Procalcitonin in Diagnosis of Post-Operative Bacterial Meningitis: A Promising but Limited Role

which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Editorial Procalcitonin (PCT) levels increase in inflammatory states following infection, tumor, burn, trauma, or surgery [1]. Many clinical studies have found that PCT levels significantly increase in patients with bacterial or fungal infection [2, 3]. Conversely, in cases of viral infection or inflammation caused by autoimmune diseases, PCT levels do not increase. Indicators related to existing inflammation, such as C-reactive protein (CRP) and white blood cell count, do not specifically respond to bacterial infection [4]. However, PCT could be a useful tool for diagnosis of sepsis since it has shown high specificity in the diagnosis and expection-ation of prognosis of bacterial infections in numerous studies [5]. PCT production is stimulated by the actions of interleu-kin (IL)-1ß, tumor necrosis factor-α, and IL-6, which are secreted according to the extent of bacterial infection, but is attenuated by interferon-γ, which is produced during viral infection. In addition, PCT levels increase within 6–12 hours in the presence of a stimulus, and fall to approximately half of the initial concentration within a day of the infection with improvement [6]. Choi et al. [7] investigated the use of PCT as a biomarker for the discrimination of non-bacterial meningitis from bacterial meningitis after brain surgery. In their study, neither type of meningitis was distinguishable by analysis of PCT alone. Many studies have investigated the utility of PCT for the differential diagnosis of bacterial meningitis and viral meningitis; such research has been prompted by the fact that PCT levels significantly increase in most cases of bacterial meningitis [8], probably due to the pathogene-sis of bacterial meningitis differing from that of viral meningitis. Bacterial meningitis arises from nasopharyngeal colonization by invasive bacteria and associated bactere-mia, and subsequent bacterial penetration of the blood– brain barrier. Therefore, community-acquired bacterial meningitis can cause systemic infection, which explains the increase in PCT levels in bacterial meningitis. In contrast , a study in patients with ventricle-peritoneal shunt infection , a non-systemic infection, did not show increased levels of PCT; this result was due to the fact that, in the absence of systemic infection, bacteria entered the meninges directly through the wound. Another reason for the inabili