Procalcitonin for patient stratification and identification of bacterial co-infection in COVID-19

Editor – an abundance of biomarkers has been measured in hospitalised patients with COVID-19. Initial reports from China have shown that most patients with COVID-19 did not have elevated procalcitonin (>0.5 μg/L).^1,2 However, elevated levels were found more frequently in severe cases and in patients who died.^2–4

Variance in procalcitonin levels have previously been proposed to differentiate systemic inflammation of bacterial origin from viral origin in community acquired pneumonia and sepsis, with a significant rise indicating bacterial infection.^5,6 The lack of a procalcitonin rise in viral infections may be due to virus-stimulated production of interferon-γ by macrophages, which inhibits TNF-α in the immune response.⁵ The presence of lower procalcitonin levels has been shown to have a 94% negative predictive value for bacterial co-infection in intensive care unit patients with confirmed influenza A(H1N1)pdm09.⁷ Therefore, we suggest that raised procalcitonin observed in COVID-19 could be due either to bacterial co-infection, which is itself causing increased severity and driving systemic sepsis, or as a direct marker of a more severe or widespread viral infection.

As such, procalcitonin measurement on admission may be a useful marker to firstly predict patient deterioration in hospital and secondly, non-elevated procalcitonin on admission may be a good predictor of the absence of bacterial co-infection and allow the more targeted use of antimicrobials thus promoting antibiotic stewardship. Further work is needed to correlate the presence of raised procalcitonin and the presence of bacterial co-infection in COVID-19 patients.