BETA(2)-GLYCOPROTEIN-I AND PLACENTAL ANTICOAGULANT PROTEIN-I IN PLACENTAE FROM PATIENTS WITH ANTIPHOSPHOLIPID-SYNDROME

Objective. To investigate the immunohistological distribution of beta( 2)-glycoprotein I (beta(2)GPI) and placental anticoagulant protein I ( PAP-I) in normal and pathological placentae of patients with antiphosp holipid (aPL) antibody associated recurrent fetal loss. These proteins are 2 natural anticoagulants able to interfere with aPL antibody bind ing. Methods. Placentae from 4 patients with primary antiphospholipid antibody syndrome (pAPS), from 2 patients with aPL negative systemic l upus erythematosus (SLE) and from 7 healthy women were studied. Cryost atic placental sections were tested by indirect immunofluorescence usi ng polyclonal anti-PAP-I and anti-beta(2)GPI antisera as well as purif ied IgG and anti-beta(2)GPI monoclonal antibody. The same tissue secti ons were also tested by direct immunofluorescence with FITC-F(ab)(2) g oat antihuman IgG. Results. We found that (a) the placental distributi on of PAP-I was comparable in normal and pathological specimens; (b) o n the contrary, increased beta(2)GPI deposition was present on the tro phoblast surfaces of placentae obtained from patients with persistent raised titers of aPL antibodies. Comparable IgG deposition on villi su rface was also found in aPL positive but not in control placentae. Con clusion. Our data are consistent with the hypothesis that high titer a PL binds to a beta(2)GPI phospholipid complex in placentae of women wi th recurrent fetal loss but that a quantitative deficiency of PAR-I do es not play a pathogenetic role in aPL associated fetal loss.