It has been hard, over the years, to truly identify a role for procalcitonin. Generally speaking, its best niche seems to be as a sort of C-reactive protein on steroids – a non-specific infectious or inflammatory marker with better sensitivity than WBC. This has led to some usage in zero-miss contexts such as neonatal sepsis, as well as a potential role in antibiotic stewardship.
These authors, many of which are supported by the manufacturers of the procalcitonin assay, evaluate its predictive power in the setting of pneumonia hospitalization, attempting to risk-stratify patients for the combined endpoint of vasopressor support or invasive ventilation. Their goal, they say, is to use procalcitonin levels to better inform level-of-care decisions – both escalated and de-escalated – at the time of hospital admission.
They analyzed 1,770 patients from a prior pneumonia study for whom banked serum samples were adequate for procalcitonin measurement, 115 of whom met their combined critical illness endpoint. They report risk of critical illness increased approximately linearly with procalcitonin from 4% when procalcitonin was undetectable, to 22.4% when procalcitonin was 10ng/mL or above. The AUC for procalcitonin alone was 0.69, as compared to WBC at 0.54. Then, they further go on to add usage of procalcitonin in conjunction with other risk-stratification scores – ATS minor criteria, PSI, and SMART-COP – provided additional discriminatory information.
This could be a potentially useful and interesting application of procalcitonin – except they don’t really make any comparisons to other available tools, other than a straw man comparison with WBC. Would the venerable CRP have a similar AUC? Or, better yet, a lab we already use nearly ubiquitously to detect occult severe sepsis – a lactic acid level? The authors do not present any specific discussion of alternative approaches – of which their friends at BioMerieux probably appreciate.
“Procalcitonin as an Early Marker of the Need for Invasive Respiratory or Vasopressor Support in Adults with Community-Acquired Pneumonia”
https://www.ncbi.nlm.nih.gov/pubmed/27107491
Hello, I usually appreciate your posts but you seem biased regarding this biomarker. Yes, its use could be better or narrowed, but its added value regarding clinical practice is unquestionable now.Or is it?
See this study recently published in a small journal : http://www.thelancet.com/journals/laninf/article/PIIS1473-30991600053-0/ppt
C.
I am hopeful for a greater role for bacterial meningitis. Could we do away with LP's in the ED?
I agree with your comment re: bias – I am biased towards skepticism, in general, not specifically towards this biomarker. I am also biased against publications confounded by conflict-of-interest.
I do not see a role for procalcitonin as described in this article, but this does not exclude its use in critical care settings to guide antibiotic stewardship. The preponderance of evidence suggests beneficial effects in antibiotic discontinuation. This may yet be an instance where gross empiric antibiotic overuse has manufactured this problem, but, regardless, it does seem as though procalcitonin trending may be a solution.
There has been some evidence presented regarding procalcitonin and meningitis, primarily in the neonatal population to help detect SBI. I am not familiar with the most recent work.