Anticardiopin antibodies: pathoetiologies for osteonecrosis in systemic lupus erythematosus?

In a cross-sectional study of 103 patients with systemic lupus erythematosus (SLE), 31 (30%) of whom had osteonecrosis (ON), our specific aim was to determine whether and to what degree anticardiolipin antibodies (aCLA) and lipoprotein (a) (Lptal) were pathoetiologies for ON. There were 97 women, 6 men, 51 black, 51 white, 1 asian. IgG aCLA and IgM aCLA were high (>22 GPL, >10 MPL) in 47 (46%) and 12 (12%) of the patients. With age, race, Lp(a), aCLA IgG, aCLA IgM, corticosteroids (ST) (ever/current), and highest ST dose as explanatory variables, by logistic regression, IgG aCLA (p=.04) and highest ST dose (p=.01) were predictors of ON. Patients with ON had higher mean (SD) IgG than those without ON (26 ±12 vs 21 ±11 GPL, p..05) and also had higher maximal ST doses (55 ±31 mg/day vs 37± 32, p=.003). Of 15 white patients with ON, 11 (73%) had IgG >22 GPL vs 16 of 36 (44%) without ON (p=.06); 6 of 15 with ON had IgM >10 MPL vs 3 of 36 (8%) without ON (p=.007). IgG and (to a lesser degree) IgM aCLA and maximal ST are determinants of ON in patients with SLE. Since aCLA-mediated thrombophilia can be ameliorated by Coumadin, we speculate that prospective MRI/X-ray followup of SLE patients with high aCLA might allow primary prevention of early ON by Coumadin Rx before irreversible segmental collapse of bone.