In premature rupture of membranes, maternal serum delta neutrophil index may be a predictive factor for histological chorioamnionitis and affect fetal inflammatory markers: A retrospective cross‐sectional study

Abstract

ProblemWe aimed to investigate the predictive value of delta neutrophil index (DNI) for histological choriomanionitis (HCAM) and the effect of maternal inflammatory markers on neonatal outcomes and fetal inflammatory parameters.Method of StudyIn this retrospective cross‐sectional study, 68 pregnant women without HCAM (group 1) and 46 pregnant women diagnosed with HCAM (group 2) were divided into two groups. Demographic stories of the groups; maternal hematological parameters; maternal DNI and systemic inflammatory index (SII) values; outcomes of newborns; fetal inflammatory markers were recorded and compared between groups.ResultsMaternal DNI, and SII levels were significantly higher in group 2 (p value < .05 for all). Admission to the neonatal unit (NICU) was higher in group 2 than in group 1 (p = .0001). We found that fetal inflammatory markers were significantly higher in group 2 (p values .001 for CRP, .0001 for DNI, and .002 for leukocyte). Maternal DNI was determined to be significantly diagnostic at a value of ≥1.3 in HCAM (p = .001). We observed that SII had a significant predictive value of 953036.6 (p = .019) for NICU admission. There is also a positive correlation between fetal inflammatory markers and maternal inflammatory markers.ConclusionsWe found that maternal inflammatory markers are high in HCAM, maternal DNI can predict patients who will develop HCAM, maternal SII value can predict NICU admission, fetal inflammatory markers are high in HCAM, and these markers are affected by maternal inflammatory markers.

Identification of circRNA Expression Profile and Potential Systemic Immune Imbalance Modulation in Premature Rupture of Membranes

“…Neutrophils are often exclusively considered as a first-line innate immune defense, able to rapidly kill or trap pathogens, and cause in case of overactivation tissue damage [ 41 ]. Increased maternal neutrophil may mediate chronic low-grade inflammation in PROM [ 9 , 42 ], gestational diabetes mellitus [ 43 , 44 ], and pre-eclampsia [ 45 ]. Neutrophil infiltration is also a key cause of fetal membrane inflammation and tissue destruction at the maternal–fetal interface [ 46 ].…”

“…It is generally accepted that PROM is a multifactorial disease with multiple causes (e.g., infection and endocrine disruption) [ 5 , 6 ], and the biological changes of membranes are the core pathological basis of PROM, including matrix degradation, cell senescence, apoptosis, autophagy, and epithelial–mesenchymal transition [ 7 , 8 ]. However, as the most common perinatal disease, research on PROM often focused on the prediction of severe maternal–fetal outcomes via common biomarkers [ 9 , 10 ], and the core etiology and key molecular mechanism of PROM remain unclear. Notably, noncoding RNAs (ncRNAs) have brought new light to PROM research, represented by miRNAs [ 11 ] and long noncoding RNAs (lncRNAs) [ 12 ].…”