P 23 Maternal vascular malperfusion in spontaneous preterm birth and outcome of subsequent pregnancy

P 23 Maternal vascular malperfusion in spontaneous preterm birth and outcome of subsequent pregnancy

48 Abstracts / Pregnancy Hypertension: An International Journal of Women’s Cardiovascular Health 9 (2017) 36–63 P 23 Maternal vascular malperfusion ...

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48

Abstracts / Pregnancy Hypertension: An International Journal of Women’s Cardiovascular Health 9 (2017) 36–63

P 23 Maternal vascular malperfusion in spontaneous preterm birth and outcome of subsequent pregnancy Laura Visser a, Hannah van Buggenum a, J. Patrick van der Voorn b, Lotte A.P.H. Heestermans a, Kees W.P. Hollander a, Maurice G.A.J. Wouters a, Christianne de Groot a, Marjon A. de Boer a (a VU Medical Center, Obstetrics and Gynaecology, Amsterdam, The Netherlands, b VU Medical Center, Pathology, Amsterdam, The Netherlands) Introduction: Spontaneous preterm birth (SPTB) common complicates pregnancy. It has several causes and its pathophysiology has not yet been elucidated. In a significant proportion of SPTB, placental histology shows signs of maternal vascular malperfusion; these signs are commonly associated with hypertensive disorders of pregnancy (HD) or fetal growth restriction (FGR). Therefore, we hypothesized that women with a SPTB and signs of maternal vascular malperfusion in the placenta are at risk for HD and FGR in a subsequent pregnancy. Objective: The objective of this study was to describe the association between placental histology of SPTB and the incidence of HD and FGR in the subsequent pregnancy. Materials and methods: We included women with a history of SPTB, and a subsequent ongoing pregnancy (n = 110). Histological placental characteristics in the pregnancy complicated by SPTB were described according to new international guidelines, and related to the outcome of the subsequent pregnancy. Results: Delivery in the index pregnancy had a median gestational age of 27.7 weeks. In 61.8% (n = 68) of the placentas signs of vascular malperfusion were observed. Maternal and respectively fetal inflammatory response was observed in 51.8 %(n = 57) and 46.4% (n = 51) and was observed as a secondary finding in 42.6% (n = 29) and 36.8% (n = 25) of the placentas with maternal vascular malperfusion. In the index pregnancy HD was present in 8.2% (n = 9), and FGR in 10.9% (n = 12). In the subsequent pregnancy HD was present in 12.7% (n = 14) and FGR in 5.5 % (n = 6). The incidence of HD or FGR in the subsequent pregnancy was not associated with histological signs of maternal vascular malperfusion in the index pregnancy. Conclusion: Women with a history of SPTB have an elevated risk on hypertensive diseases in the subsequent pregnancy, when compared to epidemiologic data on the incidence of HD in women with a prior term birth. The incidence of HD was not associated with of the presence of placental maternal vascular malperfusion in the index pregnancy. This data suggest that signs of maternal vascular malperfusion by placental histology in SPTB cannot be used as a marker for adverse outcome in a subsequent pregnancy.

doi:10.1016/j.preghy.2017.07.101

P 24 Cell renovation markers, apoptotic markers and placental expression of erythropoietin in preeclampsia Vasilii Chulkov a, Boris Medvedev b, Elena Syundyukova b, Sergei Sashenkov c (a South Ural State Medical University, Faculty Therapy Department, Chelyabinsk, Russian Federation, b South Ural State Medical University, Obstetrics and Gynecology Department, Chelyabinsk, Russian Federation, c South Ural State Medical University, Normal Physiology Department, Chelyabinsk, Russian Federation) Introduction: The role of erythropoietin (EPO) in trophoblast invasion, placental insufficiency and preeclampsia (PE) are associated with angiogenesis-stimulated and antiapoptotic effects. Objectives: To study cell renovation markers, apoptotic markers and erythropoietin placental expression in early-onset and late onset preeclampsia. Materials and methods: In a case-control study, we included 15 pregnant women with early-onset PE and 13 women – with lateonset PE. We have studied cell proliferation marker ki-67, markers of antiapoptosis bcl-2 and proapoptosis p53, placental expression of EPO in syncytium, capillaries endothelium, villi stroma macrophages. Results: In early-onset PE bcl-2 expression was lower in syncytium (5.22 ± 0.78 vs 10.21 ± 0.75, p < 0.001) and stroma macrophages (29.94 ± 0.83 vs 32.86 ± 0.75, p = 0.022) and higher in capillaries endothelium (16.72 ± 0.42 vs 15.14 ± 0.55, p = 0.02) compared to late-onset PE. In early-onset PE p53 expression was lower in syncytium (7.89 ± 0.59 vs 11.93 ± 0.63, p < 0.001), capillaries endothelium (3.89 ± 0.54 vs 6.43 ± 0.42, p = 0.002), stroma macrophages (9.94 ± 0.74 vs 15.07 ± 0.83, p = 0.001) and ki-67 expression was enhanced (24.61 ± 0.89 vs 19.85 ± 0.95, p = 0.005; 20.28 ± 0.70 vs 14.93 ± 0.62, p < 0.001; 24.33 ± 0.99 vs 17.86 ± 0.94, p. Conclusion: Despite the high expression of EPO in PE, the degree of adaptive changes, particularly in syncytium, was insufficient and that was accompanied by dystrophic changes in placenta (ischemic infarcts, immature chorionic villi) with the realization of proapoptosis and cell proliferation mechanisms. doi:10.1016/j.preghy.2017.07.102

Figure 1: Outcome subsequent pregnancy related to histological placental evaluaon in the index pregnancy.