Procalcitonin (PCT) is used as a biomarker for the diagnosis of sepsis, severe sepsis and septic shock. At the same time, PCT has also been used to guide antibiotic therapy. This review outlines the main indications for PCT measurement and points out possible pitfalls. The classic indications for PCT measurement are: (i) confirmation or exclusion of diagnosis of sepsis, severe sepsis, or septic shock, (ii) severity assessment and follow up of systemic inflammation mainly induced by microbial infection, and (iii) individual, patient adapted guide of antibiotic therapy and focus treatment. Using serially monitored PCT levels, the duration and need of antibiotic therapy can be better adapted to the individual requirements of the patient. This individualized approach has been evaluated in various studies, and it is recommended to be a part of an antibiotic stewardship program.
Postoperative induction of PCT largely depends on the type of surgery. Intestinal surgery and major operations more often increase PCT, whereas it is normal in the majority of patients after minor and primarily aseptic surgery. PCT can thus be used postoperatively for diagnostic means only when the range of PCT concentrations during the normal course of a certain type of surgery is considered and concentrations are followed up.
Endothelial activation and damage occur early during sepsis and play a major role in the pathophysiology of systemic inflammation. Various markers of endothelial activation are increased during sepsis and systemic inflammation, and in most studies, the level of markers such as soluble intercellular adhesion molecule, vascular cell adhesion molecule, and E selectin correlate well with the severity of inflammation and the course of the disease. However, to date, it remains unclear whether adhesion molecules and coagulation parameters are superior in this respect to interleukin-6 and procalcitonin, as direct comparisons are lacking. In addition, it is evident that markers of endothelial activation and coagulation parameters lack specificity for infection-induced endothelial damage and organ dysfunction.
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