Preterm birth is commonly associated with sterile intra-amniotic inflammation, a clinical condition that currently lacks approved treatments. The administration of antenatal corticosteroids, such as betamethasone, is the standard of care for women who are at risk of delivering preterm, regardless of underlying causes. Such corticosteroids are recommended for their demonstrated acceleration of fetal organ maturation, thereby reducing the risk of perinatal and neonatal death. However, the effects of betamethasone in the clinical setting of sterile intra-amniotic inflammation have not been evaluated. In this study, PRB investigators sought to evaluate the potential utility of betamethasone treatment for preventing preterm birth in an animal model of sterile intra-amniotic inflammation induced by alarmins.
The investigators first validated an established in vivo model of sterile intra-amniotic inflammation, showing that the ultrasound-guided intra-amniotic injection of the alarmin HMGB1 results in late preterm birth. Importantly, treatment with betamethasone was able to reduce the rate of HMGB1-induced preterm birth without negatively affecting neonatal survival or growth. These findings represent the first causal demonstration that betamethasone may have utility for the prevention of preterm birth in women with sterile intra-amniotic inflammation.