Etiología y biomarcadores de inflamación sistémica en las exacerbaciones leves a moderadas de la enfermedad pulmonar obstructiva crónica
Background: The etiology of acute exacerbations of chronic obstructive pulmonary disease (COPD) is heterogeneous and still under discussion. Inflammation increases during exacerbation of COPD. The identification of inflammatory changes will increase our knowledge and potentially guide therapy. Aim:...
Guardado en:
Autores principales: | , , , , , |
---|---|
Lenguaje: | Spanish / Castilian |
Publicado: |
Sociedad Médica de Santiago
2012
|
Materias: | |
Acceso en línea: | http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872012000100002 |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
Sumario: | Background: The etiology of acute exacerbations of chronic obstructive pulmonary disease (COPD) is heterogeneous and still under discussion. Inflammation increases during exacerbation of COPD. The identification of inflammatory changes will increase our knowledge and potentially guide therapy. Aim: To identify which inflammatory parameters increase during COPD exacerbations compared to stable disease, and to compare bacterial and viral exacerbations. Material and Methods: In 85 COPD patients (45 males, mean age 68 ± 8 years, FEV1 46 ± 17% of predicted) sputum, nasopharyngeal swabs and blood samples were collected to identify the causative organism, during a mild to moderate exacerbation. Serum ultrasensitive C reactive protein (CRP), fibrinogen and interleukin 6 (IL 6), neutrophil and leukocyte counts were measured in stable conditions, during a COPD exacerbation, 15 and 30 days post exacerbation. Results: A total of 120 mild to moderate COPD exacerbations were included. In 74 (61.7%), a microbial etiology could be identified, most commonly Mycoplasma pneumoniae (15.8%), Rhinovirus (15%), Haemophilus influenzae (14.2%), Chlamydia pneumoniae (11.7%), Streptococcus pneumoniae (5.8%) and Gram negative bacilli (5.8%). Serum CRP, fibrinogen and IL 6, and neutrophil and leukocyte counts significantly increased during exacerbation and recovered at 30 days post exacerbation. Compared to viral exacerbations, bacterial aggravations were associated with a systemic inflammation of higher magnitude. Conclusions: Biomarkers of systemic inflammation increase during mild to moderate COPD exacerbations. The increase in systemic inflammation seems to be limited to exacerbations caused by bacterial infections. |
---|