Severe respiratory viral infection induces procalcitonin in the absence of bacterial pneumonia

IntroductionProcalcitonin expression is thought to be stimulated by bacteria and suppressed by viruses via interferon signalling. Consequently, during respiratory viral illness, clinicians often interpret elevated procalcitonin as evidence of bacterial coinfection, prompting antibiotic administratio...

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Veröffentlicht in:Thorax 2020-11, Vol.75 (11), p.974-981
Hauptverfasser: Gautam, Samir, Cohen, Avi J, Stahl, Yannick, Valda Toro, Patricia, Young, Grant M, Datta, Rupak, Yan, Xiting, Ristic, Nicholas T, Bermejo, Santos D, Sharma, Lokesh, Restrepo, Marcos I, Dela Cruz, Charles S
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Sprache:eng
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Zusammenfassung:IntroductionProcalcitonin expression is thought to be stimulated by bacteria and suppressed by viruses via interferon signalling. Consequently, during respiratory viral illness, clinicians often interpret elevated procalcitonin as evidence of bacterial coinfection, prompting antibiotic administration. We sought to evaluate the validity of this practice and the underlying assumption that viral infection inhibits procalcitonin synthesis.MethodsWe conducted a retrospective cohort study of patients hospitalised with pure viral infection (n=2075) versus bacterial coinfection (n=179). The ability of procalcitonin to distinguish these groups was assessed. In addition, procalcitonin and interferon gene expression were evaluated in murine and cellular models of influenza infection.ResultsPatients with bacterial coinfection had higher procalcitonin than those with pure viral infection, but also more severe disease and higher mortality (p
ISSN:0040-6376
1468-3296
DOI:10.1136/thoraxjnl-2020-214896