[206-POS]: Morphological/immunohistochemical alterations of endometrial and placental site areas in preeclampsia

Objectives To study the morphological/immunohistochemical alterations of endometrial and placental sites and relation of apoptosis, proliferation and angiogenesis in preeclampsia (PE). Methods 30 women 18–40 y.o. were delivered by CS for severe PE: 15 women with early PE, and 15 with the late PE. 15 women without hypertensive disorders were matched for GA at delivery with PE-patients and formed a control group. Samples of the placental site were obtained during CS after informed consent. Morphological and immunohistochemical analysis was used. Results Dramatic thickening of spiral arterial walls with severe stenosis of the basal membrane, hyperplasia of smooth muscle cells, perivascular lymphohistiocytic infiltration dominated in the cases of late PE. Multiple sclerosis (100%), hyalinosis (100%) and intimal atheromatosis (70%) due to sharp thickness of spiral arteries with severe stenosis of the basal membrane occurred in early PE. Thrombosis was often seen equally in both groups (80%). Apoptosis predominated in the intima and smooth muscle cells of the spiral arteries. Compensatory increased formation of VEGF (5 ± 1.1 score) and IGF (6 ± 0.5 score) in myometrial stromal cells and spiral arteries was observed in all samples. Expression of VEGF in EVT cells and cytotrophoblasts significantly was reduced in patients with PE compared to the control group. Reduction of VEGF receptors in endometrial stroma and its absence in endothelial cells occurred. The levels of Apo-Cas (5% ± 1.4%, and 15% ± 2.7%), VEGF (4 ± 0.5 and 5 ± 1.1 scores) and IGF (5.5 ± 1.1 and 6 ± 0.5 scores) in myometrial stromal cells and spiral arteries in the early-onset group were slightly higher compared to the late-onset group. Conclusions These violations of utero-placental circulation were observed as a result of pathological remodeling of spiral arteries due to imbalance between proliferation and apoptosis in the placental site. These changes that have led to deficient physiologic vessel transformation are likely immunohistochemical markers of remodeling spiral arteries and endothelial dysfunction. Disclosures Z. Khodzhaeva: None. E. Kogan: None. T. Demura: None. A. Akatyeva: None. O. Vavina: None. A. Safonova: None. A. Kholin: None. G. Sukhikh: None.