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.