scholarly journals Fibronectin and C-reactive protein in pregnancy induced hypertension

2003 ◽  
Vol 22 (4) ◽  
pp. 325-328
Author(s):  
Svetlana Djuricic ◽  
Marina Stojanov ◽  
Ivana Obradovic ◽  
Aleksandar Glisic ◽  
Darko Plecas

Hypertension is the most common medical complication in pregnancy. Of the varying forms of hypertension that can effect pregnancy pre-eclampsia is the one specific to pregnant women. The differential diagnosis between pre-eclampsia and pregnancy induced hypertension (PIH) is essential to proper management of pregnancy. The aim of this study was to examine the effect of hypertension on plasma fibronectin and C-reactive protein (CRP) during gestatation. The examined groups comprised 37 patients with normal pregnancy and 30 with PIH between 24 and 36 weeks of gestation. Plasma fibronectin and CRP were both assayed by nephelometric method. The obtained results for both examined parameters were significantly higher in PIH group than in controls (p < 0.05). A positive correlation was found between fibronectin, CRP and weeks of gestation (p < 0.05). Therefore, we can conclude that plasmatic fibronectin and CRP are among useful screening parameters for estimation of the endothelial injury in hypertensive disorders of pregnancy.

2020 ◽  
Vol 15 (3) ◽  
pp. 227-239 ◽  
Author(s):  
Hader I. Sakr ◽  
Akef A. Khowailed ◽  
Reham S. Al-Fakharany ◽  
Dina S. Abdel-Fattah ◽  
Ahmed A. Taha

Background: Pre-eclampsia poses a significant potential risk of hypertensive disorders during pregnancy, a leading cause of maternal deaths. Hyperuricemia is associated with adverse effects on endothelial function, normal cellular metabolism, and platelet aggregation and adhesion. This study was designed to compare serum urate levels in normotensive pregnant women to those with pregnancy-induced hypertension, and to evaluate its value as a potential predictive marker of hypertension severity during pregnancy. Methods: A prospective, observational, case-control study conducted on 100 pregnant women in their third trimester. Pregnant women were classified into two groups (n=50) according to arterial blood pressure measurements: group I had normal blood pressure, and group II had a blood pressure of ≥ 140/90, which was further subdivided according to hypertension severity into IIa (pregnancy- induced hypertension, IIb (mild pre-eclampsia), and IIc (severe pre-eclampsia). Blood samples were obtained on admission. Serum urate, high sensitive C-reactive protein, and interleukin-1β levels, and lipid profile were compared among the groups. Results: A significant increase in the mean values of serum urate, C-reactive protein, and interleukin- 1β levels was detected in gestational hypertensives. In addition, there was a positive correlation between serum urate levels and C-reactive protein and interleukin-1β, as well as between serum urate levels and hypertension severity. Conclusion: Hyperuricemia and increased C-reactive protein and interleukin-1β serum levels correlate with the severity of pregnancy-induced hypertension, and these biomarkers may play a role in the pathogenesis of pre-eclampsia. Serum urate measurement is sensitive, reliable markers that correlate well with the severity of hypertension in pregnant females with pre-eclampsia.


Angiology ◽  
2011 ◽  
Vol 63 (1) ◽  
pp. 35-38 ◽  
Author(s):  
Velore J. Karthikeyan ◽  
Gregory Y. H. Lip ◽  
Sabah Baghdadi ◽  
Deirdre A. Lane ◽  
D. Gareth Beevers ◽  
...  

The pathophysiology of pregnancy-induced hypertension and preeclampsia may involve abnormalities in placentation and the Fas/Fas ligand system. Hypothesizing abnormal plasma Fas and Fas ligand in pregnancy-induced hypertension, we recruited 20 hypertensive pregnant women at mean week 15 and 29 at week 30: 18 were studied at both time points. Control groups were 20 normotensive pregnant women at week 20, 29 women at week 27, and 50 nonpregnant women. sFas and sFas ligand (sFasL) were measured by enzyme-linked immunosorbent assay (ELISA). The hypertensive women had lower sFasL at both stages of their pregnancy ( P < .05). There were no differences in sFas. In 18 hypertensive pregnant women, sFasL fell from week 15 to week 29 ( P < .03). We conclude that sFas and sFasL is unchanged in normal pregnancy. Hypertension in pregnancy is characterized by low sFasL, and levels fall from weeks 15 to 29. This may reflect differences in placentation in the differing physiological and pathological states.


1993 ◽  
Vol 85 (1) ◽  
pp. 63-70 ◽  
Author(s):  
L. J. Beilin ◽  
K. D. Croft ◽  
C. A. Michael ◽  
J. Ritchie ◽  
L. Schmidt ◽  
...  

1. Platelet-activating factor is a phospholipid with potent vasodilator and platelet-activating properties. To test the hypothesis that a generalized change in cellular platelet-activating factor metabolism may be involved in the systemic vasodilatation of normal pregnancy or pregnancy-induced hypertension, we studied platelet-activating factor and eicosanoid synthesis in isolated leucocytes obtained from pregnant women before and after delivery compared with age-matched non-pregnant control subjects. Parallel observations were carried out in age- and gestation-matched women with uncomplicated hypertension in pregnancy and in women with pregnancy-induced hypertension and a further set of normotensive pregnant control subjects. 2. Leucocyte counts were higher in all pregnant groups compared with non-pregnant control subjects. Neutrophil production of platelet-activating factor and metabolites of prostacyclin, prostaglandin E2 and thromboxane in response to calcium ionophore stimulation were all lower in pregnant women compared with non-pregnant control subjects, but returned to similar levels 6 weeks post partum. There was no significant difference between essential hypertensive and normotensive groups. When women with pregnancy-induced hypertension were a priori subdivided into those with or without proteinuria, subjects with proteinuria showed significantly lower levels of neutrophil platelet-activating factor synthesis. 3. Plasma levels of the platelet-activating factor metabolite (lyso-platelet-activating factor) were also lower in pregnancy, suggesting alterations in the activity of enzymes controlling synthesis or degradation of this phospholipid in pregnancy. In pregnancy-induced hypertension the levels of plasma lyso-platelet-activating factor were higher than in normal pregnancy. 4. Thus this study demonstrates a reduction in the maximum capacity of neutrophils to synthesize platelet-activating factor and the three main classes of eicosanoids in vitro and a reduction in plasma lyso-platelet-activating factor levels in normotensive and essential hypertensive pregnancies. Contrary to expectation neutrophil prostacyclin metabolite generation was reduced in normal pregnancy. In pregnancy-induced hypertension with proteinuria the suppression of neutrophil platelet-activating factor synthesis was more pronounced. The results do not support the involvement of platelet-activating factor in the vasodilatation of pregnancy, but indicate profound changes in cellular phospholipid metabolism in normal pregnancy with further disturbances in pregnancy-induced hypertension by as yet unexplained mechanisms.


1988 ◽  
Vol 74 (3) ◽  
pp. 307-310 ◽  
Author(s):  
I. Gregoire ◽  
D. Roth ◽  
G. Siegenthaler ◽  
P. Fievet ◽  
N. El Esper ◽  
...  

1. A ouabain-displacing factor (ODF) was measured in the urine of non-pregnant, normotensive pregnant and hypertensive pregnant women by a receptor-binding assay with sodium, potassium-dependent adenosine triphosphatase. 2. Urinary ODF was significantly increased in normal pregnancy. 3. Greater increases were seen in pregnancy-induced hypertension and pre-eclampsia.


2005 ◽  
Vol 94 (11) ◽  
pp. 1071-1076 ◽  
Author(s):  
Sunil Nadar ◽  
Ioannis Karalis ◽  
Eman Al Yemeni ◽  
Andrew Blann ◽  
Gregory Lip

SummaryThis study tests the hypothesis that abnormalities in plasma indices of angiogenesis, such as Vascular Endothelial Growth Factor (VEGF) and angiopoietins (Ang-1, Ang-2), as well as their soluble receptors Flt-1 (sflt-1) and Tie 2 (sTie-2) respectively, are present in women with in pregnancy-induced hypertension (PIH). We also measured platelet levels of VEGF and Ang-1 (pVEGF and pAng-1 respectively). We studied 69 consecutive women with PIH (34 without proteinuria, and 35 with proteinuria, i.e. preeclampsia) who were compared to 64 consecutive women with normotensive pregnancies and 30 normotensive non-pregnant women, in a cross-sectional study. Using ELISA, we measured levels of plasma VEGF, Ang-1 &2, Tie-2 and sflt-1, and also the levels of angiogenic markers within the platelet [platelet VEGF (pVEGF) and platelet Ang-1 (pAng1)] by lysing a fixed number of platelets with 0.5% tween. Results show that levels of plasma VEGF, Ang-1, Ang2, sFlt-1 and Tie-2 were significantly different between the study groups. Post hoc analyses revealed plasma Ang-1 was highest in the preeclampsia group (p<0.001), whilst Ang-2 was highest in the normotensive pregnant group (p-=0.018). Plasma Tie-2 was highest in the PIH group. VEGF levels were significantly different between the preeclampsia group and the PIH group (p<0.05). Platelet VEGF levels were higher in the non-pregnant group than in the pregnant group, but there were no significant differences in the platelet levels of Ang-1 between the different groups. Ang-2, sFlt-1 and Tie-2 were undetectable in the platelet lysate in any of the patient groups or controls. Blood pressure was a major determinant of the different angiogenic factors studied. Abnormal indices of angiogenesis are evident in PIH and preeclampsia, with higher levels of sFlt-1 and lower levels ofVEGF; in PIH, increased levels of Ang-1 and Tie-2, but reduced Ang-2, are evident compared to normal pregnancy. These abnormalities may have implications for the pathogenesis of PIH and preeclampsia.


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