By M. Cazzola;S. Sethi;F. Blasi;A. Anzueto
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Additional resources for Therapeutic Strategies Acute Exacerbations in Copd
Indeed, upregulation of these cytokines in smokers with airway obstruction contributes to the main- Pathophysiology of COPD exacerbations 33 tenance of the inflammatory response. This inflammatory process is amplified during exacerbations with recruitment of neutrophils and eosinophils, which become the major components of the inflammatory response [41, 42]. NEUTROPHILS There are few pathological studies that have examined COPD patients during an exacerbation. Examination of bronchial biopsies, broncoalveolar lavage and, more recently, spontaneous or induced sputum has consistently shown increased airway inflammation and elevated levels of inflammatory cytokines in these patients [41–46].
Plasma biomarkers of inflammation such as C-reactive protein (CRP) and fibrinogen are increased during COPD exacerbations, even though they appear not to be useful in predicting the clinical severity of these acute events . Nevertheless, the level of serum CRP in the presence of worsening symptoms is able to reliably differentiate exacerbation of COPD from day-to-day symptom variation and may therefore be useful in the choice of the appropriate therapeutic intervention . Moreover, patients with frequent exacerbations showed a faster rise in plasma fibrinogen over time  and it is known that increased levels of CRP and plasma fibrinogen are associated with an increased risk for cardiovascular morbidity.
Celli BR, Barnes PJ. Exacerbations of chronic obstructive pulmonary disease. Eur Respir J 2007; 29:1224–1238. Fabbri L, Beghé B, Caramori G, Papi A, Saetta M. Similarities and discrepancies between exacerbations of asthma and chronic obstructive pulmonary disease. Thorax 1998; 53:803–808. Garcia-Aymerich J, Monsó E, Marrades RM. Risk factors for hospitalization for a chronic obstructive pulmonary disease exacerbation. Am J Respir Crit Care Med 2001; 164:1002–1007. Papi A, Luppi F, Franco F, Fabbri LM.