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PS4:66 Prolonged exposure to antiphospholipid antibodies is associated with endothelial dysfunction in patients with systemic lupus erythematosus
  1. C Cho1,
  2. Y Park2,
  3. I Baek1 and
  4. W Kim3
  1. 1Yeouido St. Mary’s Hospital, Seoul, South Korea
  2. 2St. Vincent Hospital, Suwon, South Korea
  3. 3Seoul St. Mary’s Hospital, Seoul, South Korea


Objective Antiphospholipid syndrome has been shown to be associated with increased cardiovascular mortality, but the role of antiphospholipid antibodies (aPL) on endothelial dysfunction remains elusive. We investigated the association between endothelial dysfunction and aPL in systemic lupus erythematosus (SLE) patients.

Methods 188 SLE patients and 62 controls were enrolled. Endothelial function was measured by flow-mediated dilatation (FMD). Cardiovascular risk factors were assessed and quarterly measurement of anti-cardiolipin (aCL) and anti-β2 glycoprotein I Ab were used to calculate time-integrated values throughout disease duration. Circulating endothelial progenitor cell (EPC), defined by CD34+/KDR +mononuclear cells, was quantified by flow cytometry.

Results Median FMD was significantly lower in SLE patient than in controls (6.9 versus 9.3%, p<0.001). In univariate analysis, older age, hypertension and persistent positive lupus anticoagulant (LAC) were associated with decreased FMD in SLE patients (p=0.034, p=0.011, p=0.020). Time-integrated aCL value (TI-aCL), but not a single value, was correlated with decreased FMD (p=0.003). Multivariate analysis showed that hypertension and TI-aCL were independent factors for decreased FMD (p=0.011, p=0.011); addition of positive LAC increased the adjusted probability of decreased FMD (p=0.003). FMD was correlated with EPC number (ρ=0.342, p=0.005) and TI-aCL was also an independent factor of reduced EPC after multiple adjustment (p=0.024). The predicted probability of endothelial dysfunction at median EPC level was higher in group with high TI-aCL than in group with low TI-aCL (p=0.004).

Conclusion Cumulative burden of aPL was closely associated with endothelial dysfunction in SLE patients, which was mediated in part by reduction of EPC.

  • Antiphospholipid Antibody
  • Endothelial Dysfunction
  • Endothelial Progenitor Cell

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