Potential of plasma inflammatory and angiogenic mediators for predicting spontaneous preterm delivery, intraamniotic infection/inflammation, and composite neonatal morbidity/mortality in women with early preterm premature rupture of membranes

Abstract

ProblemTo assess the potential of five inflammatory and six angiogenic/antiangiogenic plasma proteins for predicting imminent spontaneous preterm delivery (SPTD; ≤14 days of sampling), microbial invasion of the amniotic cavity and/or intraamniotic inflammation (MIAC/IAI), and composite neonatal morbidity and mortality (CNMM) in women with early preterm premature rupture of membranes (PPROM).Methods of StudyThis retrospective cohort study included 76 singleton pregnant women with early PPROM (23–30 weeks). Amniotic fluid obtained via amniocentesis was cultured for microorganism detection and assayed for interleukin‐6 to define IAI (≥2.6 ng/mL). Plasma C4a, endoglin, endostatin, IGFBP‐1, IGFBP‐2, MMP‐9, PlGF, S100A8, S100A9, S100 A8/A9, and VEGFR‐1 levels were determined using ELISA.ResultsMultivariate logistic regression analyses revealed significant associations between (i) high levels of plasma S100A8/A9, SPTD ≤14 days after sampling, and shorter sampling‐to‐delivery intervals; (ii) elevated plasma MMP‐9, S100A9, and S100A8/A9 levels and MIAC/IAI, and (iii) decreased plasma endoglin levels and increased CNMM risk, while adjusting for gestational age at sampling (or delivery) and tocolytic use. The area under the curves of the aforementioned proteins ranged from 0.655 to 0.731 for each outcome. Notably, the SPTD risk increased significantly with increasing plasma S100A8/A9 levels (P for trend < .05).ConclusionsPlasma S100A8/A9, MMP‐9, S100A9, and endoglin may represent valuable biomarkers associated with SPTD, MIAC/IAI, and CNMM in women with early PPROM. Owing to their less invasive nature, repeatability, and fair‐to‐moderate diagnostic accuracy, these biomarkers may contribute to risk stratification of PPROM‐related complications in the clinical setting.

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

“…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 ].…”