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Serum Amyloid A Is a Biomarker of Acute Exacerbations of Chronic Obstructive Pulmonary Disease

¹ Department of Pharmacology, University of Melbourne, Melbourne, Australia; ² Department of Respiratory Medicine, Melbourne Health, Melbourne, Australia; ³ Victorian Infectious Disease Service and Centre for Clinical Research Excellence in Infectious Diseases, University of Melbourne, Melbourne, Australia; ⁴ Howard Florey Institute, University of Melbourne, Melbourne, Australia; ⁵ Department of Medicine, University of Melbourne, Melbourne, Australia; and ⁶ Department of Immunopathology, Westmead Hospital, Sydney, Australia

Correspondence and requests for reprints should be addressed to Steven Bozinovski, Ph.D., Department of Pharmacology, Medical Building (Level 8), University of Melbourne, Parkville, 3010 Australia. E-mail: bozis{at}unimelb.edu.au

Rationale: Much of the total disease burden and cost of chronic obstructive pulmonary disease (COPD) is associated with acute exacerbations of COPD (AECOPD). Serum amyloid A (SAA) is a novel candidate exacerbation biomarker identified by proteomic screening.

Objectives: To assess SAA as a biomarker of AECOPD.

Methods: Biomarkers were assessed (1) cross-sectionally (stable vs. AECOPD; 62 individuals) and (2) longitudinally with repeated measures (baseline vs. AECOPD vs. convalescence; 78 episodes in 37 individuals). Event severity was graded (I, ambulatory; II, hospitalized; III, respiratory failure) based on consensus guidelines.

Measurements and Main Results: Presumptively newly acquired pathogens were associated with onset of symptomatic AECOPD. In the cross-sectional study, both SAA and C-reactive protein (CRP) were elevated at AECOPD onset compared with stable disease (SAA median, 7.7 vs. 57.6 mg/L; P < 0.01; CRP median, 4.6 vs. 12.5 mg/L; P < 0.01). Receiver operator characteristics analysis was used to generate area-under-curve values for event severity. SAA discriminated level II/III events (SAA, 0.88; 95% confidence interval, 0.80–0.94 vs. CRP, 0.80; 95% confidence interval, 0.70–0.87; P = 0.05). Combining SAA or CRP with major symptoms (Anthonisen criteria, dyspnea) did not further improve the prediction model for severe episodes. IL-6 and procalcitonin were not informative.

Conclusions: SAA is a novel blood biomarker of AECOPD that is more sensitive than CRP alone or in combination with dyspnea. SAA may offer new insights into the pathogenesis of AECOPD.

Key Words: chronic obstructive pulmonary disease • exacerbation • biomarker • inflammation

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Inflammatory and other markers are currently being evaluated for their predictive value in exacerbations of chronic obstructive pulmonary disease. What This Study Adds to the Field Serum amyloid A appears to be better related to event severity in acute exacerbations of COPD than is C-reactive protein.

 

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