Discussion
This study retrospectively analyzed 157 cases of PPROM women with
gestational age between 26 0/7 and 33 6/7 weeks and investigated the
dynamic responses of maternal WBC, neutrophil,
lymphocyte, CRP and PCT to antenatal dexamethasone. We found both CON
and HCA groups had similar physiologic response to dexamethasone in WBC,
neutrophil, and lymphocyte whether they had HCA or not. On the contrary,
HCA might influence the response of CRP and PCT in PPROM women, and
notably PCT had better predictive values of HCA when compared with those
of CRP.
Membrane rupture may occur for a variety of reasons and intraamniotic
infection has been shown to be commonly associated with preterm PROM,
especially at earlier gestational ages[6, 21]. Previous studies
which have shown HCA occurred in approximately 50–60% of women with
PPROM[22, 23]. Consistent with those data, a total of 157 mothers
were involved in this study and 98 women (62.42%) were identified as
HCA. Only 5 patients (5.75%) presenting positive symptoms were
diagnosed with CCA, of whom 4 were proven to have HCA, which suggests
that diagnosis of CA solely based on clinical manifestation may
underestimate the true risks to the offspring. Hence, it is vital for
detection of HCA in PPROM women, especially in those with younger
gestational ages who were more prone to greater incidence of HCA[6].
Furthermore, limitations on the timeliness of placenta pathological
examination urges the value of early diagnosis of HCA that may help
provide timely intervention to newborn infants.
Antenatal corticosteroid therapy has shown a transient physiologic
response including an increase in maternal WBC and neutrophil, which is
caused by increasing leukocyte extravasation from bone marrow and
decreasing their clearance from blood vessels[11-13]. Some study
demonstrated WBC increased from a baseline value of
11.3×109 to 16.2×109 cell/L 24 hours
after treatment and normalized thereafter[24]. Voon et al. found
mean WBC in a preterm subgroup was initially 10.65×109cell/L, then rose to 11.99×109 cell/L at 36 hours
after dexamethasone injection, and finally returned to baseline
level[13]. Our study confirmed the physiologic leukocytosis after
administration of dexamethasone in PPROM which could differentiate from
uterine infection. In comparison, mean WBC and neutrophil counts in our
study did not return to their initial baseline levels even at 72 hours
after treatment, which is different from the aforementioned studies.
This may be explained by the fact that the preterm women recruited by
prior studies included both PPROM patients and those with intact
membranes, while women in our study only included PPROM mothers. The
results indicate the responses of maternal WBC and neutrophil in the
first 72 hours after dexamethasone injection might not be influenced by
HCA; hence they could not predict HCA in PPROM women.
Different from WBC, neutrophil and lymphocyte, CRP and PCT levels in the
HCA group were consistently higher than those in the CON group at
different time points after patients received their first injection,
indicating the responses of CRP and PCT to dexamethasone injection might
be associated with HCA. When it comes to analysis of diagnostic value,
this study showed that PCT is better than that of CRP for early
prediction of HCA. The areas under ROC curves of PCT were significantly
better than those of CRP at baseline, 48 and 72 hours, which indicate
that PCT had greater predictive value than CRP. Similarly, some scholars
found that both CRP and PCT had satisfactory accuracy, and the
diagnostic value of PCT is better than CRP for women pregnant for 28-34
weeks[17]. PCT also had both high specificity and sensitivity even
at the initial baseline, whereas CRP had high sensitivity but low
specificity, which meant PCT might be more sensitive for early diagnosis
of HCA than CRP. A previous study found PCT inversely had a poor
sensitivity and a modest specificity compared with CRP[15], but the
author included all the intrauterine infectious patients without
distinction between CCA and HCA. In the HCA group, mean CRP showed a
significant rise only at 24 hours after initial treatment before
dropping to the baseline vale where it remained stable. PCT levels
increased continually from
baseline to the peak at 72 hours post first treatment, which reflected
the dynamic response of CRP and PCT after dexamethasone and required
constantly monitoring of trends.