Esengül Türkyılmaz Şener, Müzeyyen Keçik, Salim Neşelioğlu, Esra Karakuş, Özlem Moraloğlu Tekin, Aytekin Tokmak
Pregnancies with clinically suspected IFC showed altered fetal thiol-disulfide homeostasis, increased maternal systemic inflammation, and a higher prevalence of placental inflammatory lesions. These findings support an association between suspected IFC and an altered fetal redox state but do not provide direct evidence of fetal hypoxia or generalized oxidative stress.
OBJECTIVE: To evaluate the relationship between clinically suspected intrapartum fetal compromise (IFC) requiring cesarean delivery, placental histopathological findings, maternal and fetal thiol-disulfide homeostasis, and inflammatory markers.
METHODS: This prospective observational study included 83 term singleton pregnancies delivered by cesarean section, including 35 with suspected IFC based on abnormal cardiotocography and 48 controls with non-hypoxic indications. Maternal and fetal thiol-disulfide parameters, ischemia-modified albumin (IMA), placental histopathology, obstetric characteristics and neonatal outcomes were compared. Inflammatory status was evaluated using neutrophil-to-lymphocyte ratio (NLR) and maternal and fetal inflammatory response (FIR). Multivariable logistic regression analysis was performed to identify factors independently associated with suspected IFC.
RESULTS: Baseline clinical and obstetric characteristics were comparable between groups, except for body mass index (BMI). Maternal NLR was higher, whereas fetal disulfide levels and disulfide-related ratios were lower in the IFC group. Villitis of unknown etiology (VUE), fetal vascular malperfusion (FVM), and FIR were more frequent in pregnancies with IFC. After adjustment for BMI, higher maternal NLR (aOR 1.52, 95% CI 1.11-2.10; p = 0.010), lower fetal disulfide levels (aOR 0.87, 95% CI 0.79-0.96; p = 0.007), and VUE (aOR 5.69, 95% CI 1.56-20.81; p = 0.009) remained independently associated with IFC.
CONCLUSION: Pregnancies with clinically suspected IFC showed altered fetal thiol-disulfide homeostasis, increased maternal systemic inflammation, and a higher prevalence of placental inflammatory lesions. These findings support an association between suspected IFC and an altered fetal redox state but do not provide direct evidence of fetal hypoxia or generalized oxidative stress.