The PCT level was measured on 243 patients who met the inclusion criteria, out of which 150 patients tested negative for COVID-19 and 93 patients were found to be positive. 84.9% of COVID-19 patients had negative procalcitonin levels (<0.25ng/ml). Of those, 67.7% had a procalcitonin level between 0 and 0.15ng/mL. In the absence of conditions which could potentially artificially raise PCT levels such as ESRD, trauma, burns, intra-cranial hemorrhage, and pancreatitis, PCT levels in COVID-19 patients were persistently negative despite a broad spectrum of disease severity. Based on the calculated odds ratio, a patient who presents with lower respiratory symptoms and a PCT level greater than or equal to 0.25ng/mL is 3.4 times less likely to also have COVID-19 (p<0.001). This indicates that despite the known inflammation caused by COVID-19, the low PCT with SARS-CoV-2 demonstrated here is consistent with the PCT levels in other viral respiratory infections. Moreover, the positive PCT level cut off of 0.25ng/ml used here is even lower than that of 0.5ng/ml in the existing literature on this subject . This finding is supported by one other study in the literature which analyzed characteristics of patients with COVID-19 and demonstrated that they have lower levels of plasma PCT (<0.5ng/mL) . The consistently low PCT level in these patients paired with the lowered cutoff for procalcitonin positivity suggests that serum PCT in patients with lower respiratory symptoms cases remains a quick and readily available tool in the era of COVID-19. It could also, therefore, potentially be used to guide clinicians in antibiotic initiation and discontinuation without increasing mortality or treatment failure [8, 9].
Despite the highly significant relationship between PCT and COVID-19, there were still 14 COVID-19 patients who had elevated PCT >0.25. Out of those 14 patients, 7 of them required ICU level of care due to increasing oxygen requirements and need for non-invasive positive pressure ventilation. Two patients demonstrated evidence of cytokine storm, and 3 of these patients died of hypoxemic respiratory failure. The most plausible explanation of an elevated PCT level in COVID-19 patients would be bacterial co-infection . Interestingly, blood cultures, MRSA and legionella screen in all these patients were negative. One possibility for the rise in PCT with absence of obvious infection could be due to the severe inflammation and release of pro-inflammatory cytokines such as IL-1B and IL-6—two of the inflammatory cytokines also known to trigger PCT release . A recent study of 140 Covid-19 patients noted PCT level to be increased in 25% of positive patients admitted to the ICU compared with 0% in patients who were not (p=0.029) . This could support the use of PCT as a biomarker for severe COVID-19, particularly in those patients without evidence of co-infection. However, additional studies looking specifically at this patient population are needed before any such statement can be made with statistical significance.
In conclusion, despite its inflammatory effects, SARS-CoV-2 does not significantly elevate the procalcitonin level above 0.25. These findings support the continued use of PCT as a clinical tool in the COVID-19 era.