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O2 Effect of treatment on antiphospholipid antibodies in SLE
  1. Michelle Petri1,
  2. Laurence S Magder2 and
  3. Daniel W Goldman1
  1. 1Medicine, Rheumatology, Johns Hopkins University School of Medicine, Baltimore
  2. 2Dept. Epidemiology, University of Maryland, School of Medicine, Baltimore, USA


Background Unlike primary antiphospholipid syndrome patients, most SLE patients with antiphospholipid antibodies are on one or more treatments for their SLE that might affect levels of their antiphospholipid antibodies. We examined the effect of prednisone and hydroxychloroquine on antiphospholipid antibodies in an SLE longitudinal cohort.

Methods 943 SLE patients, who were tested for each anticardiolipin isotype (aCL IgG, IgM and IgA; INOVA) and lupus anticoagulant (LAC; dRVVT with further confirmatory testing) for at least 10 quarterly clinic visits, were included. We compared visits positive for antiphospholipid antibodies (aCL>20 and aCL>40; dRVVT>45) to visits negative for antiphospholipid antibodies, with respect to treatment, using conditional logistic regression and conditioning on the patient.

Results Prednisone treatment significantly reduced the levels of aCL IgG isotypes (aCL IgG>40 and some prednisone but less than 10 mg/day, OR 0.61 95% CI 0.46–0.80 p=0.0004), but not aCL IgM, IgA, or LAC. Hydroxychloroquine treatment significantly reduced aCL IgG (aCL IgG>40, OR 0.35 95% CI 0.22–0.55 p<0.0001), aCL IgM (aCL IgM>40, OR 0.56 95% CI 0.36–0.87 p=0.010) and LAC (OR 0.71 95% CI 0.58–0.86 p=0.007) but not aCL IgA.

Conclusions Prednisone does not reduce IgM or IgA isotypes of anticardiolipin, or LAC. These results explain why prednisone does not reduce thrombosis in SLE. Hydroxychloroquine, on the other hand, significantly reduces all antiphospholipid types except for the IgA isotype of anticardiolipin. This may explain why IgA isotypes are more common in SLE. It may also explain why hydroxychloroquine leads to only a 50% reduction in thrombosis, as IgA isotypes do confer some risk of thrombosis.

Acknowledgements The Hopkins Lupus Cohort is supported by NIH Grant RO1 AR 69572.

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