REDUCED C4b-BINDING PROTEIN IN PREECLAMPSIA

Schjetlein, Rune; Haugen, Guttorm; Sandset, Per Morten; Wisløff, Finn

doi:10.1016/s0049-3848(96)00232-0

Cited by 9 publications

(6 citation statements)

References 18 publications

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“…C4b-BP is an acute phase reactant. It binds functionally active free protein S molecules, and high levels of C4b-BP may possibly induce a prothrombotic state (6,14). In our study, we observed significantly reduced levels of C4b-BP in preeclampsia compared to the normotensive control group.…”

Section: Discussionsupporting

confidence: 55%

“…The laboratory measurement of AT, TAT, fibrinogen, fibrin monomer, D-Dimer, protein C activity, total and free protein S antigen, C4b-binding protein, PAI-1 activity and PAI-2 antigen were performed as described in previous publications (5,6). TFPI-Fag was determined by the use of a solidphase two-site enzyme immunoassay with reagents donated by P. Østergaard Ph.D., Novo Nordisk, Oslo (8).…”

Section: Test Proceduresmentioning

confidence: 99%

“…We have previously reported evidence of in-creased intravascular coagulation and fibrin turnover in a group of patients with preeclampsia (5,6). In the present study, these, and some additional parameters of coagulation and lipid metabolism as well as some clinical variables, were submitted to univariate and multivariate analyses in order to examine the association with preeclampsia and FGR.…”

mentioning

confidence: 94%

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Hemostatic variables as independent predictors for fetal growth retardation in preeclampsia

Schjetlein

Abdelnoor²,

Haugen

et al. 1999

Acta Obstet Gynecol Scand

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Section: Discussionsupporting

confidence: 55%

Section: Test Proceduresmentioning

confidence: 99%

mentioning

confidence: 94%

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Hemostatic variables as independent predictors for fetal growth retardation in preeclampsia

Schjetlein

Abdelnoor²,

Haugen

et al. 1999

Acta Obstet Gynecol Scand

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“…Binding of FVII to the exposed TF on the surface of monocytes may result in the low FVII concentration seen in women with P-EC [25,26]. It could also be due to reduced production, and/or increased consumption, following placental separation [27,28], consistent with increased intravascular coagulation and fibrin turn-over [29,30].…”

Section: Discussionmentioning

confidence: 99%

Tissue factor-dependent pathway in severe preeclampsia revisited

Dusse

Godói

Gomes

et al. 2016

Blood Coagulation &Amp; Fibrinolysis

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Previously we investigated the tissue factor (TF)-dependent coagulation pathway and key haemostatic cofactors in white women with preeclampsia (P-EC) and suggested that plasma factor VII (FVII) levels can differentiate women with P-EC from healthy nonpregnant women or normal pregnant women, at the same trimester, with high sensitivity, specificity, positive and negative predictive values. Here we re-examine the TF-dependent pathway in a large cohort of Brazilian women. A total of 240 women were studied. These included healthy nonpregnant women (n = 79), normotensive pregnant women (n = 80) and women with severe P-EC (n = 81). Commercially available enzyme-linked immunosorbent assays were used to measure plasma FVII, activated factor VII (FVIIa), TF and tissue factor pathway inhibitor (TFPI). All study participants were matched for age. Pregnant women (with/without P-EC) were matched for gestational age and parity. Plasma levels of FVII, FVIIa and TFPI were significantly increased in women with severe P-EC compared with healthy nonpregnant women (P < 0.01) or normotensive pregnant women (P < 0.01). FVIIa was also higher in normotensive pregnant women compared with nonpregnant women (P < 0.01). However, no such significant trends were observed for plasma TF levels (P = 0.074). In conclusion, circulating FVII, FVIIa and TFPI were significantly elevated in women with severe P-EC in the absence of comparable changes in plasma TF levels. The present work is in agreement with our previous report on FVII levels in white women with P-EC. Thus, this lends further support to the notion that plasma FVII levels are potentially valuable diagnostic marker for P-EC, irrespective of ethnicity.

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“…Previous reports of C4bp in PE are few and inconclusive. Mellembakken et al found no difference in C4bp plasma levels of preeclamptics and controls, while Schjetlein et al reported a decrease in C4bp plasma levels with increasing severity of PE (29,34). Recently, mutations in C4bp were found to be related to recurrent pregnancy loss in certain patients (10).…”

Section: Discussionmentioning

confidence: 99%

Complement activation and regulation in preeclamptic placenta

et al. 2014

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† Anna Inkeri Lokki and Jenni Heikkinen-Eloranta have contributed equally to this work.Preeclampsia (PE) is a common disorder of pregnancy originating in the placenta. We examined whether excessive activation or poor regulation of the complement system at the maternal-fetal interface could contribute to the development of PE. Location and occurrence of complement components and regulators in placentae were analyzed. Cryostat sections of placentae were processed from 7 early-onset PE (diagnosis <34 weeks of gestation), 5 late-onset PE, 10 control pregnancies, and immunostained for 6 complement activators and 6 inhibitors. Fluorescence was quantified and compared between PE and control placentae. Gene copy numbers of complement components C4A and C4B were assessed by a quantitative PCR method. Maternal C4 deficiencies (≥1 missing or nonfunctional C4) were most common in the early-onset PE group (71%), and more frequent in late-onset PE compared to healthy controls (60 vs. 38%). Complement C1q deposition differed significantly between control and patient groups: controls and early-onset PE patients had more C1q than late-onset PE patients (mean p = 0.01 and p = 0.005, respectively). C3 activation was analyzed by staining for C3b/iC3b and C3d. C3d was mostly specific to the basal syncytium and C3b/iC3b diffuse in other structures, but there were no clear differences between the study groups. Activated C4 and membrane-bound regulators CD55, CD46, and CD59 were observed abundantly in the syncytiotrophoblast. Syncytial knots, structures enriched in PE, stained specifically for the classical pathway inhibitor C4bp, whereas the key regulator alternative pathway, factor H (FH) showed a wider distribution in the placenta. Differences in C1q deposition between late-and early-onset PE groups may be indicative of the different etiology of PE symptoms in these patients. Irregular distribution of the complement regulators C4bp and FH in the PE placenta and a higher frequency of C4A deficiencies suggest a disturbed balance between complement activation and regulation in PE.

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REDUCED C4b-BINDING PROTEIN IN PREECLAMPSIA

Cited by 9 publications

References 18 publications

Hemostatic variables as independent predictors for fetal growth retardation in preeclampsia

Hemostatic variables as independent predictors for fetal growth retardation in preeclampsia

Tissue factor-dependent pathway in severe preeclampsia revisited

Complement activation and regulation in preeclamptic placenta

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