Effect of Antenatal Corticosteroid and Antibiotics in Pregnancies Complicated by Premature Rupture of Membranes between 24 and 28 weeks of Gestation

The aim of this study was to assess the effectiveness of active intervention with antenatal maternal corticosteroid and antibiotics therapy in infants delivered between 24 and 28 weeks of gestation after premature rupture of membrane. This retrospective study included pregnant women complicated by preterm delivery at the Dong-A University Hospital from 1998 to 2002. Patients were divided into labor induction group 1 (n=20), observation group 2 (n=19), and medication group 3 (n=20). We evaluated the effects of prolongation of pregnancy and intervention with maternal corticosteroids and antibiotics therapy on perinatal and neonatal outcomes. Each group did not have a significant difference (p<0.05) in neonatal outcomes, such as respiratory distress syndrome, intraventricular hemorrhage, necrotizing enterocolitis, retinopathy of prematurity, pneumonia, bronchopulmonary dysplasia, and sepsis. The mean latency period was 4.7 days and 7.6 days in groups 2 and 3, respectively. Therefore, this study was unable to demonstrate any beneficial effects of corticosteroids in improving neonatal outcomes and prolongation of the latency period with antibiotics

Maternal hormonal milieu influence on fetal brain development

An adverse maternal hormonal environment during pregnancy can be associated with abnormal brain growth. Subtle changes in fetal brain development have been observed even for maternal hormone levels within the currently accepted physiologic ranges. In this review, we provide an update of the research data on maternal hormonal impact on fetal neurodevelopment, giving particular emphasis to thyroid hormones and glucocorticoids. Thyroid hormones are required for normal brain development. Despite serum TSH appearing to be the most accurate indicator of thyroid function in pregnancy, maternal serum free T4 levels in the first trimester of pregnancy are the major determinant of postnatal psychomotor development. Even a transient period of maternal hypothyroxinemia at the beginning of neurogenesis can confer a higher risk of expressive language and nonverbal cognitive delays in offspring. Nevertheless, most recent clinical guidelines advocate for targeted high-risk case finding during first trimester of pregnancy despite universal thyroid function screening. Corticosteroids are determinant in suppressing cell proliferation and stimulating terminal differentiation, a fundamental switch for the maturation of fetal organs. Not surprisingly, intrauterine exposure to stress or high levels of glucocorticoids, endogenous or synthetic, has a molecular and structural impact on brain development and appears to impair cognition and increase anxiety and reactivity to stress. Limbic regions, such as hippocampus and amygdala, are particularly sensitive. Repeated doses of prenatal corticosteroids seem to have short-term benefits of less respiratory distress and fewer serious health problems in offspring. Nevertheless, neurodevelopmental growth in later childhood and adulthood needs further clarification. Future studies should address the relevance of monitoring the level of thyroid hormones and corticosteroids during pregnancy in the risk stratification for impaired postnatal neurodevelopment.This work was supported by the grant "Doutoramento em Medicina Jose de Mello Saude 2014" by Jose de Mello Saude to AM