RESUMEN
AIM: We aimed to determine whether the effect of antenatal corticosteroids (ANS) differs in male and female fetuses without anomalies born before 32 weeks in terms of mortality and short-term morbidity. METHODS: This single-center retrospective study included infants born before 32 weeks' gestation and admitted to the neonatal intensive care unit between January 1, 2018, and December 31, 2020. RESULTS: The study included 210 infants with a median gestational age of 28.6 weeks (24-31.6), a birth weight of 1065 g (445-2165), and an ANS use rate of 80%. Compared to female fetuses exposed to ANS, male fetuses exposed to ANS had a lower mortality rate (23% and 11%, respectively, p = 0.038), but there were no differences in intraventricular hemorrhage, retinopathy of prematurity, necrotizing enterocolitis, respiratory distress syndrome, and APGAR scores of 1st and 5th but an increased rate of bronchopulmonary dysplasia (moderate/severe) (p = 0.008). In addition, the mortality rate was similar in exposed and unexposed female fetuses (p = 0.850). Enzyme activities and steroid levels in the placenta might be different in male and female fetuses, which could explain the results of ANS administration. CONCLUSIONS: In our study, we have shown that ANS has no effect on mortality in female fetuses younger than 32 weeks. Future studies may focus on adjusting the administration of ANS based on fetal sex, altering the dose or taking fetal sex into account when performing ANS.
RESUMEN
OBJECTIVE: Magnesium sulfate (MgSO4) provides effective fetal neuroprotection. However, there is conflicting evidence regarding the association between antenatal MgSO4 exposure and patent ductus arteriosus (PDA). Thus, herein, we aimed to evaluate the association between antenatal MgSO4 exposure and PDA. STUDY DESIGN: Preterm infants born between 240/7 and 316/7 weeks of gestation were included in this retrospective study. Infants who died within the first 72 hours of life and those with significant congenital anomalies were excluded from the study. Echocardiographic and clinical assessment parameters were used to define PDA and hemodynamically significant PDA (hsPDA). Treatments were planned according to the standard protocols of the unit. The following data were collected from hospital medical records: perinatal characteristics, neonatal outcomes, detailed PDA follow-up findings, and maternal characteristics including MgSO4 exposure and doses. RESULTS: Of the 300 included infants, 98 (32.6%) were exposed to antenatal MgSO4. hsPDA rates were similar in the infants exposed and not exposed to antenatal MgSO4, when adjusted for antenatal steroid administration, gestational age, and birth weight (OR: 1.6, 95% CI: 0.849-3.118, p = 0.146). The rates of PDA ligation and open PDA at discharge were similar between the groups. A cumulative MgSO4 dose of >20 g was associated with an increased risk of hsPDA (crude OR: 2.476, 95% CI: 0.893-6.864, p = 0.076; adjusted OR: 3.829, 95% CI: 1.068-13.728, p = 0.039). However, the cumulative dose had no effect on the rates of PDA ligation or open PDA at discharge. Rates of prematurity-related morbidities and mortality were similar between the groups. CONCLUSION: Although antenatal MgSO4 exposure may increase the incidence of hsPDA, it may not affect the rates of PDA ligation or open PDA at discharge. Further studies are required to better evaluate the dose-dependent outcomes and identify the MgSO4 dose that not only provides neuroprotection but also has the lowest risk of adverse effects. KEY POINTS: · Antenatal exposure of MgSO4 may cause PDA.. · Antenatal MgSO4 exposure may not increase the rates of PDA ligation or open PDA at discharge.. · Further studies are required to better evaluate the dose-dependent outcomes and optimal MgSO4 dose..