TY - JOUR T1 - P246 Airway and systemic inflammation in stable and exacerbated bronchiectasis: a pilot study JF - Thorax JO - Thorax SP - A167 LP - A168 DO - 10.1136/thoraxjnl-2011-201054c.246 VL - 66 IS - Suppl 4 AU - R Chitkara AU - H Batchelor AU - R J Sapsford AU - S Workman AU - A R C Patel AU - A J Mackay AU - B Grimbacher AU - J R Hurst Y1 - 2011/12/01 UR - http://thorax.bmj.com/content/66/Suppl_4/A167.4.abstract N2 - Introduction It is not known whether systemic inflammation reflects lower airway inflammation in non-CF bronchiectasis. If confirmed, blood biomarkers may provide useful information on pulmonary disease burden in both stable and exacerbated states. Serum C reactive protein (CRP) is readily measurable in many clinical settings, including at point-of-care, and procalcitonin (PCT) has a potential role with documented utility in other respiratory diseases. This study explored the relationship between airway and systemic inflammatory biomarkers in adult patients with non-CF bronchiectasis.Method Serum CRP (for systemic inflammation) and PCT, and sputum interleukin (IL)-6 (for airway inflammation) were measured in 31 well-phenotyped stable patients from The London Bronchiectasis Cohort. Six exacerbation samples were obtained from patients who had been previously sampled at baseline, with the exacerbation sample obtained at exacerbation onset, prior to initiation of additional antibiotic therapy. Sputum IL-6 was measured using ELISA, serum PCT using TRACE, and CRP using immunoturbidimetry techniques. Data were analysed using SPSS V.14.0.Results Of the 31 patients, 23 (74.2%) patients were female, with a mean (SD) age of 54.7 (14.9) years, FEV1 2.09 (0.90) l (75.71% predicted), and FVC 3.12 (1.01) l. The predominant aetiologies were primary immunodeficiency (mostly CVID, n=13, 42%), post-infectious (10, 32%) and idiopathic (4, 13%). The median (IQR) baseline sputum IL-6 was 101 (30–701) pg/ml, baseline serum PCT was 0.030 (0.021–0.040) μg/ml and CRP 3.0 (1.0–6.0) mg/l. The degree of systemic inflammation in stable bronchiectasis reflected that occurring in the airways as evidenced by a significant correlation between sputum IL-6 and serum CRP in the 31 stable samples (r=0.43, p=0.027). There was also a correlation between the two systemic markers (PCT and CRP: r=0.42, p=0.029), but the relationship between serum PCT and sputum IL-6 concentration was not statistically significant (r=0.28, p=0.127). In the six patients with paired samples, serum PCT increased significantly from baseline to exacerbation (0.031 vs 0.147 μg/ml p=0.043). Changes in sputum IL-6 and blood serum CRP did not reach statistical significance.Conclusion We report a direct relationship between airway and systemic inflammation in stable patients with non-CF bronchiectasis. This suggests that systemic biomarkers may be useful for monitoring local disease activity in this neglected condition. ER -