title: Impaired factor XIIa-dependent activation of fibrinolysis in treated antiphospholipid syndrome gestations developing late-pregnancy complications.
abstract: OBJECTIVE
  The objective of the study was to investigate the potential role of impaired factor XII-dependent activation of fibrinolysis in treated antiphospholipid syndrome gestations developing late-pregnancy complications.
  
  
  METHODS
  This was a prospective study in a third-level teaching hospital, including 75 patients: 25 pregnant patients having the antiphospholipid syndrome and carrying their pregnancies until 26 weeks' gestation or later (group 1); 25 pregnant patients having normal term pregnancies and delivery and no previous miscarriage (group 2); and 25 pregnant patients being diagnosed as having severe pre-eclampsia and/or intrauterine growth restriction but testing negative for antiphospholipid antibodies (group 3). Hemostatic evaluation was carried out from patients in groups 1 and 2 between 6 and 10 weeks, between 18 and 22 weeks, and between 28 and 32 weeks' gestation. Patients in group 3 were sampled between 28 and 32 weeks. An additional blood sample was obtained 4 to 6 months after delivery (baseline). The Mann-Whitney U test, the Friedman test, and the chi2 test were used.
  
  
  RESULTS
  Patients in group 1 were characterized by increased factor VIIa levels, increased prothrombin fragment 1+2 levels, reduced factor XIIa levels, diminished functional urokinase-type plasminogen activator levels, and decreased levels of plasmin/alpha-2-plasmin inhibitor complexes. These abnormalities were more evident in patients in group 1 developing pre-eclampsia and/or intrauterine growth restriction.
  
  
  CONCLUSIONS
  Impaired factor XIIa-dependent activation of fibrinolysis seems to be a key mechanism related to late-pregnancy complications in patients with the antiphospholipid syndrome.
authors.affiliation: Institut Clínic of Gynecology, Obstetrics, and Neonatology, Barcelona, Spain.
authors.forename: Francisco
authors.initials: F
authors.lastname: Carmona
authors.forename: Isabel
authors.initials: I
authors.lastname: Lázaro
authors.forename: Juan C
authors.initials: JC
authors.lastname: Reverter
authors.forename: Dolors
authors.initials: D
authors.lastname: Tàssies
authors.forename: Josep
authors.initials: J
authors.lastname: Font
authors.forename: Ricard
authors.initials: R
authors.lastname: Cervera
authors.forename: Juan
authors.initials: J
authors.lastname: Balasch
mesh_terms: D000328:Adult; D016736:Antiphospholipid Syndrome / Q000175:diagnosis / Q000503:physiopathology*; D001779:Blood Coagulation Factors / Q000032:analysis; D015956:Factor XIIa / Q000502:physiology*; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans; D011225:Pre-Eclampsia / Q000503:physiopathology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology*; D011262:Pregnancy Trimester, Second; D011446:Prospective Studies
chemical_list: D001779:Blood Coagulation Factors; D015956:Factor XIIa