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Procalcitonin (PCT) is the 116–amino-acid precursor of calcitonin. In health, it is produced in thyroid C-cells and rapidly cleaved, so circulating levels are negligible. In systemic bacterial infection, however, PCT is synthesised ubiquitously by parenchymal tissues (lung, liver, kidney, adipose), making it a useful biomarker of bacterial-driven inflammation.
Bacterial endotoxin and pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) upregulate CALC-1 gene expression outside the thyroid, leading to a rapid rise in circulating PCT. Crucially, interferon-γ—prominent in viral infections and autoimmune disease—suppresses PCT production. This physiological “brake” explains why PCT tends to remain low in viral illness and sterile inflammation, unlike CRP.
In the NHS, PCT is most useful when embedded in protocol-driven pathways (e.g. ICU sepsis bundles) rather than as a stand-alone test. It should never override clinical judgement, cultures, or imaging.
📌 Makindo pearl: CRP tells you there is “fire” (inflammation). PCT helps decide whether the “smoke” is bacterial. Use both, trend them, and always interpret in clinical context.