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FRI0319 The analysis of risk and protective factors for thrombosis in systemic lupus erythematosus with or without antiphospholipid antibodies
  1. T. Watanabe1,
  2. K. Oku1,
  3. O. Amengual1,
  4. S. Shimamura1,
  5. I. Nakagawa1,
  6. A. Noguchi1,
  7. Y. Kanetsuka1,
  8. M. Kono1,
  9. T. Kurita1,
  10. Y. Fujieda1,
  11. T. Bohgaki1,
  12. S. Yasuda1,
  13. T. Horita1,
  14. T. Atsumi1
  1. 1Division of Rheumatology, Endocrinology and Nephrology, Hokkaido University Graduate School of Medicine, Sapporo, Japan

Abstract

Background Thrombosis is one of the most frequent manifestations in patients with systemic lupus erythematosus (SLE). In this study, we examined the several risk factors for thrombosis in patients with SLE. Further, we investigated whether some factors could play a protective thrombotic role in SLE.

Objectives To identify risk and protective factors for thrombosis in SLE.

Methods Ninety-seven newly diagnosed consecutive patients with SLE without history of thrombotic events were recruited at our hospital from 2001 to 2012. All patients, 87 woman and 10 men, fulfilled the 1997 American College of Rheumatology revised criteria for SLE. Fifty-four patients (55.7%) had antiphospholipid antibodies (aPL). All patients were follow-up since the inclusion until December, 2012. The development of thrombosis were defined as the study endpoint.

Results The median follow-up period in all patients was 46 months (IQR 17-84 months). In 54 patients with aPL, the median follow-up period was 57 months (IQR 28-99 months). 10 patients with aPL (18.5%) developed thrombosis during the follow-up period. Cerebral infarction (CI) was observed in 5 patients, pulmonary embolism (PE) in 4 and deep vein thrombosis in 3. Multivariate analysis with Cox’s proportional hazards model showed that older age at SLE onset and anticardiolipin antibodies (aCL)-IgG positivity, (HR 1.89 for every ten age, 95%C.I. 1.07-3.33) and (HR 5.68, 95%C.I. 1.28-25.3), respectively, are statistically significant risk factor for thrombosis. Statin therapy appears as a statistically significant protective thrombotic factor (HR 0.093, 95%C.I. 0.01-0.82) (Figure 1.). Disease activity, anti-thrombotic agents and risk factors for atherosclerosis were not related to thrombosis. On the other hand, in 43 patients without aPL (median follow-up period 26 months, IQR 12-66 months), 4 patients (9.3%) developed thrombosis. Three patients had CI and one PE. None of the evaluated risk factors correlated to the development of thrombosis in aPL-negative patients.

Conclusions This study suggests that, in patients with aPL, the late disease onset and the presence of aCL-IgG represent additional risk factors for thrombosis. Statin treatment appears as a thrombotic protective factor.

Disclosure of Interest: None Declared

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