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  • br Materials and methods This is a


    Materials and methods This is a retrospective case-controlled study. The cases were selected based on the presence or absence of preeclampsia. Women enrolled in the study delivered singleton pregnancies at our institution from June 2003 to July 2004. Preeclampsia is defined as elevated blood pressure recorded on at least two occasions (separated by at least 6h) of at least 140/90mmHg and proteinuria of ⩾2+in a catheterized specimen or at least 300mg in a 24–h urine collection. Controls were women who were normotensive during pregnancy. Exclusion criteria were the presence of an autoimmune disease, collagen vascular disease, recent blood transfusion, chronic renal diseases, multiple gestations, isolated intra-uterine growth restriction and malignancies. Demographic parameters and pregnancy outcome data were extracted from patients’ medical records. We identified 45 subjects, of which 23 women had preeclampsia and 22 were normotensive. Results were not available on all 45 subjects as the DNA was degraded in several samples. All analyses had at least 43 test results available. We used descriptive statistics, Student’s “t” test for continuous variables and Chi square and Fisher’s exact for categorical variables. A P value of <0.05 was considered significant.
    Results We enrolled 45 patients in our study. There were 23 women with preeclampsia (cases) and 22 women that were normotensive (controls). There were no significant differences in the demographic characteristics of the cases and controls except for the rate of cesarean delivery and gestational age at delivery (Table 1). However, we do not have the parity, fetal weight and placental weight in this study. Preeclamptic women were more likely to have a cesarean delivery and be delivered at a younger gestational age. We present the Forskolin and allele frequencies for each of the polymorphisms tested in Table 2, Table 3, Table 4, Table 5, Table 6, Table 7.
    Comment Preeclampsia is proposed to be maternal immune mal-adaptation during placental invasion as proposed by Redman et al. [8] Superficial placentation is a powerful but not mandatory trigger for the maternal response syndrome ‘preeclampsia’, i.e. there is also a ‘maternal preeclampsia’ phenotype that typically does include significant placental involvement or for that matter ‘immune maladaptation’. Normal placental development involves differentiation and invasion of the trophoblast. In vitro assays show that placental cytotrophoblast cells from preeclamptic patients fail to up regulate integrin and matrix metalloproteinase-9 proteins that promote cell invasion [9]. They also fail to up regulate HLA-G protein that may act to protect cytotrophoblast cells from natural killer cell lysis [9]. Normal placental development is characterized by active apoptosis of trophoblast cells [10]. This active apoptosis is required for tissue homeostasis, and we thus hypothesized that abnormal homeostasis may be the product of dysregulated apoptosis [11], [12]. Normal homeostasis eventually leads to immune tolerance and regulates survival during invasion and subsequent placentation. Abnormal levels of placental apoptosis have been linked to pathologic conditions of pregnancy including preeclampsia and intrauterine growth restriction [12], [13]. The Fas–Fas ligand pathway is central to normal pregnancy and dysregulation of this pathway has been linked to pathologic conditions of pregnancy. In normal pregnancy, Fas ligand from invading trophoblasts incites apoptosis contributing to the loss of smooth muscle from the walls of spiral uterine arteries [14]. Sziller et al. suggested that the maternal Fas-670 GG genotype was expressed more in pregnancies where preeclampsia had developed before 37weeks [7]. They noted that the maternal Fas −670 single nucleotide polymorphism (SNP) reduced the expression of Fas and was associated with preeclampsia. Robinson et al. recently noted that maternal Fas −670 SNP mutation was associated with intrauterine growth restriction [4]. However, placental Fas–Fas ligand gene polymorphism was not reported in these studies. As preeclampsia is believed to be a placental disorder due to faulty trophoblastic invasion, we sought to investigate if placental multiple Fas–Fas ligand gene polymorphisms were associated with preeclamptic pregnancies. We found that placental Fas and Fas ligand gene polymorphisms did not appear to play as important a role in the pathogenesis of preeclampsia as that of the maternal immune cell Fas expression. Our findings support Hu et al. that there was no difference of Fas or Fas ligand expression between preeclamptic and normotensive placentas [15].