When using procalcitonin (PCT) assays to support clinical decisions, speed and accuracy counts. That’s where PCT kinetics come into play—one factor that makes PCT unique from other inflammatory biomarkers. Unlike other tests, PCT provides timely information specific to systemic bacterial infection, with respect to its presence, course, and severity.1 For example, after a bacterial insult, cytokine IL-6 rises and falls too quickly, whereas C- reactive protein (CRP) levels rise much later and decline much slower than the actual resolution of the episode. PCT, on the other hand, is subject to stimulation by competing causes of inflammation to a lesser degree than other biomarkers.2
Serial PCT testing provides valuable information regarding patient response to treatment and outcome risk.3
Healthy subjects/non-infected patient: < 0.1 µg/L4
Critically ill patients with a PCT > 2.0 µg/L have a high risk of progression to sepsis or septic shock.5-7
In the presence of a bacterial infection, PCT levels will begin to increase in the first 3 to 6 hours after the onset of infection. The levels will continue to rise rapidly, reaching a peak at 12 to 24 hours. The half-life of PCT is approximately 24 hours.5
PCT has prognostic implications, with higher levels correlating to severity of infection and rapidly declining levels after treatment indicating a positive prognosis.3
Assessing PCT trend over time provides another key insight: patients whose PCT levels fail to decline under treatment may face therapeutic failure and increased mortality risk.6
In particular, it was demonstrated that PCT levels that decline less than 80% from the baseline within four days are associated with increased all-cause 28-day mortality—especially when the baseline PCT measurement is > 2.0 µg/L.3
Daily variations of PCT levels during ICU hospitalization in patients admitted with sepsis and septic shock that survived or did not survive.6
PCT kinetics also lead to greater insights around antibiotic therapy decision-making. Because PCT blood levels rise within 3 to 6 hours after bacterial infection, the levels mirror the host response and severity of infection. Once infection is controlled and the patient is adequately responding to antibiotics, PCT levels decrease by about 50% per day.8
In LRTI patients, when the PCT levels have decreased to < 0.25 µg/L, or ≥ 80% below the peak value, it appears to be acceptable and safe to stop antibiotic therapy, assuming patients also show a favorable clinical response.9,10
Similarly, in patients with suspected or confirmed sepsis, when PCT levels have decreased to < 0.5 µg/L, or > 80% below the peak value, stopping antibiotic therapy appears to be safe and acceptable, assuming patients also show a favorable clinical response.9,10
It is important to note that if PCT levels do not decrease by more than 80% at Day 4 of a patient’s illness, treatment failure should be considered and patient re-assessment is recommended.11 Using PCT to decide when to stop antibiotics has been shown to reduce total antibiotic usage and decrease the duration of antibiotic therapy.12
While other biomarkers have been used to target the use of antibiotics, improve clinical outcomes, and lower costs, their impact has been limited. In contrast, the inclusion of PCT in antimicrobial stewardship is a game-changer. But it’s not enough to understand the kinetics of PCT—you need to see for yourself what PCT can do for your antibiotic administration, your patients, and your bottom line.
Antibiotic therapy should be considered regardless of PCT result if the patient exhibits one of the following:13
If antibiotics are withheld, reassess the patient if symptoms persist or worsen and repeat PCT measurement within 6 to 24 hours. To assess treatment success and to support a decision to discontinue antibiotic therapy, follow up tests should be performed once every 1 to 2 days, based upon physician discretion in considering the patient’s evolution and progress.13 Note that PCT levels may not be elevated in patients infected by certain atypical pathogens, such as Chlamydophila pneumoniae and Mycoplasma pneumoniae.14