PT6:07 Maternal vascular malperfusion of the placenta but not chorioamnionitis is associated with small for gestational age infants in systemic lupus erythematosus

Objectives Giving birth to a small for gestational age (SGA) infant is a common adverse pregnancy outcome in women with SLE, but the local underlying pathogenetic mechanisms are largely unknown. We aimed to determine whether specific placental histopathological patterns of injury are associated with SGA in SLE pregnancy.Methods We prospectively followed 83 SLE and 67 healthy pregnancies and placentas were collected unselectively without clinical indication. Placental pathology reports were available from 63 SLE and 46 healthy pregnancies. SGA was defined as a birth weight less than the 10th percentile of expected. Placentas were evaluated by a placental pathologist who recorded placental weight and the presence of maternal vascular malperfusion (MVM, defined as a small placental disc and at least one of: accelerated villous maturation, placental disc infarction and decidual vasculopathy), chorioamnionitis and funisitis. Soluble FMS-like tyrosine kinase-1 (S-Flt1) and placental growth factor (PlGF) were quantified using Legendplex.Results In SLE pregnancies, placental weight was reduced compared to healthy controls, and the most common complication was giving birth to a small for gestational age (SGA) infant (SLE 17% vs. controls 3%). Placental weight was lower in SLE pregnancy resulting in SGA compared to those not, and placentas were more often small for their gestational age. Among placentas from women with SLE who gave birth to SGA infants, 80% displayed signs of MVM compared to 20% of placentas of patients who had children who were normal or large for gestational age. Chorioamnionitis and funisitis were not evident in placentas of women with SGA. Women with SLE and evidence of MVM, compared to those without, gave birth to infants with lower birth weight and shorter birth length. The ratio of S-Flt1/PlGF was higher in women with SLE who gave birth to an SGA infant compared to women who did not, and in women with placental MVM compared to no MVM.Conclusions Impaired placental perfusion and spiral artery development may contribute to SGA in women with SLE, a conclusion further supported by an altered balance of the pro- and antiangiogenic factors S-Flt1/PlGF during SLE pregnancy resulting in SGA.