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Abstracts / Placenta 36 (2015) A1eA14
CD56+CD16+ of PE were lower than those of NP, both in decidual cells and peripheral blood. Conclusion: Changes of NK cells with NCR in preeclampsia may relate to roles in the pathology of this disorder.
JPA2015-53. C-REACTIVE PROTEIN LEVELS CAN BE USED AS MARKER FOR DIAGNOSIS OF PREGNANCY INDUCED HYPERTENSION Masayoshi Arizawa. Tokyo Metropolitan Ohtsuka Hospital, Japan
JPA2015-52. EXPRESSION OF ANGIOGENIC AND IMMUNOLOGICAL FACTORS IN PLACENTA WITH PREECLAMPSIA AND/OR FETAL GROWTH RESTRICTION Naoyuki Iwahashi, Aya Kobayashi, Yuko Tanizaki, Michihisa Shiro, Nami Ota, Yasushi Mabuchi, Shigetaka Yagi, Sawako Minami, Kazuhiko Ino. Department of Obstetrics and Gynecology Wakayama Medical University, Japan Objectives: Impaired placental angiogenesis is associated with preeclampsia (PE) and fetal growth restriction (FGR). Immunosuppressive factors such as indoleamine 2, 3-dioxygenase (IDO) may also play a role in placental development. Our objective was to determine the differences in fms-like tyrosine kinase receptor-1 (Flt-1), vascular endothelial growth factor (VEGF), TGF-b, and IDO expressions among normal, preeclampsia (PE), and fetal growth restriction (FGR) placentas. Methods: Immunohistochemical studies were performed in human placenta from the 3rd trimester of pregnancies complicated with either PE alone (n¼28), FGR alone (n¼20) or both PE/FGR combined (n¼34) compared to gestational age-matched controls (n¼23). Results: Flt-1, VEGF, and TGF-b were mainly located on trophoblast cells, while IDO was located on endothelial cells in villous stroma. Flt-1 and TGFb were strongly expressed in PE alone, FGR alone, and PE/FGR combined groups compared to control group. Furthermore, PE/FGR combined group showed higher Flt-1 expression compared to FGR alone group. PE alone group showed significantly lower IDO expression compared to FGR alone group. Among patients with PE, high Flt-1 expression was concerned with the existence of maternal nephropathy, but not with hypertention. There was no significant difference in VEGF expression among the groups. Conclusion: Higher Flt-1/lower IDO expression seems to be related to PE, and these findings suggest that both angiogenic and immunosuppressive factors may play a role in pathophysiology of PE complicatedly.
Background: There are two main causes of premature delivery; CAM (chorioamnionitis) and PIH (pregnancy induced hypertension) CAM is usually associated with elevated levels of CRP(C-reactive protein). However sometimes we find higher than normal CRP levels in cases without CAM, i.e. PIH. I had previously tried to find possible reasons for premature delivery without CAM but which had elevated levels of CRP. Recently I noticed tissue damage, such as infraction, can also increase levels of CRP. I examined cases of PIH with premature delivery and found elevated CRP levels with placental infarction. In this paper I make clear that most PIH cases include elevated levels of CRP. Infarction can be seen pathologically in pictures as well as by elevated CRP in blood samples. Materials: I examined the placenta and clinical records of 144 cases of PIH and 19 cases of HELLP syndrome. I checked the level of CRP in all these cases. I defined the normal level to be under 0.3mg/ dL. Results: 1) 144 PIH cases The average CRP from the 144 cases was 0.84 mg /dL. There were 55 cases with decidual vascular abnormality 2) 19 HELLP syndrome cases The average CRP from the 19 cases was 3.0mg/dL. Out of the 19 HELLP syndrome cases: There were 18 cases of CRP positive. Placenta pathology showed there were 19 cases of ischemia or infarction. There were 14 cases of decidua thrombosis Conclusion: The main cause of PIH is from vascular problems in the decidua and villous ischemia. This kind of tissue damage elevates CRP levels. Out of uterus vascular damage, such as liver necrosis, also elevates CRP. That is why in this study we found higher levels of CRP in the HELLP syndrome cases than in the PIH cases without HELLP syndrome. These results show how the CRP level is useful for predicting the development of PIH and HELLP syndrome.