Original Paper

Neonatology 2019;116:85–91 Received: October 2, 2018

Accepted after revision: January 25, 2019
DOI: 10.1159/000497237 Published online: May 21, 2019

Serial C-Reactive Protein Measurements

in Newborn Infants without Evidence of
Early-Onset Infection
Kathryn Macallister a, b Adam Smith-Collins c, d Helen Gillet c Linze Hamilton c
       

Jonathan Davis a, e  

a Neonatal Directorate, King Edward Memorial and Perth Children‘s Hospitals, Women and Newborn Health Service,
Perth, WA, Australia; b Neonatal Department, Gloucestershire Royal Hospital NHS Foundation Trust, Gloucester,
 

UK; c Regional Neonatal intensive Care Unit, St. Michael’s Hospital, University Hospital Bristol, NHS Foundation
 

Trust, Bristol, UK; d Department of Neonatal Neuroscience, School of Clinical Sciences, University of Bristol, Bristol,
 

UK; e Centre for Newborn Research and Education, School of Child and Paediatric Health, University of Western
 

Australia, Perth, WA, Australia

Keywords derived. Comparisons of median CRP values between groups

C-reactive protein · Newborn · Postnatal ·
Negative blood culture
Abstract
Background: C-reactive protein (CRP) is used to assist the
diagnosis and monitoring of newborn infection. Little is
known about CRP activity after birth in the absence of infec-
tion. Objective: The aim of this work was to describe postna-
tal CRP responses in the first days of life in asymptomatic
infants with a negative blood culture. Methods: Data were
collected from infants who had a blood culture taken at
<72 h of age in a UK maternity hospital. All CRP values and
their time from birth were recorded. Infants with signs of in-
fection, positive blood culture, or major congenital anoma-
lies were excluded. Infants were analysed by gestation
(greater or less than 37 weeks). Normalised CRP curves were
generated by linear interpolation and centile curves were
were made by Mann-Whitney U test at 24, 36, and 48 h. Re-
sults: During the study period a total of 219 babies were
screened. After exclusions, 73 infants (58 term, 15 preterm)
were analysed. In asymptomatic term neonates the CRP
(mg/L) peaked at 9.4 after 34.6 h. In preterm babies the CRP
peak was 1.75 at 43 h. The median (IQR) values were higher
in the term group at 24 and 36 h: 2.5 (1–10.5) versus 0 (0–2.2;
p = 0.02) and 3 (0–8.6) versus 0 (0–2.8; p = 0.031). Conclu-
sions: A CRP rise was demonstrated in term and preterm in-
fants without evidence of infection. This rise was greatest in
term infants. CRP values must be interpreted in the context
of an infant’s clinical condition and not used alone to guide
clinical decision making. © 2019 S. Karger AG, Basel
K.M. and A.S.-C. contributed equally to this study.
130.235.66.10 - 7/20/2019 2:05:48 PM

© 2019 S. Karger AG, Basel Jonathan Davis

Centre for Newborn Research and Education, University of Western Australia
Lund University Libraries

c/o King Edward Memorial Hospital

E-Mail karger@karger.com
374 Bagot Road, Subiaco, Perth, WA 6008 (Australia)
www.karger.com/neo
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E-Mail jonathan.davis @ uwa.edu.au

Table 1. Risk factors and clinical indicators of early-onset neonatal infection, adapted from NICE guidance, which recommends treating
babies with one red flag (in bold) or more than one risk factor/clinical indicator
Risk factors
Maternal GBS colonisation
Invasive GBS infection in previous baby
Pre-labour rupture of membranes
Rupture of membranes for more than 18 h in a preterm birth
Preterm birth <37 weeks gestation
Maternal pyrexia in labour
Maternal IV antibiotics for suspected invasive bacterial
infection in labour
Early-onset newborn sepsis (EONS) has been defined
by the Committee on the Fetus and Newborn and Com-
mittee on Infectious Diseases of the American Academy
of Paediatrics as “a blood or cerebrospinal fluid culture
obtained within 72 h of birth growing a pathogenic bacte-
rial species” [1] and is a significant cause of morbidity and
mortality worldwide. Bacteria are acquired from the
mother, most commonly ascending from the cervix or,
more rarely, transplacentally. The most common caus-
ative organism is Group B Streptococcus (GBS), with an
incidence of 0.57 cases per 1,000 live births and case fatal-
ity of 5.2% in the UK and Republic of Ireland [2].
The diagnosis of EONS remains a challenge. Symp-
toms, when present, are non-specific and overlap with
those of other non-infective neonatal pathology, or may
be absent entirely [3]. Clinical diagnosis depends on a
combination of perinatal risk factors, clinical evaluation,
and biochemical markers.
One of the most widely used biochemical tests in the
investigation of EONS is C-reactive protein (CRP). The
National Institute for Health and Care Excellence (NICE)
in the UK recommends that CRP is measured prior to
commencing antibiotics for suspected infection and
again at 18–24 h [4].
Data on CRP in healthy term or preterm infants is in-
complete. There is evidence that even in well term or
near-term neonates there may be a physiological rise in
CRP after birth [5–7]. CRP levels in newborns with non-
infective complications, such as meconium aspiration
syndrome, perinatal asphyxia, and intraventricular haem-
orrhage, have been shown to be elevated [8–10].
Infants with a rise in CRP without evidence of infec-
tion may receive unnecessary antibiotic treatment as a
result. This may lead to a prolonged hospital stay, disrup-
86 Neonatology 2019;116:85–91
DOI: 10.1159/000497237
Clinical indicators
Respiratory distress
Increased oxygen requirement or respiratory support
Increased apnoeas or bradycardias
Hypotension
Glucose intolerance
Impaired peripheral perfusion
Lethargy
Temperature instability
Ileus/feed intolerance
Decreased urinary output
Metabolic acidosis
tion of maternal-infant bonding, increased risk of iatro-
genic complications, and propagation of antibiotic resis-
tance. The aim of this study was to establish CRP centiles
in a population of term babies who had no clinical signs
of infection or bacterial growth on blood culture.
Methods
This retrospective cohort study was conducted at St Michael’s
Hospital Neonatal Intensive Care Unit in Bristol, UK, a regional
referral (level III) neonatal unit in the southwest of England. Data
were collected for all infants in the hospital who had a blood cul-
ture taken <72 h after birth during two discrete 2-month time pe-
riods: September 2012 to October 2012, and April 2013 to May
2013. The local procedure at this time was based on the UK na-
tional NICE guidance that infants with specific perinatal risk fac-
tors for infection or clinical indicators of infection (Table 1) should
have blood taken for culture and CRP and be commenced on in-
travenous (IV) antibiotics [4].
Information regarding pregnancy, labour, clinical status of the
infant, and laboratory blood results were obtained from medical
notes, nursing charts, the Badger database (digital neonatal data-
base), and the laboratory results system. Collected data included
gestation, perinatal risk factors for infection, clinical indicators of
infection, blood culture, and serial CRP results. All babies were
commenced on IV antibiotics after the blood cultures had been
taken. Infants born at <37 completed weeks gestation were defined
as being preterm.
Blood cultures were collected in a paediatric blood culture bot-
tle (BacT/ALERT®, Biomérieux Inc., Craponne, France). They
were incubated for 5 days and were classified as positive if an or-
ganism was grown during this time. The recommended volume of
blood collected for culture was 1 mL. Blood (0.5 mL) was collected
for CRP analysis via a venous or capillary sample into a lithium
heparin tube (Vacuette, Greiner Bio-One, Kremsmünster, Aus-
tria). CRP was measured using a standard laboratory assay (Roche
Diagnostics, Basel, Switzerland).
Infants with major congenital malformations, those who had
any clinical indicators of infection (Table 1), and those with posi-
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Table 2. Reasons for blood culture
sampling, n (%) Term Preterm
(n = 58) (n = 15)

Preterm birth following spontaneous

labour (<37 weeks) 0 (0) 10 (66.7)
Maternal GBS colonisation 8 (13.8) 0 (0)
Prolonged rupture of membranes (>18 h) 11 (18.9) 3 (20)
Maternal pyrexia in labour (>38° C) 21 (36.2) 1 (6.7)
Maternal IV antibiotics in labour 2 (3.4) 1 (6.7)
No documented reason 16 (27.6) 0 (0)

Table 3. Demographic characteristics of the

infants, and peak and time of peak CRP Term Preterm

n 58 15
Median gestational age (range), weeks 40.4 (37.3-43) 34.3 (27.7–36.6)
Median birthweight (range), g 3,550 (2,620–4,480) 1,814 (975–3,020)
Median peak CRP (IQR), mg/L 3 (1–13.6) 0 (0–3)
Mean time to peak CRP (SD), h 34.6 (7.1) 41.9 (12.6)

tive blood cultures were excluded from analysis. Serial CRP values
and the time from birth were obtained for each infant and used to
generate CRP values at 0, 6, and 12 h from birth, and then every
12 h thereafter. The CRP at t = 0 h was assumed to be 0 in each
case, as CRP does not cross the placenta [11]. At least 2 measure-
ments of CRP were performed in each infant (median 2 measures/
infant, range 2–6), with further measurements taken if it was felt
they would guide clinical decision making, for example to identify
a rising or falling trend in CRP.
Remaining values were determined by linear interpolation be-
tween the closest two measures taken at known time points. For
example, if an infant had a CRP measured at 24 h of 10 mg/L and
at 48 h of 20 mg/L, with no measures taken in between, a calcu-
lated value of 15 mg/L would be generated for the 36-h time point.
Where no further data existed (i.e., past the time point of the
final actual CRP measure), CRP was assumed to decay exponen-
tially with a half-life of 19 h, derived from previous data [12]. Once
CRP values fell (or were predicted to fall) to below 1, they were
considered to be 0. For each group of interest, the data at each time
point were ranked. Data were then generated for the 10th, 25th,
50th, 75th, 90th, and 95th centiles. Where these data fell between
actual subject data rows, these were generated by linear interpola-
tion (for example, in a group of 55 infants, the 10th centile would
fall on the 5.5th infant, so the mean of the values of the 5th and 6th
would be used to generate the centile data).
Statistics
The CRP distribution was truncated at 0 and showed a marked
positive skew. Therefore, differences between CRP at time points
(24, 36, 48, and 72 h) were tested for statistical significance using
the Mann-Whitney U test for independent samples, and the Bon-
ferroni correction was applied for multiple comparisons. Test sta-
tistics are given as original U values but also reported as normalised
z-scores for ease of interpretation.
Results
A total of 219 infants (157 term, 62 preterm) had a
blood culture taken during the 2 study periods. After the
exclusion of 128 symptomatic infants (12 infants with
positive blood cultures, 4 with major congenital anoma-
lies, and 2 infants who were > 72 h of age when the cul-
tures were taken), 73 asymptomatic infants with nega-
tive blood cultures remained. These were subdivided
into term infants (n = 58) and preterm infants (n = 15).
The reasons for taking blood cultures are outlined in
Table 2.
The characteristics of the infants together with the
peak CRP and time to peak CRP are shown in Table 3.
Normalised CRP curves, generated by linear interpola-
tion of measured values and exponential decay, were gen-
erated as described above (Fig. 1, 2). These demonstrate
that in our sample 25% of asymptomatic term infants,
screened due to risk factors for infection (Fig.  1), had
raised CRP levels >10 mg/L at 24 and 36 h from birth.
These infants would have been considered for a lumbar
puncture in accordance with the UK national (NICE)
guidance.
Median (IQR) CRP values were significantly higher in
the term than the preterm group at 24 h [2.5 (1–10.5) vs.
0 (0–2.2) mg/L, U = 343, z = 2.56; p = 0.02, corrected for
multiple comparisons] and at 36 h [3 (1–13.6) vs. 0 (0–
2.8) mg/L, U = 356, z = 2.41; p = 0.03]. These differences
were no longer significant at 48 h [1.89 (0–8.6) vs. 0 (0–
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CRP in Newborn Infants without Signs of Neonatology 2019;116:85–91 87

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 Color version available online
35
10th centile
30 25th centile
50th centile
25 75th centile
90th centile

CRP, mg/L
20 95th centile

15

10

0
0 20 40 60 80 100 120 140 160 180
Fig. 1. Normalised CRP curves for asymp-
Time from delivery, h
tomatic term infants without evidence of
sepsis (with or without risk factors); n = 58.

Color version available online

20
18 50th centile
75th centile
16 90th centile
95th centile
14
12
CRP, mg/L

10
8
6
4
2
0
Fig. 2. Normalised CRP curves for asymp- 0 20 40 60 80 100 120
tomatic preterm infants without evidence of Time from delivery, h
sepsis (with or without risk factors); n = 15.

2.4) mg/L, U = 431, z = 1.56; p = 0.24] or 72 h [0.5 (0–3.4) Discussion

vs. 0 (0–1) mg/L, U = 455.5, z = 1.32; p = 0.38].
Subgroup analysis was undertaken to separately con-
sider the term infants with and without clearly identifi-
able antenatal risk factors for sepsis. In the group with
clearly identifiable risk factors (n = 42) the median
(IQR) peak CRP was 3 (0.5–13.5) mg/L and mean (SD)
time to peak CRP (for those with peak > 5 mg/L) was
23.1 (13.8) h. Those without identified risk factors (n =
16) had a median (IQR) peak CRP of 2.3 (1.1–5.8) mg/L
and the mean (SD) time to peak CRP (for those with
peak > 5 mg/L) was 42 (12) h. Median CRP values be-
tween the subgroups did not differ at 24, 36, 48, or 72 h.
There was, however, a significantly earlier median
(IQR) CRP peak in the group with risk factors versus no
risk factors [30 (6–36) vs. 48 (36–48) h, U = 12, z = 1.9;
p = 0.03; Fig. 3).
The CRP response in this group of infants suggests that
there is an inflammatory response following birth that is
independent of infection. The normalised CRP curves for
term infants demonstrate that at least 25% of well term
babies without evidence of infection had a peak CRP
greater than 10 mg/L. Under the current NICE guidelines
many of these babies would therefore have had a lumbar
puncture performed. In addition, these babies may well
have had prolonged antibiotic courses while waiting for
the CRP to fall. Prolonged use of intravenous antibiotics
requires a longer hospital stay for the infant and possibly
the mother. It also increases the risk of iatrogenic infection
secondary to intravenous cannulae and exerts an influ-
ence on antibiotic sensitivity. In addition, having to un-
dergo a lumbar puncture can be a traumatic experience for
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25
20
15
CRP, mg/L
10
0
Fig. 3. 90th centile CRP values over time for
term infants with (n = 42) and without (n =
16) risk factors for sepsis.
infants and their parents, and may also risk the introduc-
tion of iatrogenic central nervous system infection.
CRP is an acute-phase reactant produced in the liver
in response to pro-inflammatory cytokines such as inter-
leukin (IL)-6 and, to a lesser extent, IL-1 [13]. These cy-
tokines are produced in response to acute tissue injury,
which may be infectious, inflammatory, or traumatic in
origin. In adults, CRP levels greater than 5 mg/L can be
detected 6 h after a single insult and reach peak levels at
around 48 h [14]. The sensitivity of CRP in detecting neo-
natal infection varies widely between studies. One study
found that an initial CRP value had a sensitivity of 39.4%
for detecting proven or probable EONS, but that this is
improved to 92.9% if the CRP was repeated after 24 h [15].
This was corroborated in a study of the CRP response of
491 infants [16], concluding that the sensitivity of CRP in
EONS was improved by the use of serial measurements.
A recently published study reported CRP values in 859
healthy term newborns at 12, 24, and 48 h of life [17]. CRP
levels in these babies were significantly higher at 48 h than
at 12 or 24 h. CRP levels were higher if a baby had been
born by vaginal delivery or emergency caesarean section
compared to an elective caesarean, and higher if there had
been pre-labour rupture of membranes, prolonged la-
bour, or meconium-stained amniotic fluid. CRP in these
infants was significantly lower if their mother had com-
pleted a full course of intrapartum antibiotics.
CRP is part of an inflammatory cascade and stimu-
lated by IL-6, which in turn is stimulated by catechol-
amine production [18–19]. Serum concentrations of
adrenaline and noradrenaline are higher at birth in babies
born by vaginal delivery compared to those born by cae-
sarean section [20]. We compared, albeit with a small
sample, infants with and without pro-inflammatory risk
CRP in Newborn Infants without Signs of
Infection
Color version available online
No risk factors
Risk factors
0 50 100 150 200
Time from delivery, h
factors (prolonged rupture of membranes, preterm la-
bour, and GBS colonisation). There was a difference in
CRP levels between these groups and the time to peak
CRP was earlier in infants with risk factors, possibly as a
result of the related maternal inflammatory response be-
fore delivery. CRP may also be affected by the physical
stress of labour and delivery. We did not collect these data
and cannot comment on their influence on the CRP re-
sponse in the infants described in this study.
The results for the preterm infants show that fewer
well preterm infants mounted a substantial CRP response
after birth in our study population when compared to the
well term infants. This supports previous evidence that
CRP responses may be reduced in preterm infants [21].
However, one preterm infant did mount a CRP response
to 19 mg/L despite being clinically well throughout.
CRP responses appear to be less pronounced in pre-
term infants, making the role of CRP in detection of pre-
term infection less clear. There is evidence that elevations
of CRP in response to birth, infection, or non-infectious
conditions are lower and shorter in preterm infants com-
pared to term infants, and that the CRP response increas-
es with each week of gestational age [21]. Thus, CRP may
not be a sensitive marker of infection in this group of in-
fants.
Most of the asymptomatic term infants who had blood
cultures taken had risk factors for infection as per the cur-
rent NICE guidance [4], which recommends screening
for infection and commencing antibiotics in all babies
with more than one risk factor for infection or a single red
flag risk factor (see Table 1). It is therefore common prac-
tice for healthy babies to receive at least 48 h of antibiotics
while waiting for blood culture results, and serial CRPs
are measured during this time. Some of the term babies
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included did not have any documented risk factors for
infection and antibiotics were commenced at the treating
physician’s discretion. In these cases, it is likely that po-
tential risk factors were cautiously interpreted and anti-
biotics commenced as a result. For the preterm infants,
many of those who had a blood culture taken did not have
documented risk factors for infection. A blood culture
was taken and antibiotics commenced because these in-
fants demonstrated respiratory distress (likely due to im-
maturity).
There are several limitations of this study. Firstly, the
retrospective nature meant that it was sometimes difficult
to elucidate the initial concern which led to asymptom-
atic infants without risk factors for infection having a
blood culture taken. Secondly, all of the infants included
were on antibiotics following blood culture, so we cannot
say whether they would have had an altered CRP response
or perhaps become clinically unwell had they not been on
antibiotics, although all of their blood cultures taken pri-
or to commencing antibiotics were negative. Thirdly, the
number of infants included was small, especially in the
case of the preterm infants, but the population is reflec-
tive of the demographics of infants receiving antibiotics
in a tertiary neonatal unit at any given time.
The infants in this study had a negative blood culture
and no clinical signs of infection, yet demonstrated a rise
in CRP. This suggests that there may be a CRP response
following birth in some infants. Clinicians should be
aware of this when making treatment decisions based on
a CRP result. This response appears more pronounced in
term compared to preterm infants and with the addition
of maternal pro-inflammatory factors. An isolated rise in
CRP should not be used to determine investigations or
the length of antibiotic treatment, and it must be inter-
preted in view of the clinical condition of the infant to aid
decision making.
Acknowledgements
The authors would like to thank the contribution of the staff of
St. Michael’s Regional NICU for assistance in the conduct of this
study.
Statement of Ethics
The authors have no ethical conflicts to disclose. This project
was undertaken as part of a quality improvement project and ap-
proved by the governance infrastructure of the University Hospital
Bristol NHS Foundation Trust.
Disclosure Statement
The authors have no conflicts of interest to declare.
Funding Sources
The authors received no funding for the presented study.
Author Contributions
K.M. wrote the initial report and collected data. A.S.-C. per-
formed the statistics and assisted in writing the report. H.G. and
L.H. collected data and assisted in writing the report. J.D. envi-
sioned the project and supervised the collection of data and ap-
proved the report.

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