Clinical Chemistry 46:10
1583–1587 (2000)
Evidence-based
Laboratory Medicine
and Test Utilization
Serum Procalcitonin Concentrations in Term
Delivering Mothers and Their Healthy Offspring:
A Longitudinal Study
Marcello Assumma,1 Fabrizio Signore,2 Lucia Pacifico,3,5 Naila Rossi,1
John F. Osborn,4 and Claudio Chiesa3,5*
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 ⬇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
Divisions of 1 Neonatology and 2 Obstetrics, S. Camillo Hospital, 00152
Rome, Italy.
Institutes of 3 Pediatrics and 4 Hygiene, “La Sapienza” University of Rome,
00161 Rome, Italy.
5
Institute of Experimental Medicine, National Research Council, 00161
Rome, Italy.
* Address correspondence to this author at: Institute of Pediatrics, La
Sapienza University of Rome, Viale R. Elena, 324 00161 Rome, Italy. Fax
39-06-49-218-480; e-mail Claudio.Chiesa@Uniroma1.it.
Received May 12, 2000; accepted July 31, 2000.
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 agematched 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.
© 2000 American Association for Clinical Chemistry
High serum concentrations of procalcitonin (PCT),6 the
prohormone of calcitonin, have been reported in adults
and children with invasive bacterial or fungal infections
(1– 6 ). Although it has been suggested that PCT may be a
useful marker of septicemia in newborns, the estimates of
sensitivity and specificity for the diagnosis of neonatal
infection vary widely, especially during the 48-h period
after birth (7–14 ) when the majority of diagnostic problems are encountered. In a previous cross-sectional study
(9 ), we showed that in the healthy neonates circulating
concentrations of PCT increase gradually from birth to
reach peak values at about 24 h of age and then decrease
gradually by 48 h of life, primarily reflecting a physiologic
postnatal surge of PCT. However, many questions remain
unanswered about maternal and perinatal factors that
may influence the normal PCT kinetics during the immediate postnatal period. Given the low molecular mass
(⬇12 kDa) of PCT (15 ), it is not surprising that transplacental passage has been suggested as a possible source of
6
Nonstandard abbreviations: PCT, procalcitonin; GBS, group B streptococcus; CI, confidence interval; TNF-␣, tumor necrosis factor-␣; and IL-6,
interleukin-6.
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Assumma et al.: Procalcitonin in Mother-Newborn Pairs
the postnatal increase of PCT (16 ), although we are not
aware of any study dealing specifically with this issue.
The main objective of the present study was to investigate the association, if any, between serum PCT concentrations in mothers at delivery and serum PCT in their
healthy babies at birth as well as at 24 and 48 h of age. The
three fixed neonatal ages 0, 24, and 48 h could provide this
information given that the half-life of PCT is 22–29 h (17 ).
Also, we investigated whether maternal and perinatal
factors could confound these associations.
Materials and Methods
patients
This study was performed at the Obstetric Unit and the
well-baby nursery of the Saint Camillo Hospital, Rome.
As part of an ongoing prospective investigation of serum
PCT values in complicated and uncomplicated pregnancies, mothers were eligible for enrollment if: (a) they
agreed to participate in the study and signed consent
forms approved by the Institutional Review Board of the
Saint Camillo Hospital; and (b) they delivered singleton
term newborns with normal birth weights (ⱖ2500 g) and
with normal results on physical examination at birth
implying, therefore, no need of empiric management. The
mother-infant pair was included in the present study if all
the following criteria were met: (a) a blood sample was
collected at the time of delivery from the mother; (b) a
blood sample was obtained at birth, at 24 h, and at 48 h
after birth from each infant; and (c) the neonate had a
continuous, uncomplicated hospital stay until discharge
on day 3 after vaginal or day 4 after cesarean delivery and
also normal assessments at the 2- and 4-week follow-up
visits. We excluded parturients with: (a) multiple preexistent or pregnancy-related noninfectious complications; or (b) clinically evident intraamniotic infection
[defined as intrapartum fever (ⱖ38 °C) accompanied by at
least two of the following: tachycardia (maternal, ⱖ100
beats/min; fetal, ⱖ160 beats/min), uterine tenderness,
purulent amniotic fluid, or increased peripheral white
blood cell count (⬎15 000/mm3)].
All antepartum and intrapartum data were collected
prospectively and included maternal age, pre-existent or
pregnancy-related diseases, mode of delivery, use of
anesthesia, duration of active labor (18 ), interval between
rupture of membranes and delivery, maternal group B
streptococcus (GBS) colonization, intrapartum antimicrobial administration, and abnormalities in intrapartum
fetal heart monitoring. The institutional policy was to give
term women with rupture of membranes ⱖ18 h intrapartum penicillin or broad-spectrum antibiotics, if results of
GBS cultures were not known at the time of labor (19 ).
Late prenatal cultures (35–37 weeks) including vaginal
specimens for GBS culture (20 ) were considered a part of
good antenatal care. For those with poor or no antenatal
care, intrapartum vaginal specimens were obtained for
culture. For term women with rupture of membranes ⬍18
h, the institutional policy was to treat those patients with
late prenatal cultures positive for GBS. Neonatal data
collected included gestational age, birth weight, gender,
and Apgar scores at 1 and 5 min.
pct determination
Blood for PCT determination was centrifuged within 30
min of collection, and the serum was stored at ⫺70 °C
until analysis. PCT was first determined by the LUMItest威
PCT method (BRAHMS Diagnostica) as described in
detail elsewhere (9 ). According to the manufacturer, this
immunoluminometric assay has a detection limit of 0.1
␮g/L. Interassay and intraassay variations at both low
and high concentrations were ⬍8% and 7%, respectively.
Samples with PCT concentrations below the detection
limit of the LUMItest PCT assay were subsequently tested
with the LUMItest ProCa-S assay (BRAHMS Diagnostica),
which has been developed in a prototype format only.
This immunoluminometric test is more sensitive (limit of
detection, 0.005 ␮g/L) than the LUMItest PCT assay.
Duplicate determinations of PCT were performed for each
serum sample, without knowledge of the maternal and
neonatal clinical characteristics.
statistical analysis
The PCT values (Fig. 1) were distributed with a long tail
to the right (positive skew), but the logarithms of the
values of PCT were approximately normally distributed.
Fig. 1. Distribution of crude PCT values among 121 delivering mothers
and their healthy offspring at the three neonatal ages 0, 24, and 48 h.
Œ, 10 subjects; F, 1 subject.
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Clinical Chemistry 46, No. 10, 2000
Thus, the data were analyzed after a logarithmic transformation, and the results were expressed as geometric
means with 95% confidence intervals (CIs). The geometric
mean concentration of PCT in the mothers was compared
with that of the babies at birth and at 24 and 48 h of age
by applying a matched-pairs t-test to the logarithms of the
PCT values, from which the mean percentage difference
and its CI can be derived. The nonparametric Wilcoxon
test was also applied to confirm the result of the t-test.
The association between the serum PCT values obtained from mothers and serum PCT in their healthy
offspring at birth and at ages 24 and 48 h were investigated by multiple regression of the log PCT of the baby on
the log PCT of the mother, whereas dummy variables
were used to take account of the possible confounding
effects of: gestational diabetes, pregnancy-induced hypertension, intrapartum fetal distress, maternal GBS colonization, type of delivery (spontaneous vaginal, elective
cesarean section, emergency cesarean section, and induced delivery), duration of active labor, interval (h)
between rupture of the membranes and delivery, intrapartum antimicrobial administration, and use of epidural
or general anesthesia. All statistical tests were considered
significant if P ⬍0.05.
Results
One hundred fifty-two neonates born on 42 randomly
selected study days were enrolled at birth. Thirty-one
neonates were subsequently excluded from the study
because: 6 infants were transferred to the intermediate
nursery 12–18 h after birth, in 20 infants the PCT measurements were not made according to the protocol
design, and 5 infants were inadequately followed-up after
discharge from hospital. Thus, data from a total of 121
mother-newborn pairs were available for analysis.
The characteristics of mothers and their healthy infants
are summarized in Table 1. Table 2 shows the geometric
mean PCT concentration in delivering mothers and in
their healthy newborns at each postnatal age. PCT concentrations in the babies at birth were significantly higher
than in the mothers (P ⬍0.0001 by t-test; P ⬍0.0001 by
Wilcoxon test), with even larger differences at 24 and 48 h
of life. At 24 and 48 h after birth, the geometric mean
concentration of PCT in the babies was 220 and 76 times
higher than the concentration observed in the delivering
mothers, respectively (Table 2).
By multiple regression analysis, none of the variables
identified from maternal and perinatal history had a
significant effect on PCT response in parturient mothers.
Multiple regression analysis of PCT values observed in
the babies at delivery on the mother’s PCT and the
confounders identified from antepartum and intrapartum
data (see Statistical Analysis) revealed that the variables
that significantly affected PCT concentrations in the babies at birth were the PCT concentrations in the delivering
mothers, maternal GBS colonization, and rupture of membranes for 18 h or longer. The crude product–moment
Table 1. Maternal and neonatal characteristics.
Maternal
Mean age, years
Complications during pregnancy
Gestational diabetes
Pregnancy-induced hypertension
Mode of delivery
Spontaneous vaginal
Induced vaginal
Emergency cesarean section
Elective cesarean section
Use of epidural anesthesia
Use of general anesthesia
Mean length of active labor, h
Mean time of ruptured membranes, h
Ruptured membranes ⱖ18 ha
GBS colonizationa
(35–37 weeks of gestation)
Intrapartum antibimicrobial administration
Infant
Mean birth weight, g
Mean gestational age, weeks
Male gender
Apgar scores
ⱕ7 at 1 min
ⱕ8 at 5 min
a
31.0 (SD, 4.6)
5 (4.1%)
9 (7.4%)
54 (44.6%)
24 (19.8%)
12 (9.9%)
31 (25.6%)
23 (19.0%)
20 (16.5%)
2.9 (SD, 2.6)
4.9 (SD, 11.2)
13 (10.7%)
11 (9.0%)
24 (19.8%)
3230 (SD, 396)
39.2 (SD, 1.2)
65 (53.7%)
0
0
Occurring as an isolated event.
coefficient of linear correlation, r, between the mother’s
PCT values and those of the baby at birth was 0.32 (P
⬍0.01), and the Spearman rank correlation was 0.38. The
baby’s PCT concentration at birth was increased by a
factor of 1.45 (95% CI, 1.05–1.99; P ⬍0.05) if the mother
had GBS colonization and 1.50 (95% CI, 1.12–2.0; P ⬍0.01)
if the time from rupture of the membranes was ⱖ18 h. In
contrast, the multiple regression showed that the mothers’
PCT had no significant association with the baby’s concentration at both 24 (r ⫽ 0.021; P ⫽ 0.41) and 48 (r ⫽
0.025; P ⫽ 0.40) h of age. Likewise, the rank correlation
coefficients were 0.023 and 0.004, respectively. Indeed, at
both postnatal hours 24 and 48, the only variable found to
be associated with the babies’ values of PCT was the time
since rupture of the membranes. If this time was ⱖ18 h,
the concentration of PCT was increased by a factor of 2.84
Table 2. Geometric mean PCT values in 121 delivering
mothers and their healthy newborns at ages 0, 24, and
48 h of life and the ratios of the geometric means of the
newborns to that of the mothers.
PCT (␮g/L)
Geometric mean (95% CI)
Mothers
Newborns
At birth
At 24 h
At 48 h
Ratio newborn/mother
(95% CI)
0.010 (0.009–0.013)
0.094 (0.084–0.10)
2.47 (1.97–3.09)
0.83 (0.67–1.02)
8.5 (7.1–10.2)
220 (163–297)
76 (57–102)
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Assumma et al.: Procalcitonin in Mother-Newborn Pairs
(95% CI, 1.50 –5.48; P ⬍0.01) at 24 h of life and by 2.47
(95% CI, 1.29 – 4.73; P ⬍0.01) at 48 h. In fact, for babies
born to mothers with rupture of the membranes ⱖ18 h,
the geometric mean PCT values were 5.96 ␮g/L (95% CI,
2.50 –14.18) at 24 h of age and 1.82 ␮g/L (95% CI,
0.73– 4.53) at 48 h. In contrast, if the time since rupture of
the membranes was ⬍18 h, the geometric mean values of
PCT were 2.16 ␮g/L (95% CI, 1.74 –2.69) at 24 h of age and
0.74 ␮g/L (95% CI, 0.61– 0.92) at 48 h.
Discussion
In the early neonatal period, especially in the first 2 days
after birth, various kinds of laboratory values may change
considerably, and their mean “normal” values differ from
those measured in later periods. Variable intervals that
change rapidly have been, for example, observed for
bilirubin, aspartate aminotransferase, oxygen tension, hemoglobin, and neutrophilic cells as well as for hormones
and cytokines (21, 22 ). Some of the differences are attributable to direct stress on the baby during the perinatal
period or to maladaption to the extrauterine environment,
causing the activation or suppression of certain substances. Creatine kinase and thyroid-stimulating hormone
are in this category. Other changes are attributable to
influx from the placenta. For example, immunoglobulin G
that crosses the placenta raises the concentrations in the
infants toward the concentrations in the mother. The
modest positive association between PCT values in paired
maternal and cord sera found in our study suggests that
PCT may cross the placental barrier, but the findings of
higher PCT concentrations in cord sera compared with
maternal samples, with even larger differences at 24 and
48 h of age, cannot be explained on the basis of maternal
transfer alone. Therefore, the postnatal surge of PCT most
likely represents endogenous synthesis.
Most previous studies did not assess the postnatal
course of PCT (7, 8, 10 –14 ) in the healthy term baby,
neither did they provide information as to whether maternal and perinatal factors may affect the interpretation
of what constitutes the abnormal (and as importantly the
normal) postnatal PCT value. Consequently, the reported
“normal” ranges have been relatively broad and have
made uncertain the use of PCT as a discriminatory tool for
differentiating infected from uninfected neonates during
the immediate postnatal period. The present study, which
is the first to analyze the PCT response of a cohort of
healthy, full-term neonates born under different clinical
scenarios, shows that pathologic prenatal noninfectious
conditions, such as gestational diabetes or pregnancyinduced hypertension, do not affect the babies’ PCT
concentration during the 48-h period after birth. Additionally, perinatal stress, surgical trauma, and anesthesia
did not significantly alter PCT response in such neonatal
population. However, the novel finding observed in the
current investigation is that neonates born to intrapartumtreated mothers with isolated risk factors for infection,
although totally asymptomatic, had significantly in-
creased PCT concentrations when compared with those
who were born to mothers who were either risk factor
negative or who had only noninfectious clinical conditions.
The exact site of PCT release during sepsis is unclear.
Recently, Brunkhorst et al. (23 ) mentioned that one possible site of PCT production during inflammation is
peripheral blood mononuclear cells, whereas Nijsten et al.
(24 ) suggested that the liver is a major source of PCT
production. There are few data to support either possibility. Likewise, the mechanism of PCT release remains
uncertain. Dandona et al. (25 ) first showed that when
endotoxin was administered to apparently healthy human volunteers, the expected release of tumor necrosis
factor (TNF)-␣ and interleukin (IL)-6 was followed by an
increase and prolonged peak of concentrations of circulating PCT. A tenable interpretation was that endotoxin
might release PCT directly, without cytokine mediation.
More recently however, Nijsten et al. (24 ) showed that,
directly or indirectly, IL-6 and TNF-␣ release PCT. Whatever the site(s) and mechanism(s) of PCT release, the
amount of PCT produced and the degree of increase in
serum concentrations have been correlated with the extent of the inflammatory reaction to infection (1, 26 ).
Al-Nawas et al. (2 ) reported higher PCT concentrations
in adult patients with clinically documented infection
than in those merely fulfilling the criteria of systemic
inflammatory response syndrome. Similar observations
have been reported recently by Martin-Denavit et al. (27 )
in neonates with unspecified gestational age. These authors showed that, among neonates born to intrapartumtreated mothers who presented a risk factor for infection
(including premature rupture of membranes or maternal
GBS colonization), mean PCT values at both 24 and 72 h
of life were much higher in those with clinical signs of
infection than in the ones without. In the current study,
the magnitude of PCT response observed during the first
48 h of life among healthy term babies born to mothers
with either rupture of membranes ⱖ18 h or GBS colonization remained modest, being well below the concentrations reached in symptomatic neonates with early-onset
(i.e., within the first 48 h of life) infection (9 ). Nonetheless,
it would be reasonable to postulate that the increased PCT
concentrations in such neonates specifically represent a
host inflammatory response to the infectious stimuli, and
their presence may then remain a potential marker of
infection. We cannot rule out subclinical infection in some
of these infants born to intrapartum-treated mothers;
however, none of them became symptomatic or received
antibiotic treatment. Serum PCT values obtained in this
longitudinal study from healthy neonates born to mothers
without infectious risk factors are comparable with those
reported in a previous cross-sectional study of the whole
population of healthy neonates born after uncomplicated
pregnancy and labor (9 ). The pattern(s) of PCT response
and temporal course of the increase in PCT concentrations
in the healthy neonate should be taken into account to
Clinical Chemistry 46, No. 10, 2000
optimize the use of PCT in the diagnosis of early-onset
neonatal sepsis.
Mothers delivering at term had circulating PCT concentrations similar to those observed in the apparently
healthy adult population (1, 3 ). The maternal concentration of PCT did not appear to be affected by pregnancyrelated disorders, mode of delivery, use and type of
anesthesia, duration of active labor, and stressful labor.
Importantly, although maternal GBS colonization per se
or rupture of membranes ⱖ18 h per se appeared to be
associated with a significant increase in the neonatal PCT
concentration at or after birth, neither risk factor was
associated with a significant increase in maternal PCT
concentration at the time of delivery. Possibly the fetal
compartment responds differently than the maternal compartment in the presence of such infectious risk factors.
Future studies would be useful to clarify the role of
maternal serum PCT in preterm and term labor under
conditions of clinically overt or subclinical chorioamnionitis.
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