Decreased fertility in women with cesarean scar syndrome is associated with chronic inflammation in the uterine cavity

Aim To analyze the effectiveness of amniotic fluid neutrophil gelatinase‐associated lipocalin and L‐type fatty acid‐binding protein as predictive factors for fetal inflammatory response syndrome. Methods We classified single pregnancy cases into the fetal inflammatory response syndrome and nonfetal inflammatory response syndrome groups. We collected amniotic fluid at vaginal delivery and cesarean section and compared the patient characteristics, maternal white blood cell count, C‐reactive protein level, and amniotic fluid interleukin‐6; neutrophil gelatinase‐associated lipocalin; and L‐type fatty acid‐binding protein levels between the groups. We further analyzed the relationship between L‐type fatty acid‐binding protein levels and neonatal clinical outcomes. Results We analyzed 129 pregnancies, of which 36 and 93 (27.9% and 72.1%, respectively) were classified into the fetal inflammatory response syndrome and nonfetal inflammatory response syndrome groups, respectively. We observed significant differences in the maternal white blood cell counts and amniotic fluid interleukin‐6 and neutrophil gelatinase‐associated lipocalin levels. On the multivariate analysis, the useful predictive factors were maternal white blood cell count and amniotic fluid interleukin‐6 and neutrophil gelatinase‐associated lipocalin levels. Furthermore, the level of L‐type fatty acid‐binding protein was significantly higher in the transient tachypnea of the newborn and postnatal respiratory support group than in the control group. Conclusions The maternal white blood cell count and amniotic interleukin‐6 and neutrophil gelatinase‐associated lipocalin levels were effective predictors of fetal inflammatory response syndrome. Amniotic fluid L‐type fatty acid‐binding protein level was an effective predictor of neonatal respiratory support.

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BackgroundThe pathophysiology of neonatal hypoxic-ischemic encephalopathy (HIE) has been studied in several rodent models to develop novel treatments. Although it is well known that high ambient temperature results in severe HIE, the effect of subtle changes in ambient temperature during a hypoxic-ischemic (HI) insult has not been studied. Therefore, in order to clarify the difference of pathophysiological change among the HIE models due to the influence of small changes in chamber temperature, three-step gradual change of 0.5°C each were prepared in ambient temperature during hypoxic exposure.MethodsBlood flow in the left common carotid artery (CCA) of neonatal mice was interrupted using bipolar electronic forceps under general and local anesthesia. The mice were subsequently subjected to 10% hypoxic exposure for 50 min at 36.0, 36.5, or 37.0°C. A control group was also included in the study. The size of the striatum and hippocampus and the volume reduction rate of the hemisphere in the section containing them on the ischemic side were evaluated using microtubule associated protein 2 (MAP2) immunostaining. The accumulation of Iba1-positive cells was investigated to assess inflammation. Additionally, rotarod and open-field tests were performed 2 weeks after HI insult to assess its effect on physiological conditions.ResultsMAP2 staining revealed that the higher the temperature during hypoxia, the more severe the volume reduction rate in the hemisphere, striatum, and hippocampus. The number of Iba1-positive cells in the ipsilateral lesion gradually increased with increasing temperature, and there was a significant difference in motor function in the 36.5 and 37.0°C groups compared with the sham group. In the open-field tests, there was a significant decrease in performance in the 37.0°C groups compared with the 36.0°C and sham groups.ConclusionsEven a small gradual change of 0.5°C produced a significant difference in pathological and behavioral changes and contributed to the accumulation of Iba1-positive cells. The arrangement of ambient temperature is useful for creating a rodent model with the appropriate severity of the targeted neuropsychological symptoms to establish a novel therapy for HIE.

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