Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease of unknown cause, which mainly affects women of childbearing age, especially between 15 and 55 years of age. During pregnancy, SLE is associated with a high risk of perinatal morbidity and mortality. Among the most frequent complications are spontaneous abortion, fetal death, prematurity, intrauterine Fetal growth restriction (FGR), and preeclampsia (PE). The pathophysiology underlying obstetric mortality and morbidity in SLE is still under investigation, but several studies in recent years have suggested that placental dysfunction may play a crucial role. Understanding this association will contribute to developing therapeutic options and improving patient management thus reducing the occurrence of adverse pregnancy outcomes in this group of women. In this review, we will focus on the relationship between SLE and placental insufficiency leading to adverse pregnancy outcomes.

Background Pregnancy in systemic sclerosis (SSc) patients is no more an infrequent event as it used to be, but literature data on pregnancy outcomes in women with SSc are scarce. The rate of preterm deliveries and intrauterine growth restriction (IUGR) seems to be increased, while the risk of miscarriages is controversial. Moreover, no study compared pregnancy outcomes in SSc with antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE). We performed a retrospective study to compare the pregnancy and disease outcomes of women with SSc with a cohort of age-matched women with systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS), and healthy controls (HC). Methods A total of 154 pregnancies from SSc, SLE, APS patients, and HC were prospectively followed at the High-Risk Pregnancy Unit of our center from 2008 to 2019. The primary outcome was a composite endpoint of miscarriages, fetal deaths, intrauterine growth restriction (IUGR), preeclampsia, neonatal deaths, preterm birth, and small-for-gestational-age (SGA) newborns. Single adverse pregnancy outcomes (APO) represented secondary endpoints. SSc activity variations in relation to pregnancy were assessed. Results The risk of APO was significantly higher in SSc patients compared to HC (60.6% vs 10.0%; OR = 14.42; 95% CI 3.70–56.18, p = 0.001) and SLE patients (60.6% vs 37.5%; OR = 3.56; 95% CI 1.29–9.83, p = 0.014). Compared to HC, women with SSc had an increased frequency of first trimester miscarriage (15% vs 0 %; p = 0.016), preeclampsia (12% vs 0%, p = 0.038), and SGA newborns (21.2% vs 0%; p = 0.003). Preterm deliveries were more frequent in SSc pregnancies in comparison with HC (24.2% vs 5%; OR = 6.08; 95% CI 1.19–31.02, p = 0.036) and SLE patients (24.2% vs 7.5%, OR = 5.68; 95% CI 1.1–29.38, p = 0.038). Disease remained stable in all SSc patients during pregnancy and up to 1 year after delivery. Conclusions We found an increased risk of APO in our SSc cohort in comparison with HC (with higher rates of miscarriages, preeclampsia, SGA newborns, and preterm deliveries) and SLE patients (presenting a higher rate of preterm deliveries). High-risk multidisciplinary management of SSc pregnant women is highly recommended.

Objective To compare the fetal brain structures assessed in routine sonographic scans during the second and third trimesters in fetuses with and without congenital heart disease (CHD). Methods This is a retrospective cross-sectional single-center study. We measured the head circumference (HC), the transversal diameter of the cerebellum (TCD) and the sizes of the cisterna magna (CM), the cavum septi pellucidi (CSP) and the posterior ventricles (PV) between 20 and 41 weeks of gestation. We compared 160 fetuses with CHD (case group) to 160 fetuses of normal pregnancies (control group). Every patient was matched with a control, considering the gestational age at which the ultrasound was performed. We divided the CHD group into 3 subgroups: retrograde flow in the aortic arch (group 1), right heart anomaly with the antegrade flow in the aortic arch (group 2) and other CHDs with the antegrade flow in the aortic arch (group 3). Results The mean width of the PV was larger in fetuses of groups 1 and 3 in comparison to the control group (P < 0.001, P = 0.022; respectively). We found that the APGAR score at 5 min (P < 0.001, P < 0.001; respectively) and gestational age at delivery (P = 0.006, P = 0.001; respectively) were inferior in groups 1 and 3 compared to controls. Conclusions Central nervous system biometry is altered in fetuses with CHD. PV is enlarged in CHD fetuses especially with decreased oxygen levels in the aortic arch.