers, compared to non-smokers (p<0.001) among the control group. Moreover, SP-D was significantly positively correlated with pack-year in both SCOPD and AECOPD (rs= 0.543, rs= 0.509, p<0.01, p<0.05, respectively).
Correlative study within SCOPD and AECOPD groups revealed that SP-D had a highly significant negative correlation with pulmonary functions (rs= -0.647, rs= -0.625, p<0.001, p<0.01, respectively).
Assessment of the diagnostic performance of serum SP-D in SCOPD (Gp Ia) versus control subjects (Gp II) using ROC curve analysis revealed that the best cutoff level of SP-D was 8.5 ng/mL. At this cutoff, the diagnostic sensitivity was 93.3%, specificity was 100.0%, positive predictive value was 100.0%, negative predictive value was 93.8% and diagnostic efficiency was 96.7%.
In conclusion, serum SP-D is considered a promising biomarker for the evaluation and follow-up of COPD patients, especially in diagnosis of acute exacerbation.