Systemic Cytokines, Clinical and Physiological Changes in Patients Hospitalized for Exacerbation of COPD
Background:Systemic inflammation in patients with COPD may worsen during exacerbations, but there is limited information relating levels of systemic inflammatory markers with symptoms and physiologic changes during an exacerbation Methods:We measured dyspnea using the visual analog scale, pulmonary...
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Veröffentlicht in: | Chest 2007-01, Vol.131 (1), p.37-43 |
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Zusammenfassung: | Background:Systemic inflammation in patients with COPD may worsen during exacerbations, but there is limited information relating levels of systemic inflammatory markers with symptoms and physiologic changes during an exacerbation
Methods:We measured dyspnea using the visual analog scale, pulmonary function tests, hemograms, and plasma levels for interleukin (IL)-6, IL-8, leukotriene B4(LTB4), tumor necrosis factor-A, and secretory leukocyte protease inhibitor (SLPI) in 20 patients on admission to a hospital for exacerbation of COPD (ECOPD), 48 h later (interim), and 8 weeks after hospital discharge (recovery).
Results:Dyspnea was present in all patients. Inspiratory capacity improved faster than FEV1. Compared to recovery, there was a significant increase in the mean (± SD) hospital admission plasma levels of IL-6 (6.38 ± 0.72 to 2.80 ± 0.79 pg/mL; p = 0.0001), IL-8 (8.18 ± 0.85 to 3.72 ± 0.85 pg/mL; p = 0.002), and LTB4 (8,675 ± 1,652 to 2,534 ± 1,813 pg/mL; p = 0.003), and the percentages of segmented neutrophils (79 to 69%; p < 0.02) and band forms (7.3 to 1.0%; p < 0.01) in peripheral blood, with no changes in TNF-A and SLPI. There were significant correlations between changes in IL-6 (r= 0.61; p = 0.01) and IL-8 (r= 0.56; p = 0.04) with changes in dyspnea and levels of IL-6 (r= −0.51; p = 0.04) and TNF-A (r= −0.71; p < 0.02) with changes in FEV1.
Conclusions:Hospitalized patients with ECOPDs experience significant changes in systemic cytokine levels that correlate with symptoms and lung function. An ECOPD represents not only a worsening of airflow obstruction but also increased systemic demand in a host with limited ventilatory reserve. |
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ISSN: | 0012-3692 1931-3543 |
DOI: | 10.1378/chest.06-0668 |