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Clot lysis time and thrombin activatable fibrinolysis inhibitor in severe preeclampsia with or without associated antiphospholipid antibodies

M. Angeles Martínez-Zamoraa, Dolors Tassiesb, Francisco Carmonaa, Gerard Espinosac, Ricard Cerverac, Juan Carlos Reverterb, Juan BalaschaCorresponding Author Informationemail address

Received 14 February 2010; received in revised form 18 May 2010; accepted 18 May 2010. published online 10 June 2010.
Corrected Proof

Abstract 

We investigated clot lysis time, thrombin activatable fibrinolysis inhibitor antigen (TAFI) levels and TAFI gene polymorphisms in pregnant patients with severe preeclampsia, with or without associated antiphospholipid syndrome (APS). The study groups included 82 pregnant patients without antiphospholipid antibodies with severe preeclampsia (PE group) and 10 pregnant APS patients who developed severe preeclampsia (APS-PE group). Controls included 76 primary pregnant APS patients (APS group) and 89 healthy pregnant patients (NOR group) with uneventful term pregnancy and delivery. Patients in the APS-PE, APS and NOR groups were sampled during each trimester of pregnancy and at 4–6 months and 12 months after delivery. Patients in the PE group were sampled during the third trimester and after delivery. Significantly prolonged clot lysis time after delivery was found in the PE, APS-PE and APS groups compared to the NOR group. The PE and APS-PE groups had longer clot lysis time than the APS group. Levels of TAFI were found to be higher after delivery in patients of the PE and APS-PE groups compared to the APS and NOR groups. Allele distribution of the TAFI gene polymorphisms was similar among the four study groups. We conclude that increased TAFI antigen levels and impaired fibrinolysis are pathogenetic factors in preeclampsia, regardless of whether or not preeclampsia is associated with the presence of antiphospholipid antibodies.

a Institut Clínic of Gynecology, Obstetrics and Neonatology, Faculty of Medicine, University of Barcelona, Hospital Clínic, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain

b Department of Hemotherapy and Hemostasis, Faculty of Medicine, University of Barcelona, Hospital Clínic, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain

c Deparment of Autoimmune Diseases, Faculty of Medicine, University of Barcelona, Hospital Clínic, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain

Corresponding Author InformationCorresponding author at: Institut Clínic of Gynecology, Obstetrics and Neonatology, Faculty of Medicine, University of Barcelona, Hospital Clínic, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Villarroel, 170, 08036 Barcelona, Spain. Tel.: +34 932275436; fax: +34 932279325.

PII: S0165-0378(10)00095-1

doi:10.1016/j.jri.2010.05.002

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