View Abstract

A2749 - Phenotyping COPD Exacerbations Using Molecular Pathogen Detection Methods
Author Block: N. M. Alotaibi1, V. Chen2, Z. Hollander2, C. Hague3, J. Leipsic3, D. Murphy3, M. Demarco4, M. Fitzgerald5, B. McManus2, R. Ng2, D. D. Sin1; 1Department of Medicine, University of British Columbia, Vancouver, BC, Canada, 2PROOF Center of Excellence, Vancouver, BC, Canada, 3Department of Radiology, University of British Columbia, Vancouver, BC, Canada, 4Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada, 5Respiratory Medicine Institute for Heart and Lung Health, University of British Columbia, Vancouver, BC, Canada.
Rationale
Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are heterogeneous, with a variety of infectious and non-infectious causes; non-infectious causes are implicated in roughly a third of AECOPD. Our aim was to phenotype AECOPD using the CE-IVD marked Randox Respiratory Multiplex Array.
Methods
Subjects who were hospitalized with a primary diagnosis of AECOPD at St. Paul’s Hospital or Vancouver General Hospital in Vancouver, Canada were enrolled in the Rapid Transition Cohort. Of these, 72 subjects had sputum samples collected. The samples were tested on the Randox Respiratory Multiplex Array to detect various bacterial and viral pathogens. The subjects were classified into positive or negative microbiology groups based on the results. The pathogen-positive group was further subdivided into virus group if a virus was detected exclusively or with bacteria, and bacteria group if only bacteria were detected. Admission day 1 blood samples were assayed for N-terminal prohormone brain natriuretic peptide (NT-proBNP), C-reactive protein (CRP), and complete blood counts. We also examined the relationship of the Randox sputum data with length of hospital stay, and 1-year mortality.
Results
The subjects were 64% male with a mean age of 65.8 ± 11.5 years and a mean FEV1% predicted of 46.6 ± 16.7; 61% were current smokers at the time of assessment. 52 subjects had a positive result on the array, while 20 subjects had no pathogens detected. Of the 52 pathogen-positive subjects, 26 were classified into the virus group, and 26 were classified into the bacteria group. The pathogen-negative group had higher NT-proBNP concentrations (1216.5 [311-1920] vs. 369 [183-843] ng/L) (P=.042), lower hemoglobin concentrations (114 [95-133] vs. 128 [111-138] g/L) (P=.031), and higher red blood cell distribution width (RDW) values (16.2 [14.4-20] vs. 14.6 [13.9-16.1] %) (P=.029) compared to the pathogen-positive group. The pathogen-negative group had a longer hospital stay measured in days compared to the bacteria group (6 [5-14] negative group, 6 [3-11] virus group, 5 [3-7] bacteria group) (P=.046 on ANOVA, P=.02 on post hoc LSD). The pathogen-negative group had increased 1-year mortality compared to the bacteria group (P=.053).
Conclusions
Subjects with a negative result on a sputum pathogen array test had clinical and biochemical results strongly suggestive of a non-infectious etiology and generally had a worse prognosis than those with bacterial AECOPD. Molecular pathogen detection methods have the potential to aid in better identifying non-infectious etiologies of AECOPD, leading to better therapeutic decisions.