s / Placenta 35 (2014) A1eA112 A88 P2.84. PLACENTAL EXPRESSION OF SOLUBLE ENDOGLIN IN HIV ASSOCIATED PREECLAMPSIA Thajasvarie Naicker, Nalini Govender, Jagidesa Moodley University of KwaZulu-Natal, Durban, South Africa Introduction: Preeclampsia, a placental disease is related to increased maternal and neonatal morbidity and mortality. In South Africa, majority of the 14% of maternal deaths arising from hypertension are attributed to pre-eclampsia. Increased placental levels of the anti-angiogenic factors, sEng and sFlt-1 are correlated with interrupted angiogenic balance in preeclampsia development. Inconsistent data exist on the impact of HIV infection on the incidence of preeclampsia. Furthermore, the effects of HIV infection on placental levels of sEng in both normotensive and preeclamptic pregnancies are unknown. Objective: We examined the placental immunoexpression of sEng, in HIV negative and positive normotensive (Nand N+ respectively) and preeclamptic (Pand P+ respectively) pregnancies at term using immunohistochemistry and immunoelectron microscopy. Results and discussion: Strong immunoreactivity was located within endothelial cells, syncytioand cytotrophoblasts. All extravillous trophoblasts were also immunopositive for sEng. Subcellularly, gold particles were immunolocalised primarily within the endoplasmic reticulum; mitochondria and within the cytoplasm of syncytiotrophoblasts. No significant effect of HIV status on sEng immunoexpression within exchange villi [F(1,123)1⁄42.964, p1⁄40.088]. . Furthermore, sEng immunoexpression differed significantly within exchange [F(1,123)1⁄45.545, p1⁄40.020] and stem villi [F(1,123)1⁄413.161, p<0.001] . Higher sEng immunoexpression was observed in the pre-eclamptic [(exchange villi: mean1⁄414.04, 95% CI: 13.25-14.83) and stem villi (mean1⁄416.73, 95% CI: 15.43-18.02)] compared to normotensive groups [exchange (mean1⁄412.80, 95% CI: 12.13-13.48) and stem villi (mean1⁄413.60, 95% CI: 12.50-14.71)]. No interaction between HIV status and pregnancy type (normotensive vs preeclampsia) on sEng immunoexpression in both exchange [F(1,123)1⁄41.61, p1⁄40.207] and stem villi [F(1,123)1⁄40.65, p1⁄40.421] was observed. There was no correlation of sEng intensity between the exchange and stem villi (r21⁄40.02; p1⁄40.07). Increased placental sEng immunoexpression results in placental vascular maladaptation and the reduced blood flow and consequent hypoxia. Subsequent discharge of trophoblastic/necrotic tissue and antiangiogenic molecules lead to abnormal placentation and endothelial dysfunction evident in preeclampsia. However, irrespective of the HIV status, placental sEng1 remains high in preeclampsia compared to normotensive pregnancies.