Abstract

Preeclampsia is a heterogeneous syndrome ranging from mild hypertension and proteinuria to severe preeclampsia with complications (1). It has also been reported that this severe pregnancy complicationmay be associated with an enhanced maternal inflammatory response and endothelial cell activation (2, 3), in that the placental tissue produces a variety of cytokines and hormones which are essential for the regulation of the feto-maternal unit by modulating the immune, reproductive and endocrine systems (4). Overall, preterm birth, preeclampsia, pregnancy loss and adverse neonatal outcomes have all been associated with inflammation (2). High-sensitivity C-reactive protein (hsCRP) has been reported to be increased in many patients with preeclampsia, even in the absence of manifest infection, and it could be used as a severity marker (5). Procalcitonin (PCT), a 14.5-kDa protein, is the 116 amino acid polypeptide precursor of calcitonin, a calcium regulatory hormone. Production is regulated by the Calc-1 gene, located on chromosome 11. Calc-1 codes for prePCT, which undergoes proteolytic cleavage of its signal sequence to produce the definitive PCT molecule (6). Current evidence suggests that PCT might be useful for detecting and evaluating severity of systemic bacterial infections. However, additional studies indicate that PCT may be a cytokine-like mediator of inflammation rather than a simple marker of infection (7, 8).

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