Evaluation of Lp-PLA2 mass, vitronectin and PAI-1 activity levels in patients with preeclampsia
Purpose The aim of the current study is to determine, correlate and compare the plasma lipoprotein-associated phospholipase A2 (Lp-PLA2), vitronectin (Vn), Plasminogen activator inhibitor-1 (PAI-1) activity and tissue plasminogen activator (t-PA) levels in early-onset preeclampsia, late-onset preecl...
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Published in | Archives of gynecology and obstetrics Vol. 292; no. 1; pp. 53 - 58 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.07.2015
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Purpose
The aim of the current study is to determine, correlate and compare the plasma lipoprotein-associated phospholipase A2 (Lp-PLA2), vitronectin (Vn), Plasminogen activator inhibitor-1 (PAI-1) activity and tissue plasminogen activator (t-PA) levels in early-onset preeclampsia, late-onset preeclampsia and in control pregnant women.
Methods
A total of 79 individuals, 30 early-onsets, and 22 late-onset preeclamptic and 27 control pregnant women were included into the scope of this study. Enzyme-linked immunosorbent assay procedure was used to determine the serum Lp-PLA2 and plasma Vn, t-PA antigen and PAI-1 activity levels. Serum C-reactive protein (CRP) levels were measured immunoturbidimetrically in routine clinical chemistry analyser.
Results
In patients with preeclampsia, Lp-PLA2, PAI-1, t-PA, CRP and blood pressures levels were increased (
p
= 0.000) and correlated with each other. Vn levels were decreased (
p
= 0.016) but not correlated with other parameters in preeclamptic patients.
Conclusion
We are of the opinion that increased Lp-PLA2 levels may partially contribute to endothelial dysfunction by the progression of inflammation. In addition, increased complex formation with Vn is likely to bring about the increase of PAI-1 activity in patients with preeclampsia. Moreover, increased t-PA and decreased Vn levels may also be the consequences of compensatory mechanisms against disease progression. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0932-0067 1432-0711 |
DOI: | 10.1007/s00404-014-3601-1 |