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publication name Study of anti nuclear and anti smooth muscle antibodies in patients with chronic obstructive pulmonary disease
Authors Tahany M. Gouda a, Ayman A. Yousof a, Mahmoud M. Al Salahy a, Gehan F. Al mehy a, Tarek S. Essawy a,*, Osama S. El-Shaer b
year 2014
keywords COPD; ANA; ASMA; Autoimmune
journal Egyptian Journal of Chest Diseases and Tuberculosis
volume 63
issue Not Available
pages 49-56
publisher Not Available
Local/International International
Paper Link Not Available
Full paper download
Supplementary materials Not Available
Abstract

Background/aim: Autoimmunity is a disease in which the immune system mistakenly attacks the body’s own cells and tissues. Sometimes the whole body is attacked, and sometimes only one organ. The aim of the work: The aim of this study was to evaluate antinuclear and anti smooth muscle antibodies, two common markers of autoimmunity, in COPD and their relation with different components of the disease and disease severity. Methods: The study included 50 clinically stable COPD patients classified into two groups mild to moderate (group A) and severe to very severe (group B) according to GOLD (2009) [13] criteria plus 30 healthy control subjects (15 smokers and 15 non smokers). Blood levels of ANA and ASMA (measured by ELISA) were recorded. Results: Levels of both ANA and ASMA were significantly higher in patients than in controls as a whole group but smoker controls showed significantly higher levels of both antibodies than mild to moderate COPD group (group A) indicating that not only smoking is responsible for COPD but other factors also play a role. Also high levels of these antibodies in smoker controls than in non smokers indicate a role of smoking in their development which is augmented by the direct relation with smoking index both in patients and controls. Conclusion: Both ANA and ASMA levels are elevated in COPD patients compared to controls (smokers and non smokers) and levels elevated in healthy smokers compared to group A COPD patients. Autoimmunity plays a role in the pathogenesis of COPD.

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