Upper-respiratory viral infection, biomarkers, and COPD exacerbations

Abstract

Background: Respiratory viruses frequently are recovered in the upper-respiratory tract during acute exacerbations of COPD (AECOPD), but their role as contributing pathogens remains unclear. The usefulness of procalcitonin and C-reactive protein as indicators of the presence or absence of viral infection in this setting also needs to be evaluated.

Methods: The study was of a prospective cohort of patients with COPD admitted to the ED for AECOPD. Reverse transcriptase-polymerase chain reaction (RT-PCR) for 14 respiratory viruses was performed on nasopharyngeal swabs collected at admission and after recovery in stable condition.

Results: Eighty-six patients (mean age, 72 years; male, 64%) were included. During AECOPD, upper-respiratory viral infections were detected in 44 (51%) patients: picornavirus in 22, metapneumovirus in seven, coronavirus in eight, influenza A/B in two, parainfluenza in two, and respiratory syncytial virus in three. A dual infection was present in three patients. After recovery, viruses were detected in only eight (11%) of 71 patients (P < .001 compared with AECOPD phase). In five of these patients, no virus had been identified during the initial exacerbation, thus suggesting a new viral infection acquired during follow-up. During AECOPD, procalcitonin and C-reactive protein levels did not differ significantly between patients with or without a proven viral infection.

Conclusions: Prevalence of upper-respiratory viral infection, as detected from nasopharyngeal swab by RT-PCR, is high in AECOPD and low after clinical recovery, suggesting that AECOPD frequently are triggered by viral infections initiated in the upper-respiratory tract. In our study, serum procalcitonin and C-reactive protein did not discriminate virus-associated exacerbations from others.

Trial registration: clinicaltrials.gov; Identifier: NCT00448604.

Figures

Figure 1

Flowchart of patients included in the study. “Follow-up impossible” refers to patients transferred to another hospital.

Figure 2

Viruses detected by polymerase chain reaction (PCR) in nasopharyngeal samples of 86 patients admitted for acute exacerbations of COPD (AECOPD) (black bars) and 71 patients who completed follow-up (white bars, stable period). RSV = respiratory syncytial virus.

Figure 3

Seasonal variability of viruses detected by reverse transcriptase-polymerase chain reaction (RT-PCR) of nasopharyngeal swabs in patients admitted for AECOPD. See Figure 2 legend for expansion of abbreviations.

Figure 4

Seasonal variability of samples at baseline during admission (A) and at 4-month follow-up (B).

Figure 5

Serum CRP (n = 86) and procalcitonin (PCT) (n = 81) in patients with AECOPD. Five values are missing for PCT (two in the virus-positive group; three in the virus-negative group). Patients with (n = 20) and without bacterial infection (n = 68) identified by semiquantitative bacterial analysis of sputum at admission for AECOPD (A). Patients with (n = 44) and without (n = 42) viral nucleic acids identified by RT-PCR of nasopharyngeal swabs at admission for AECOPD (B). Data are expressed as medians (interquartile range).