References[1] Hnat MD, Sibai BM, Caritis S, Hauth J, Lindheimer MD, MacPherson C, et al. Perinatal outcome in women with recurrent preeclampsia compared with women who develop preeclampsia as nulliparas. Am J Obstet Gynecol 2002;186(3):422-6. [2] Odendaal HJ, Pattinson RC, Bam R, Grove D, Kotze TJ. Aggressive or expectant management for patients with severe preeclampsia between 28-34 weeks' gestation: a randomized controlled trial. Obstet Gynecol 1990;76(6):1070-5. [3] Sibai BM, Mercer BM, Schiff E, Friedman SA. Aggressive versus expectant management of severe preeclampsia at 28 to 32 weeks' gestation: a randomized controlled trial. Am J Obstet Gynecol 1994;171(3):818-22. [4] Thomas T, Jophy R, Mhaskar A, Misquith D. Are we increasing serious maternal morbidity by postponing termination of pregnancy in severe pre-eclampsia/eclampsia? J Obstet Gynecol 2005;25(4):347-51. [5] Bassaw B, Roopnarinesingh S, Sirjusingh A. An audit of perinatal mortality. West Indian Med J 2001;50(1):42-6.
Background and purpose: Were to assess the association between homocysteine levels and development of preeclampsia, to determine homocysteine levels in fetal circulation, to differentiate homocysteine levels in mild and severe preeclampsia and to compare homocysteine levels in pregnant women with preeclampsia with homocysteine levels measured in the same group of women six months after delivery. Material and methods: IntroductIon Since the 1990s, homocysteine has been associated with disorders of the fetomaternal unit (1). Studies on recurrent abortions also found clear association between elevated homocysteine levels and the risk of abortion (2,3). Later on, Vollset et al. (4) found the levels of homocysteine to be associated with the prevalence of preeclampsia, preterm delivery, low birth weight, intrauterine growth restriction (IUGR), stillbirth, congenital malformations and abruptio placentae. The association of mild hyperhomocysteinemia with cardiovascular disease and related mortality was demonstrated in a number of studies (5-11).Hyperhomocysteinemia alters vascular morphology, stimulates inflammation, activates endothelium and blood clotting cascade, and inhibits fibrinolysis. Hyperhomocysteinemia results in the loss of endothelial antithrombin function and induction of a procoagulant setting (9,12). The pathogenetic action of homocysteine also includes interference with the nitric oxide (NO) system (homocysteine reduces NO bioavailability by interfering with its synthesis), activation of transcrip- (13,14). The aims of the study were to assess the association between elevated homocysteine levels and development of preeclampsia; to determine homocysteine levels in fetal circulation; to differentiate homocysteine levels in mild and severe preeclampsia; and to compare homocysteine levels in pregnant women with preeclampsia with homocysteine levels measured in the same group of women six months after delivery. methodsThe study included 55 pregnant women with verified milde preeclampsia (blood pressure measured on two occasions at least 4 h apart ≥140/90 mm Hg after 20 th week of gestation, and positive proteinuria) and severe preeclampsia (blood pressure ≥160/110 mm Hg, proteinuria ≥++). Control group consisted of 50 healthy pregnant women, as approved by the Ethics Committee of the Osijek University Hospital. All pregnant women are taking folate supplements and vitamins, including B6 and B12 during pregnancy and puerperium (Elevit®, Bayer, Germany). In both preeclampsia and control group, homocysteine levels were measured after at least 12-h fasting. Umbilical blood homocysteine levels were determined in the same groups of women after delivery, during third stage. In the group of women with preeclampsia, blood homocysteine was also determined six months after delivery. Homocysteine levels were determined by the FPIA (fluorescence polarization immunoassay) technology on an AxSYM device (Abbott Laboratories) using reagents of the same manufacturer . According to Khong and Hague (15), hyperhomocyst...
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