Annexin V expression in growth restricted fetuses is inversely related with neonatal and placental weight

Abstract

WITH NEONATAL AND PLACENTAL WEIGHT FRANCESCA SALA, GABRIELE URBAN, PATRIZIA VERGANI, FRANCESCA MOLTRASIO, BIAGIO EUGENIO LEONE, Universita di Milano-Bicocca, Obstetrics and Gynecology, Monza, Milan, Italy, University of Milano-Bicocca, Pathology Unit, Monza, Milan, Italy OBJECTIVE: Recently increased Annexin V (A5) levels in amniotic fluid have been shown to predict subsequent FGR. We investigated the placental expression of A5 in singleton growth restricted fetuses. STUDY DESIGN: Twenty nine small for gestational age (SGA) newborns were matched with 30 appropriate for gestational age (AGA) controls based on gestational age at delivery. Placental samples were obtained at three different sites: marginal, central and close to the insertion of the umbilical cord. Samples were stored at 80 C and in paraffin. Immuno-hystochemical analysis was performed blinded to the clinical condition. The localization of A5 in placenta was determined by immunoperoxidase staining with ABC peroxidase system using monoclonal antibodies anti-Human A5. The mean reactivity among 10 fields for sample was calculated. Maternal and neonatal blood and clotting markers were evaluated in cases and controls. Statistical analysis was performed with Spearman correlation and chi square (p!0.05). RESULTS: There were no significant differences in gestational age, parity, gravity, maternal age between SGA and AGA. In SGA but not AGA placentas, A5 was inversely correlated with birth weight (r=-0.4, p=0.04) and placental weight (r= 0.3, p=0.04), but not with gestational age (p=0.2). None of coagulation or blood markers were related with A5 expression except for the maternal LDH (r=0.4, p=0.04). CONCLUSION: Our results show that placental expression of A5 is increased in SGA neonates, and it is related to the severity of the condition regardless of the gestational age. The present results in the context of similar previous amniotic fluid findings suggest a role for A5 in the homeostatic placental regulation to vascular or hypoxic insults.