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Tüberküloz ve toraks · Jan 2011
Does airway colonization cause systemic inflammation in bronchiectasis?
- Begüm Ergan Arsava and Lütfi Cöplü.
- Department of Chest Diseases, Faculty of Medicine, Hacettepe University, Ankara, Turkey. erganb@hacettepe.edu.tr
- Tuberk Toraks. 2011 Jan 1;59(4):340-7.
AbstractRecent evidence suggests the presence of accompanying systemic inflammation in chronic inflammatory airway diseases such as chronic obstructive pulmonary disease and asthma; however little is known regarding the presence of systemic inflammation in bronchiectasis. Although bronchiectasis was initially considered a stationary process, chronic bacterial colonization causes airway inflammation and progressive airway damage. The aim of this study was to determine the level of systemic inflammation in bronchiectasis patients and identify its relationship with colonization. White blood cell (WBC) count, erythrocyte sedimentation rate, serum C-reactive protein (CRP), plasma fibrinogen, interleukin-8, tumor necrosis factor-α and leptin levels were determined in clinically stable bronchiectasis patients (n= 50), and age- and sex-matched controls. Bronchiectasis patients were also analyzed according to colonization in sputum samples. There was no significant difference between bronchiectasis and control groups with respect to inflammatory markers but median (interquartile range-IQR) WBC count, CRP and fibrinogen levels were significantly higher in colonized patients (n= 14) when compared to non-colonized patients [8.2 (6.4-9.5) vs. 6.4 (5.8-7.7) x 103/mm3, 0.91 (0.45-1.29) vs. 0.42 (0.30-0.77) mg/dL, 433.5 (390.3-490.3) vs. 392.0 (327.0-416.0) mg/dL, respectively; p< 0.05]. There was no evidence supporting the presence of systemic inflammation in the overall bronchiectasis group when compared to controls. However, elevated WBC count, CRP and fibrinogen levels in patients with colonization suggest the presence of a systemic inflammatory response in clinically stable bronchiectasis patients with colonization.
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