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Background: Better identification of immunological and inflammatory changes in chronic obstructive pulmonary disease (COPD) exacerbations will help identify exacerbations phenotypes associated with bacteria, viruses and sputum eosinophilia in order to predict prognosis, guide therapy and provide new therapeutic targets. This study aimed to identify systemic and local immunological and inflammatory changes during COPD exacerbations, and to compare clinical COPD exacerbation phenotypes especially those with infectious etiology. Methods: This study included 30 patients with acute COPD exacerbations and 16 stable COPD patients as controls. Sputum samples from exacerbation patients were analyzed for bacterial and viral infections. IL-1?, IL-6, TNF-?, apolipoprotein A1, lipocalin-1 and CXCL-10 were assessed in serum and sputum samples from patients and controls. Results: Acute COPD exacerbation patients had significantly higher levels of serum CXCL-10, and sputum IL-1?, IL-6, TNF-?, CXCL-10, apolipoprotein A1 and lipocalin-1 with areas under the receiver operating characteristic curves (AUC) of 1, 0.93, 1, 1, 0.766, 1 and 0.94, respectively. Bacterial exacerbation patients had significantly higher levels of sputum IL-6 and TNF-? with an AUC of 0.845, 0.839 respectively. Serum lipocaline-1 was significantly lower in patients with viral exacerbation compared to non-viral exacerbations with an AUC of 0.752. Peripheral percentage eosinophils were significantly higher in eosinophilic exacerbations with an AUC of 0.72. Conclusion: Acute COPD exacerbations were associated with higher increase in the local inflammatory reaction rather than systemic inflammation. Sputum IL-6 and TNF-? can predict bacterial exacerbations while lipocalin-1 in blood can predict viral exacerbations. Peripheral percentage eosinophils are the best predictor for eosinophilic exacerbations.
[Marwa Salah Mostafa, Khaled M Hassanein, Alaa Abdel Monaeim (2014); Role of Immunological and Inflammatory markers in the Identification of Acute COPD Exacerbations with Infectious Etiology Int. J. of Adv. Res. 2 (10). 0] (ISSN 2320-5407). www.journalijar.com
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