Does airway colonization cause systemic inflammation in bronchiectasis?

Recent 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-alpha 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 10(3)/mm(3), 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

Amfizemli Hastalarda α1-Proteinaz İnhibitörü Aktivitesi ve Fenotiplerinin Belirlenmesi

In our study, functionally active α1-proteinase inhibitor (α1-PI) levels and phenotypeswere determined in sera of patients with emphysema and in that of healthy subjects. Patients were classified according to their smoking habits: Group I consistedof 7 nonsmoking (or limited history of smoking) patients. Group II consisted of heavily smoking 14 patients. Four patients having intermediate smoking habits were considered independently (Group III). Two of these patients were siblings with a history of familial emphysema. The Control group consisted of 28 healthy nonsmokingsubjects. Active serum α1-PI levels were assayed spectrophotometrically, by determining the extent of trypsin inhibition. α1-PI phenotypes were determined by isoelectric focusing on polyacrylamide gels. Once the serum α1-PI levels have been compared, the differences between Group I and Group II and the Control group were statistically insignificant (p >0.05). Isoelectric focusing results showed that all but 4 patients had the M1M1 or M1M2 phenotype. (The siblings in the Group III had the ZZ phenotype and 2 patients in Group II had undefined phenotypes). Considering these results, we concluded that, with the exception the siblings expressingthe ZZ variant, the development of emphysema in our patients was caused by an increase in elastase load rather than a deficiency in antielastase capacity. The increase in elastase load was most likely due to biological and chemical oxidants in the lung