Procalcitonin direct antibiotic therapy in immunocompromised patients
Abstract
Procalcitonin (PCT) is a prohormone produced by the C-cells of the thyroid. Once split it becomes calcitonin and is responsible for calcium homeostatic. In response to pro-inflammatory cytokines extrathyroidal nonendocrine tissue produces immature PCT which can be detected in the circulation, reaching a maximum within approximate 12–24 hours after the onset of inflammation. Uniquely, interferon-gamma, which is released during viral infections, inhibits the production of PCT thereby making elevations in PCT useful in detecting bacterial infections as opposed to viral infections.1 Despite these potential benefits the role of PCT in the intensive care unit (ICU) has not been fully established. The problem is that PCT elevations can take place because of non-infective systemic inflammation, as seen during major trauma or after cardiac bypass, thereby making it difficult to differentiate bacterial from nonbacterial causes.2 This, together with the 24–48 hour time lag after the onset of an infection, as well as the persistent elevation seen after a major episode of systemic inflammation, limits the diagnostic accuracy of PCT.
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