Introduction

‘Calcitonin’ was first identified during studies of parathyroid function in dogs1 – a new parathyroid hormone that caused a transient hypocalcaemia. Subsequently demonstrated in the human serum of patients with medullary thyroid carcinoma, its heterogeneity hinted at the existence of multiple forms of this new hormone and of a precursor prohormone.2 The identification of this procalcitonin (PCT) in the hypocalcaemia of Staphylococcal toxic shock syndrome3 first drew the association of PCT with sepsis and inflammatory states, which was confirmed by subsequent studies. The first prospective study of PCT in children with sepsis revealed a rapid and dramatic increase in the levels of PCT, which normalised with appropriate antibiotic therapy.4 Elevated PCT has been demonstrated following the injection of endotoxin into healthy volunteers, that is detectable at 4 h with a peak at 6 h postadministration.5

Demonstration of its rapid increase in response to inflammatory stimuli and favourable comparisons of its performance as an indicator of serious infection with established markers such as C-reactive protein (CRP) have encouraged the ongoing investigation of PCT as a reliable and discriminatory diagnostic and prognostic tool in childhood and adult infection. Furthermore, the study of PCT has begun to explain its role as a mediator of sepsis. Antibodies that bind PCT have markedly reduced mortality from sepsis in animal models suggesting that immunoneutralisation may be a promising adjunctive therapy.6 This paper seeks to elucidate the current understanding of PCT as a marker of childhood infection and to draw attention to areas of ongoing research.