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Serum procalcitonin concentrations in term delivering mothers and their healthy offspring: a longitudinal study
M Assumma1, F Signore, L Pacifico
1Divisions of Neonatology and Obstetrics, S. Camillo Hospital, 00152 Rome, Italy.
Insights
Procalcitonin (PCT) levels rise in healthy newborns, influenced by maternal PCT and prolonged membrane rupture. Understanding normal PCT kinetics is crucial for accurate neonatal sepsis diagnosis.
Area of Science:
- Neonatal Medicine
- Biochemistry
- Infectious Disease
Background:
- Procalcitonin (PCT) sensitivity and specificity for neonatal infection diagnosis vary.
- Normal postnatal PCT kinetics in healthy term newborns are not fully understood.
- Maternal and perinatal factors influencing neonatal PCT require further investigation.
Purpose of the Study:
- To investigate the association between maternal and neonatal serum PCT levels.
- To analyze the impact of obstetric and perinatal factors on PCT kinetics.
- To clarify normal PCT patterns in healthy term neonates.
Main Methods:
- Prospective study of 121 mother-infant pairs.
- Serum PCT measurements at delivery, 24, and 48 hours postpartum.
- Analysis of maternal and perinatal factors affecting PCT levels.
Main Results:
- Neonatal PCT levels were significantly higher than maternal levels at all time points.
- Maternal PCT, group B streptococcus colonization, and prolonged membrane rupture (>18h) affected neonatal PCT at birth.
- Prolonged membrane rupture was the only factor altering PCT at 24 and 48 hours.
- PCT levels in healthy neonates with risk factors remained below those in sepsis.
Conclusions:
- The postnatal rise in neonatal PCT is likely endogenous synthesis.
- Normal PCT kinetics and response patterns in healthy neonates are essential for accurate sepsis diagnosis within 48 hours of life.
Background:
The reported sensitivities and specificities of procalcitonin (PCT) concentrations for the diagnosis of neonatal infection vary widely. A postnatal increase of PCT has been observed in healthy term newborns with a peak at approximately 24 h of age, and many questions remain regarding maternal and perinatal factors that may influence the normal PCT kinetics during the immediate postnatal period.
Methods:
We prospectively investigated the association between the serum PCT values obtained from 121 mothers at delivery and serum PCT in their healthy, term offspring at birth as well as at 24 and 48 h of age. We also analyzed whether obstetric and perinatal factors would alter maternal and neonatal PCT response.
Results:
PCT concentrations in the babies at birth were significantly higher than in the mothers (P <0.0001), with even larger differences at 24 and 48 h of age. None of the variables identified from maternal and perinatal histories had a significant effect on maternal PCT response. In the healthy neonate, the variables that significantly affected the concentration of PCT at birth were the mothers' PCT (P <0.01), maternal group B streptococcus colonization (P <0.05), and rupture of membranes >/=18 h (P <0.01). The coefficient of linear correlation between the mother's PCT concentration and that of the baby at birth was 0. 32 (P <0.01). The only variable that significantly altered the PCT concentration at both 24 (P <0.01) and 48 (P <0.01) h of age was rupture of membranes >/=18 h. Nonetheless, the PCT response observed during the 48-h period after birth among healthy babies born to mothers with risk factors for infection was well below that reported previously among age-matched neonates with sepsis.
Conclusions:
The postnatal increase of PCT observed in the healthy neonate with peak values at 24 h of age most likely represents endogenous synthesis. In estimating the sensitivities and specificities of PCT for diagnosis of sepsis throughout the initial 48 h of life, it is important to consider the normal PCT kinetics and the pattern(s) of PCT response in the healthy neonate.