β2 Glycoprotein I and placental anticoaglant protein I in placentae from patients with antiphospholipid syndrome

Objective. To investigate the immunohistological distribution of beta₂-glycoprotein I (β₂GPI) and placental anticoagulant protein I (PAP-I) in normal and pathological placentae of patients with antiphospholipid (aPL) antibody associated recurrent fetal loss. These proteins are 2 natural anticoagulants able to interfere with aPL antibody binding. Methods. Placentae from 4 patients with primary antiphospholipid antibody syndrome (pAPS), from 2 patients with aPL negative systemic lupus erythematosus (SLE) and from 7 healthy women were studied. Cryostatic placental sections were tested by indirect immunofluorescence using polyclonal anti-PAP-I and anti-β₂GPI antisera as well as purified IgG and anti-β₂GPI monoclonal antibody The same tissue sections were also tested by direct immunofluorescence with FITC-F(ab)₂ goat antihuman IgG. Results. We found that (a) the placental distribution of PAP-I was comparable in normal and pathological specimens; (b) on the contrary, increased β₂GPI deposition was present on the trophoblast surfaces of placentae obtained from patients with persistent raised titers of aPL antibodies. Comparable IgG deposition on villi surface was also found in aPL positive but not in control placentae. Conclusion. Our data are consistent with the hypothesis that high titer aPL binds to a β₂GPI phospholipid complex in placentae of women with recurrent fetal loss but that a quantitative deficiency of PAP-I does not play a pathogenetic role in aPL associated fetal loss.