Published ahead of print on November 15, 2007, doi:10.1164/rccm.200705-678OC Am. J. Respir. Crit. Care Med., Volume 177, Number 3, February 2008, 269-278 A more recent version of this article appeared on February 1, 2008
Submitted on May 7, 2007 Serum Amyloid A is a Biomarker of Acute Exacerbations of COPDSteven Bozinovski1*,1 Department of Pharmacology, The University of Melbourne, Parkville, Victoria, Australia, 2 Department of Respiratory Medicine, Melbourne Health, Parkville, Victoria, Australia; Victorian Infectious Disease Service and Centre for Clinical Research Excellence in Infectious Diseases, The University of Melbourne, Parkville, Victoria, Australia, 3 Department of Respiratory Medicine, Melbourne Health, Parkville, Victoria, Australia, 4 Victorian Infectious Disease Service and Centre for Clinical Research Excellence in Infectious Diseases, The University of Melbourne, Parkville, Victoria, Australia, 5 Howard Florey Institute, The University of Melbourne, Parkville, Victoria, Australia, 6 Department of Immunopathology, Westmead Hospital, Wentworth, NSW, Australia, 7 Department of Pharmacology, The University of Melbourne, Parkville, Victoria, Australia; Department of Medicine, The University of Melbourne, Parkville, Victoria, Australia * To whom correspondence should be addressed. E-mail: bozis{at}unimelb.edu.au.
Rationale: Much of the total disease burden and cost of COPD is associated with acute exacerbations (AECOPD). Serum Amyloid A (SAA) is a novel candidate exacerbation biomarker identified by proteomic screening. Objective: To assess SAA as a biomarker of AECOPD. Methods: Biomarkers were assessed (i) cross-sectionally (stable vs. AECOPD; in 62 individuals) and (ii) repeated-measure longitudinally (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. Results: Presumptively newly acquired pathogens were associated with onset of symptomatic AECOPD. In the cross-sectional study both SAA and CRP were elevated at AECOPD onset compared to 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 (ROC) analysis was used to generate Area Under Curve (AUC) values for event severity. SAA discriminated Level II/III events (SAA; 0.88, 95% CI, 0.80 to 0.94 vs. CRP; 0.80, 95% CI, 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. Conclusion: 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
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