State of the Art Lectures, Plenary Presentations and Oral Communications / Pregnancy Hypertension 1, Supplement 1 (2010) S1–S41 S3 preeclampsia. Although the exact mechanism(s) of Nifedipine on anti- hypertensive treatment in preeclampsia is unclear these data suggest it may act through the regulation of the level of sICAM-1 secretion from endothelial cells. M5.4 Correlation of free fatty acid and adiponectin in hypertensive pregnancy: key molecules for homeostatic inflammatory linkage Katsuhiko Naruse, Akira Onogi, Toshiyuki Sado, Taketoshi Noguchi, Satomi Komeda, Emi Koyama, Kazuhiro Nishioka, Takashi Kitanaka, Hidekazu Oi, Hiroshi Kobayashi. Department of OB/GYN, Nara Medical University, Japan Background: Recently, roles of adipocytes in hypertensive disease have been described elsewhere. We reported an increase of Adiponectin, an adipocyte-derived insulin-sensitizing and anti-inflammatory cytokine, in lean severe preeclamptic patients (Naruse K., et al, J Reprod Immunol 65-75, 2005). However, a systemic pathway to activate adipocyte in the disease remains unclear. On the other hand, lipid linkage including free fatty acid (FFA) signalling between adipocytes and macrophages is regarded as a part of homeostatic inflammation, a new theory for pathophysiology of metabolic syndromes. Aims: In the pathophysiology of preeclampsia, adipocyte may play a key role via several factors. Our study is to reveal a FFA-central pathway in preeclampsia, which states that preeclampsia is a disease after deviated homeostatic inflammation. Methods: 17 severe preeclamptic patients (PE) were compared with 27 gestational-age matched normal pregnant women (NP). Serum samples are taken on admission or at the routine medical examination with informed consent. Serum FFA was measured with enzyme-based method (BioVi- sion Research Products, CA; Palmitic Acid was used as a standard) with collection of albumin (Alb) concentrations. High Molecular-Weight (active form)-Adiponectin (HMW-Adn) was measured with Protease-pretreated ELISA (Sekisui Medical, Tokyo, Japan). All data are shown as mean ± S.E.M. Results: Mean FFA value were 153.8±15.5 μM in NP and 264.0±27.6 μM in PE. FFA (μM) / Alb (g/dL) was significantly increased in PE (124.4±12.1) than NP (58.7±5.8, p<0.001). HMW-Adn was also significantly increased in PE (3.57±0.29 μg/mL) than NP (2.04±0.20, p<0.001). FFA/Alb ratio and HMW-Adn were positively correlated when values both in NP and PE were included (p<0.005, r=0.44). Conclusion: FFA was increased in PE, and it might be positively correlated with adipocyte stimulation. This linkage suggested that the immoderate homeostatic inflammation is a possible trigger or plays a key role in the pathophysiology of hypertensive pregnancy. M6.1 Are early and late pre-eclampsia distinct sub-classes of the disease – what does the placenta reveal? David Hall 1 , Hannes van der Merwe 1 , Colleen Wright 2 , Pawel Schubert 2 , Debbie Grove 1 . 1 Dept. of Obstetrics & Gynaecology, 2 Division of Anatomical Pathology, Stellenbosch University & Tygerberg Hospital, South Africa Background: Pre-eclampsia presents clinically in an early or a late onset form. Early pre-eclampsia is generally severe with increased risks and therefore referred to specialized centres, while late-onset disease is often mild-moderate disease with good maternal and perinatal outcomes. Certain investigators have even proposed separate pathogenic paths for early and late onset pre-eclampsia. Early onset pre-eclampsia has been associated with abnormal placentas and fetal growth restriction, while abnormal placental morphology may be absent in women presenting with late onset pre-eclampsia. If it is clearly shown that early and late onset pre-eclampsia are indeed different sub-classes of the condition, this could motivate different approaches in management. Objective: To compare histopathological differences in placentas from early and late onset pre-eclampsia, as well as late onset pre-eclampsia and normal term deliveries. Methods: This prospective study was performed at Tygerberg Hospital, a secondary and tertiary referral centre in South Africa. Placentas from 100 women, 25 each with early and late onset pre-eclampsia, and an equal number of controls matched for gestational age, underwent routine preparation and were evaluated independently by two pathologists in a strictly predetermined, standardised manner. Results: Compared to late pre-eclampsia, placentas in the early pre- eclampsia group were smaller (p<0.01), had more infarction (OR=4.03, 95%CI=1.2-13.5) and inappropriate maturation (OR=16.62, 95%CI=4.1-68.0). Placentas from the late onset pre-eclampsia group showed increased de- cidual arteriopathy (OR=5.09, 95%CI=1.45-17.92) and abruptio placentae (OR=5.41, 95%CI=1.01-28.79) compared to controls. Conclusions: The early and late onset pre-eclampsia placentas showed clear histopathological differences, while late onset pre-eclampsia and normal term placentas differed less. These findings support the contention that early and late onset pre-eclampsia are different sub-classes of disease. M6.2 The mRNA expression of placental proteoglycans in pre-eclampsia Amy Chui 1 , Padma Murthi 1 , Shaun Brennecke 1 , Vera Ignjatovic 2 , Paul Monagle 2 , Joanne Said 1 . 1 Department of Perinatal Medicine, Pregnancy Research Centre and Department of Obstetrics and Gynaecology, The University of Melbourne, The Royal Women’s Hospital, Parkville, Australia; 2 Murdoch Children’s Hospital and Department of Clinical Haematology and Department of Paediatrics, The Royal Children’s Hospital and The University of Melbourne, Parkville, Australia Introduction: Pre-eclampsia (PE) is one of the leading causes of ma- ternal and perinatal morbidity and mortality. PE is clinically defined as the onset of hypertension and proteinuria after 20 weeks of gestation and is associated with altered maternal spiral artery remodelling, which may lead to reduced blood flow and increased thrombosis within the uteroplacental vasculature. Proteoglycans (PGs) are macromolecules which have (in combination with glycosaminoglycans) important anticoagulant roles in vascular endothelial environments, including the uteroplacental circulation. The hypothesis under consideration in this study was that a deficiency in placental PGs may contribute to the uteroplacental vascular thrombodysregulation seen in PE. Aim and Methods: The aim of this study was to determine the mRNA expression of placental PGs in the placentae of pre-eclamptic women compared with gestation-matched controls. RNA was obtained from 21 PE and 21 control placentae and reverse transcribed into cDNA. Real-time PCR was used to determine the mRNA expression of the proteoglycans in the placentae, relative to the housekeeping gene, GAPDH, according to the 2 -CT method [1]. Data are represented as mean ± SEM with statistical analysis by the Student’s t-test. Results: The table shows the relative mean mRNA expression of placen- tal proteoglycans in pre-eclamptic placentae compared with gestation- matched controls. Proteoglycan Control PE P Value ( ttest) Glypican 1 2.50±0.28 0.63±0.12 0.0003* Glypican 3 2.03±0.16 1.51±0.13 0.02* Biglycan 1.93±0.17 1.53±0.14 0.05 Perlecan 3.04±0.20 2.43±0.19 0.04* Decorin 2.08±0.17 1.17±0.09 0.00007* Syndecan 1 2.04±0.15 1.62±0.18 0.06 Syndecan 2 2.77±0.30 1.02±0.15 0.0001* Syndecan 3 0.67±0.05 0.72±0.06 0.93 Syndecan 4 0.43±0.05 0.42±0.04 0.81 *Denotes significant findings. Conclusion: These data demonstrate the differential mRNA expression of placental proteoglycans in human pre-eclamptic placentae compared with controls. These data support the concept that a placental PG deficiency may contribute to the placental thrombotic lesions characteristic of PE. Reference(s) [1] Livak, K.J. and T.D. Schmittgen, Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods, 2001. 25(4): p. 402-8. M6.3 Hydrogen sulfide: a protective gas for preeclampsia? Titia Lely 1 , Carry Ris-Stalpers 2 , Joris van der Post 3 , Marijke Faas 4 , Gerda Zeeman 1 , Bert Timmer 4 , Harry van Goor 4 . 1 Department of Obstetrics and Gynecology, University Medical Center Groningen, The Netherlands; 2 Molecular Obstetrics Research Group, Academic Medical Center, University of Amsterdam, The Netherlands; 3 Department of Obstetrics and Gynecologym, Academic Medical Center, University of Amsterdam, The Netherlands; 4 Department of Pathology and Laboratory Medicine, University Medical Center Groningen, The Netherlands Background: Hydrogen sulfide (H 2 S), the third gasotransmitter in addition