Reduced Number of Endothelial Progenitor Colony-Forming Units in Patients with Preeclampsia

PURPOSE: Endothelial progenitor cells (EPCs), which mediates neovascularization of uterine endometrium may be involved in the neovascularization in the utero-placental circulation. Low numbers of endothelial progenitor colony-forming unit (CFU) in culture are predictive biomarker of vascular disease. The aim of the present study was to evaluate whether the number of CFU in preeclampsia differed from that in normal pregnancy. MATERIALS AND METHODS: Women with singleton normal (n=26) or preeclamptic (n=20) pregnancies were studied during the third trimester. The number of EPCs was quantified by CFU methodology. Plasma levels of angiogenic factors, vascular endothelial growth factor (VEGF), soluble fms-like tyrosine kinase-1 (sFlt-1), and placental growth factor (PlGF) were determined by enzyme-linked immunoassay. RESULTS: CFU numbers were significantly decreased in the preeclamptic patients compared with the controls (median, 3; range 1-12 vs. 31; 3-81 CFU/well, P<0.001). A majority of the cells comprising individual colonies were positive for endothelial characteristics (Ulex europaeus lectin staining and acetylated low-density lipoprotein uptake). Plasma levels of the sFlt-1 were highly elevated (P<0.001) in patient with preeclampsia compared to controls, whereas PlGF were highly reduced (P=0.004), but these factors did not associate with CFU numbers. CONCLUSION: Our results suggest that reduced numbers of CFU obtained from maternal peripheral blood may contribute to the development of preeclampsia.

Polymorphisms of 5, 10-Methylentetrahydrofolate Reductase (MTHFR C677T) and Methionine Synthase Reductase (MTRR A66G) as Maternal Risk Factors for Fetal Aneuploidy

PURPOSE: Aneuploidy is the cause of diseases such as Down syndrome or Edward syndrome and, more generally, is a major cause of mental retardation and fetal loss. The purpose of this study was to evaluate the association between MTHFR (C677T) or MTRR (A66G) polymorphisms and fetal aneuploidy. MATERIALS AND METHODS: Data was collected from 37 women who had a fetus with aneuploidy (cases) and 78 women who had previously delivered at least two healthy children without aneuploidy and did not have a history of miscarriage or abnormal pregnancy (controls). The MTHFR (C677T) or MTRR (A66G) polymorphisms were analyzed by PCR-restriction fragment length polymorphism assay. RESULTS: The frequencies of the MTHFR 677 CC, CT, and TT genotypes were 30.7%, 48.7%, and 20.6% in the control group and 37.8%, 48.6%, and 13.5% in the case group, respectively. There were no significant differences in genotype frequencies between the two groups. For the MTRR A66G polymorphism, the frequencies of the AA, AG and GG genotypes were 50%, 46.1%, and 3.9% in the control group and 13.5%, 81.1%, and 5.4% in case group, respectively. The frequency of the MTRR AG mutant was significantly increased in the case group, with an odds ratio of 6.5 (95% CI: 2.3-18.6, P<0.05). CONCLUSION: The results of this study suggest that mother carriers with the MTRR G allele have an increased risk of fetal aneuploidy, while the MTHFR T allele is not associated with increased risk of fetal aneuploidy. The MTRR A66G polymorphism may be a risk factor for producing a child with chromosomal aneuploidy.

Maternal Serum and Amniotic Fluid Inhibin A Levels in Women who Subsequently Develop Severe Preeclampsia

The purpose of this study was to evaluate whether maternal serum (MS) and amniotic fluid (AF) inhibin A levels are elevated in patients who subsequently develop severe preecalmpsia, and to investigate the correlation between MS and AF inhibin A levels in the second trimester. The study included 40 patients who subsequently developed severe preecalmpsia and 80 normal pregnant women. Inhibin A levels in MS and AF were measured with enzyme-linked immunosorbent assay (ELISA). The MS and AF inhibin A levels in patients who developed severe preeclampsia were significantly higher than those in the control group (both for p<0.001). There was a positive correlation between MS and AF inhibin A levels in patients who developed severe preeclampsia (r=0.397, p=0.011), but not in the control group (r=0.185, p=0.126). The best cutoff values of MS and AF inhibin A levels for the prediction of severe preeclampsia were 427 pg/mL and 599 pg/mL, respectively; the estimated ORs that were associated with these cut-off values were 9.95 (95% CI 3.8-25.9, p<0.001) and 6.0 (95% CI 2.3-15.8, p<0.001). An elevated level of inhibin A in MS and AF at the time of second trimester amniocentesis may be a risk factor for the subsequent development of severe preeclampsia.

A Clinical Report of Pregnancy Induced Hypertension according to the Severity / 대한주산의학회잡지

The aim of present study was to establish the baseline data for pregnancy induced hypertension (PIH). From November 2000 through October 2001, a total of 212 women diagnosed as PIH and delivered at Samsung Cheil Hospital were included in this study. We reviewed the obstetric and neonatal records, then analyzed the incidence, maternal complications, and neonatal outcomes according to the severity of PIH. The incidence of PIH was 2.6% (mild and severe form was 59% and 41%, respectively). In maternal age, parity, number of fetus (singletone or multiple pregnancy), and gestational diabetus, there was no significant different incidence between mild and severe form of PIH. But, the women with severe PIH delivered more frequently at 21~28 and 33~36 gestational weeks than in mild form (p<0.05). Among fetuses with intrauterine growth restriction (IUGR), a group with birth weight below the population 5 percentile was more frequent in severe than in mild form of PIH (p0.05). As to maternal, fetal and neonatal complications of PIH, maternal anemia, preterm labor, and IUGR were more frequently founded in severe form of PIH than in mild. We could not found significant different frequency in other complication (disseminated intravascular coagulation, abruptio placenta, pulmonary edema, low apgar score, meconium stained, respiratory distress syndrome, and intracranial hemorrhage) between mild and severe form of PIH.