C34 synthesis br Acknowledgements Funding for this study is

Acknowledgements Funding for this study is gratefully acknowledged from the Department of Employment and Learning (QC) and the Northern Ireland Chest Heart and Stroke Association (2008107).
Introduction Preeclampsia is a major human pregnancy-specific disorder that occurs in at least 5–10% of pregnancies and leads to maternal and fetal morbidity and mortality (Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy, 2000). It is characterized by the onset of proteinuria and hypertension after the 20th week of gestation. Infants are at increased risk of growth restriction and the adverse effect of preterm delivery (Stella and Sibai, 2006, Ilekis et al., 2007). The etiology remains poorly understood, although the involvement of immune, angiogenic, metabolic, and genetic factors is suggested (Sibai et al., 1997, Roberts and Cooper, 2001, Tyurin et al., 2001, Kaufmann et al., 2003, Maynard et al., 2003, Bdolah et al., 2004, Chaouat et al., 2004, Redman and Sargent, 2005). In preeclampsia, there is incomplete invasion of the uterine spiral C34 synthesis by endovascular trophoblasts. As a result, decidual vessels, but not myometrial vessels, become lined with endovascular trophoblasts (Meekins et al., 1994). The magnitude of defective trophoblastic invasion of the spiral arteries is likely associated with the severity of the hypertensive disorder (Madazli et al., 2000). It is thought that these changes cause placental perfusion to be pathologically diminished, which eventually leads to the pre-eclampsia syndrome (Redman and Sargent, 2003). Increased placental trophoblastic apoptosis has been suggested as a possible cause (Huppertz and Kingdom, 2004). The Fas–Fas ligand system is the major signal transduction pathway involved in apoptosis. Fas and FasL (CD95) are classical trans-membrane proteins that belong to the tumor necrosis factor receptor super family (TNFRSF) of proteins. Fas is ubiquitously expressed, while FasL is limited to certain leukocytes (activated T lymphocytes, natural killer [NK] cells) and tissues with immune privilege, including the human trophoblast throughout gestation (Sziller et al., 2005). As the Fas and FasL might represent candidate genes involved in the pathogenesis of preeclampsia, the presence of a genetic variant might increase susceptibility to the development of the pathology (Ashton et al., 2005). The Fas 670 G variant was found to be associated with a decreased Fas production in activated T lymphocytes (Pinti et al., 2002, Lai et al., 2003). Thus, we and others have hypothesized that genetic polymorphisms affecting Fas or Fas ligand might increase the risk of preeclampsia.
Patients and methods The diagnosis of preeclampsia was established before 37 weeks of gestation in cases using (1) blood pressure of 140/90mmHg (twice on separate occasions >6h apart) and urinary protein >300mg/l, or ≥2+ on dipstick urine analysis. Severe preeclampsia was defined as BP ≥160/110mmHg with proteinuria >5g in 24h, with or without other features like oliguria (<500ml/24h), cerebral or visual disturbances, pulmonary edema or cyanosis, epigastric or right upper quadrant pain, HELLP syndrome, or intrauterine growth restriction. The fetal outcomes assessed were intrauterine growth retardation (IUGR), intrauterine fetal death (IUFD), and prematurity (delivery <37 weeks’ gestation). IUGR was diagnosed in neonates when their birth weight was below the 10th percentile value for the given gestational age (Sziller et al., 2005).
Results Table 1 shows selected clinical features of the cases and controls. There were no differences in mean maternal age or parity between the two groups. As expected, the systolic and diastolic blood pressures were significantly higher in preeclamptic women compared with the control group (P<0.001 for both). There were no statistically significant differences between the two groups regarding hematocrit (P=0.072), platelet count (P=0.645) or ALT (P=0.091). Statistically significant differences were found regarding creatinine (P=0.012), and regarding total bilirubin and AST.