DETECTION OF BETA-2-GLYCOPROTEIN-I-DEPENDENT ANTIPHOSPHOLIPID ANTIBODIES AND ANTI-BETA-2-GLYCOPROTEIN-I ANTIBODY IN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS AND IN PATIENTS WITH SYPHILIS
J. Matsuda et al., DETECTION OF BETA-2-GLYCOPROTEIN-I-DEPENDENT ANTIPHOSPHOLIPID ANTIBODIES AND ANTI-BETA-2-GLYCOPROTEIN-I ANTIBODY IN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS AND IN PATIENTS WITH SYPHILIS, International archives of allergy and immunology, 103(3), 1994, pp. 239-244
We investigated whether or not antiphospholipid antibodies (aPLs; anti
phosphadidylserine antibody, aPS; antiphosphatididylinositol antibody,
aPI; antiphosphatidic acid antibody, aPA, and antiphosphadidylethanol
amine antibody, aPE) were beta(2)-glycoprotein-I (GPI)-dependent antib
odies like anticardiolipin antibody (aCL) in patients with systemic lu
pus erythematosus (SLE). None of the patients with syphilis or healthy
controls was positive for any GPI-dependent aPL. By contrast, GPI-dep
endent aCL (40%), aPS (20%), aPI (18%), aPA (12%) and aPE (8%) were de
tected in patients with SLE. Among these, 4 patients were negative for
aCL, but positive for aPS. Those who were positive for more than 2 ty
pes of aPL, along with lupus anticoagulant, had a high incidence of ar
teriovenous thrombosis, fetal loss, thrombocytopenia and biological fa
lse-positive reaction to syphilis. From these findings we conclude tha
t GPI-dependent aPLs, other than aCL, are present in patients with SLE
, and we should examine more than 2 types of aPL, such as a combinatio
n of aCL and aPS, to avoid overlooking aPL. Furthermore, we confirmed
that GPI-independent aPL was not rare in SLE patients, but the clinica
l significance of this type of aPL in this clinical setting is unclear
.