Fetal sex and inflammatory responses in preterm prelabor rupture of membranes.

BACKGROUND

Fetal sex influences placental development and immune regulation. Although sex-related differences in placental vascular pathology have been described, their influence on intra-amniotic inflammation and placental inflammatory responses in pregnancies complicated by preterm prelabor rupture of membranes (PPROM) remains poorly understood.

OBJECTIVE

To determine whether fetal sex is associated with differences in the intensity of the intra-amniotic inflammatory response, the distribution of intra-amniotic categories defined according to the presence or absence of microbial invasion of the amniotic cavity and intra-amniotic inflammation, acute placental inflammatory lesions, and short-term neonatal outcomes in PPROM.

STUDY

DESIGN

This retrospective cohort study included 852 singleton pregnancies complicated by PPROM between 23 + 0 and 36 + 6 weeks of gestation that underwent transabdominal amniocentesis. Pregnancies complicated by maternal hypertensive disorders or diabetes mellitus were excluded from the analysis. The intra-amniotic inflammatory response was assessed by amniotic fluid interleukin-6 levels. Placental inflammatory lesions were evaluated according to the histopathological criteria described by Salafia et al.

RESULTS

The distribution of intra-amniotic categories (P = 0.28) and amniotic fluid interleukin-6 levels did not differ between pregnancies carrying female and male fetuses. The prevalence of most acute placental inflammatory lesions was comparable between the groups. However, pregnancies carrying female fetuses had a higher prevalence of early-stage funisitis (11% vs. 5%; P = 0.002). Female newborns also had a higher prevalence of bronchopulmonary dysplasia (7% vs. 3%; P = 0.002).

CONCLUSION

In PPROM, fetal sex was not associated with differences in the intra-amniotic environment. However, female fetuses exhibited a higher prevalence of early-stage funisitis, suggesting that fetal sex may modulate the earliest histopathological manifestation of the fetal inflammatory response despite comparable intra-amniotic inflammatory exposure.