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Severe Preeclampsia (severe + preeclampsia)
Selected AbstractsMaternal Mortality Associated with Eclampsia and Severe Preeclampsia of PregnancyJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 5 2000Dr. H. Sawhney Abstract Objective: To analyse factors associated with maternal mortality in eclampsia and preeclampsia. Method: Retrospective analysis of 69 maternal deaths due to (eclampsia-61; severe preeclampsia-8) was carried out during a period of 17 years (1982,1998). Maternal condition on admission, associated complications and principal cause of death was analysed in each case. Results: Mean time interval between hospitalization and maternal death was 49.56 + 62.01 hrs (1,240 hrs). Twenty (28.9%) women died undelivered. Twenty-three (37.7%) women were in grade IV coma and 52.4% of eclampsia patients had recurrent convulsions (> 10) prior to admission. Associated complications in form of hemorrhage, cerebrovascular accidents, acute renal failure, jaundice, aspiration pneumonia and pulmonary oedema were 30.4, 31.8, 34.8, 18.8, 17.8, and 5.8%, respectively. Maternal mortality in eclampsia was significantly low in time period B (4.1%) when magnesium sulphate was used as an anticonvulsant. Conclusions: Maternal condition on admission and associated complications are the major determinant of maternal outcome. Use of magnesium sulphate is associated with significant reduction of maternal mortality. [source] Double inherited thrombophilias and adverse pregnancy outcomes: Fashion or science?JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 5 2010Giovanni Larciprete Abstract Aim:, To determine to what extent double inherited thrombophilias are associated with adverse obstetric complications correlated with fetoplacental insufficiency, such as preeclampsia, hemolytic anemia elevated liver enzymes and low platelet count (HELLP) syndrome, gestational hypertension, fetal growth restriction (FGR), intrauterine death (ID), abruptio placentae and disseminated intravascular coagulopathy. Methods:, Pregnant women coming to delivery were retrospectively divided into two groups: group A (controls) and group B (cases). Patients belonging to group B had one of the following: severe preeclampsia, HELLP syndrome, gestational hypertension, FGR, intrauterine death, abruptio placentae of disseminated intravascular coagulopathy. We detected methylenetetrahydrofolate reductase (MTHFR) A1298C, MTHFR C677T, factor V Leiden, PAI-1, mutant prothrombin G20210A, plasma homocysteine, antithrombin III, protein S and activated protein C resistance. Normal pregnant women or pregnant women with double defects were enrolled in this study. Results:, The combination of MTHFR C677T mutation with PAI-1 (5G/5G) mutation was significantly linked with the occurrence of ID. HELLP syndrome was significantly related to the simultaneous presence of factor VIII and X mutations. The combination of MTHFR C677T with factor VIII mutation and the combination of factor II and V mutations were significantly related to the occurrence of abruptio placentae. We found an association between double isoforms MTHFR mutation and FGR. Conclusion:, It seems that some thrombophilias and a combination of thrombophilic factors carry a greater risk than others for a given adverse outcome. Further studies are needed to check the link between thrombophilic gene mutations and adverse pregnancy outcomes, such as recurrent miscarriages and deep venous thrombosis. [source] Changes of serum melatonin level and its relationship to feto-placental unit during pregnancyJOURNAL OF PINEAL RESEARCH, Issue 1 2001Yasuhiko Nakamura Serum melatonin concentrations were studied in normal pregnant women and in women with several types of pathologic pregnancies, e.g., twins, preeclampsia or intrauterine growth retardation (IUGR). Blood samples were collected from the maternal antecubital vein at 14:00 hr (daytime) and 02:00 hr (nighttime) during pregnancy, and also from the umbilical vein and artery immediately after delivery. Serum melatonin concentrations were measured by radioimmunoassay. Daytime serum melatonin levels in normal (single fetus; singleton) pregnancies were low. While the levels showed an increasing tendency toward the end of pregnancy, no statistically significant changes occurred. On the other hand, the nighttime serum melatonin levels increased after 24 weeks of gestation, with significantly (P<0.01) high levels after 32 weeks; these values decreased to non-pregnant levels on the 2nd day of puerperium. Nighttime serum melatonin levels were significantly (P<0.05) higher in twin pregnancies after 28 weeks of gestation than in singleton pregnancies, whereas the patients with severe preeclampsia showed significantly (P<0.05) lower serum melatonin levels than the mild preeclampsia or the normal pregnant women after 32 weeks of gestation. Melatonin concentrations in umbilical vessels showed a higher tendency in neonates who were born during at night compared with the other neonates; moreover, those in the umbilical artery were generally higher than those in the umbilical vein. The present results indicate that in humans, the maternal serum melatonin levels show a diurnal rhythm, which increases until the end of pregnancy, reflecting some pathologic states of the feto-placental unit. Fetuses may produce melatonin with a circadian rhythm. [source] The G20210A prothrombin-gene mutation and the plasminogen activator inhibitor (PAI-1) 5G/5G genotype are associated with early onset of severe preeclampsiaJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 4 2005A. GERHARDT Summary., Hereditary risk determinants of venous thrombosis have been reported to be associated with severe preeclampsia. So far there are no data to support whether these risk determinants are related to the time of onset of severe preeclampsia. We used a case,control design, studying 97 women with severe preeclampsia in previous pregnancies and 277 normal women, to assess hereditary risk factors of venous thrombosis as risk determinants for severe preeclampsia. A case-only design comprising solely the 97 women with a history of preeclampsia was used to evaluate these risk factors as risk determinants for early onset of severe preeclampsia. Using the case,control design, there was no significant risk association of the hereditary risk factors with severe preeclampsia [factor V Leiden, odds ratio (OR) 0.9, 95% confidence interval (CI) 0.4, 2.2; prothrombin mutation, OR 1.9, 95% CI 0.5, 7.0; methylentetrahydrofolate reductase 677TT genotype, OR 0.8, 95% CI 0.4, 1.8; plasminogen activator inhibitor (PAI-1) 4G/4G genotype, OR 1.2, 95% CI 0.7, 2.1; PAI-1 5G/5G genotype, OR 1.0, 95% CI 0.5, 1.8]. However, the onset of severe preeclampsia was significantly earlier in women with the G20210A prothrombin gene mutation (24.5 weeks vs. 30.1 weeks, P = 0.046) and in women with the PAI-1 5G/5G genotype (25.7 weeks vs. 30.8 weeks, P = 0.024). Hereditary risk factors for venous thrombosis do not predispose for severe preeclampsia. However, women who are carriers of the G20210A prothrombin gene mutation and the PAI-1 5G/5G genotype are at risk for early onset of severe preeclampsia. It appears that these risk factors do not induce the pathomechanism but accelerate the course of preeclampsia. [source] The relationship of the level of circulating antiangiogenic factors to the clinical manifestations of preeclampsiaPRENATAL DIAGNOSIS, Issue 5 2009Young Nam Kim Abstract Objective This study investigated whether the antiangiogenic factors' concentrations differ according to the clinical manifestations of preeclampsia. Methods This study included 62 preeclampsia and compared the soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng), and placental growth factor (PlGF) concentrations among patients with different clinical manifestations of preeclampsia. We also compared the patients with preeclampsia to 62 controls matched by age, gestational age, and parity after 20 weeks of gestation. Results The sEng concentrations were significantly elevated in early-onset than in late-onset preeclampsia (105.4 ± 37.9 vs 66.3 ± 36.0 ng/mL, p = 0.0008). Moreover, the sEng levels were also higher in severe preeclampsia compared to mild (42.5 ± 31.0 vs 79.2 ± 38.6 ng/mL, p = 0.0013) and in the small for gestational age (SGA) group compared to the group without SGA (68.3 ± 39.3 vs 85.7 ± 38.2 ng/mL, p = 0.0273). The sFlt-1 levels, however, did not reveal significant difference according to the onset-time, severity, and presence of SGA. The antiangiogenic factors' concentrations were not related with the degree of hypertension or proteinuria. Conclusion Altered antiangiogenic factors might be involved in the pathogenesis of preeclampsia with synergistic, but different roles. Especially, sEng may be more related with early and severe preeclampsia. Copyright © 2009 John Wiley & Sons, Ltd. [source] Decreased expression of heparin-binding epidermal growth factor,like growth factor as a newly identified pathogenic mechanism of antiphospholipid-mediated defective placentationARTHRITIS & RHEUMATISM, Issue 5 2010N. Di Simone Objective Heparin-binding epidermal growth factor,like growth factor (HB-EGF) plays a role in blastocyst implantation and is down-regulated in preeclampsia and in hypertensive pregnancy disorders associated with defective extravillous trophoblast invasion. Defective placentation and severe preeclampsia are also features of the antiphospholipid syndrome (APS). The purpose of this study was to investigate whether abnormal HB-EGF expression plays a pathogenic role in antiphospholipid antibody (aPL),mediated defective placentation. Methods HB-EGF expression in placental tissue was evaluated by Western blotting and messenger RNA analysis in normal and APS placentae. Polyclonal IgG fractions or monoclonal ,2 -glycoprotein I,dependent aPL and their respective controls were investigated for the following 4 features: their binding to human trophoblast monolayers, as determined by cell enzyme-linked immunosorbent assay (ELISA); their effect on HB-EGF expression by Western blotting in trophoblast cell extracts as well as by ELISA as a protein secreted in the culture supernatants; their inhibitory effect on in vitro trophoblast invasiveness, as evaluated by Matrigel assay; and their inhibitory effect on matrix metalloproteinase (MMP) levels, as measured by gelatin zymography. Experiments were also performed in the presence of serial concentrations of heparin or recombinant HB-EGF. Results Placental APS tissue displayed reduced expression of HB-EGF. Polyclonal and monoclonal aPL bound to trophoblast monolayers and significantly reduced the in vitro synthesis and secretion of HB-EGF. Heparin inhibited aPL binding and restored HB-EGF expression in a dose-dependent manner. Addition of recombinant HB-EGF reduced the in vitro aPL-induced inhibition of Matrigel invasiveness as well as MMP-2 levels. Conclusion These preliminary findings suggest that the reduction of aPL-mediated HB-EGF represents an additional mechanism that is responsible for the defective placentation associated with APS and that heparin protects from aPL-induced damage by inhibiting antibody binding. [source] Serum iron and copper status and oxidative stress in severe and mild preeclampsiaCELL BIOCHEMISTRY AND FUNCTION, Issue 3 2006Zehra Serdar Abstract Our aim was to investigate parameters of iron and copper status and oxidative stress and antioxidant function in women with healthy pregnancy, mild and severe preeclampsia with a view to exploring the possible contribution of these parameters to the aetiology. Thirty healthy, 30 mild preeclamptic and 30 severe preeclamptic pregnant women were included. Serum and placental lipid peroxides, and serum vitamin E and total carotene levels were measured by colorimetric assay. Cholesterol, copper, iron, total iron binding capacity (TIBC), ceruloplasmin and transferrin concentrations were measured by commercially available procedures. Data were analysed statistically using one-way analysis of variance and Pearson correlation test. Logistic regression procedures were used to calculate odds ratios. Lipid peroxides in serum and placental tissue, and iron, copper and ceruloplasmin levels in serum were significantly increased, and transferrin, TIBC, vitamin E/total cholesterol and total carotene/total cholesterol ratios in serum were significantly decreased especially in women with severe preeclampsia. Significant correlations were detected between serum iron and lipid peroxidesin serum and placental tissue and between serum iron and vitamin E/total cholesterol in severe preeclamptic pregnancy. Furthermore, there were significant correlations between serum malondialdehyde and ceruloplasmin and vitamin E/total cholesterol in women with severe preeclampsia, and changes in serum and placental lipid peroxides and serumiron concentrations were significantly associated with preeclampsia. In conclusion, ischaemic placental tissue may be a primary source of potentially toxic iron in preeclampsia and the released iron species may contribute to the aetiology and would exacerbatelipid peroxidation and endothelial cell injury, which may be abated by antioxidant supplementation. Copyright © 2005 John Wiley & Sons, Ltd. [source] | |||||||||||||