The aim of this study was to examine potential links between antiOxLDL anti
bodies and the clinical and biological features of secondary antiphospholip
id syndrome (II APLS) associated with systemic lupus erythematosus (SLE).
A cohort study was done of 98 SLE patients followed-up for 1 y, including 1
8 with definite II APLS and 13 patients with definite primary APLS (I APLS)
. IgG anticardiolipin, IgG anti beta2 GPI, lupus anticoagulant, VDRL and Ig
G antiOxLDL were measured in all 98 study subjects.
High antiOxLDL titers were found in seven (39%) of the 18 patients with II
APLS vs 10 ( 12.5%) of the 80 patients without APLS (P < 0.01; OR = 4.45; 9
50% CI = 1.4-14.1) and none of the 13 patients with I APLS (P < 0.02). The
mean antiOxLDL titer was not significantly higher in the SLE patients with
than without II APLS (P > 0.05). A high antiOxLDL titer was correlated with
deep venous thrombosis (P < 0.01; OR= 5.77; 95% CI = 0.54-61) but not with
arterial thrombosis (P > 0.05 OR = 1; 95% CI = 0.29-3.09), thrombocytopeni
a, central nervous system involvement, livedo reticularis, or a positive Co
ombs test, The antiOxLDL antibody titer was correlated with the IgG anticar
diolipin antibody titer (r = 0.235; P = 0.02) and with the IgG anti-beta2 G
PI antibody titer (r = 0.224, P = 0.026).
AntiOxLDL elevation was found in 17% of SLE patients and was significantly
associated with II Introduction APLS and venous thrombosis, We found no evi
dence suggesting that antiOxLDL may be associated with atherosclerosis.