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81 Antiphospholipid syndrome in systemic lupus erythematosus leads to a more severe disease
  1. Leyre Riancho-Zarrabeitia1,
  2. Víctor M Martínez-Taboada2,
  3. Iñigo Rua Figueroa3,
  4. Fernando Alonso4,
  5. Maria Galindo Izquierdo5,
  6. Juan Ovalles-Bonilla6,
  7. Alejandro Olivé-Marqués7,
  8. Antonio Fernandez Nebro8,
  9. Jaime Calvo9,
  10. Javier Narváez-García10,
  11. Eva Tomero Muriel11,
  12. Esther Uriarte Isacelaya12,
  13. Alina Boteanu13,
  14. Mariano Andrés14,
  15. Mercedes Freire González15,
  16. Gregorio Santos Soler16,
  17. María E Ruiz-Lucea17,
  18. Mónica Ibáñez-Barcelo18,
  19. Ivan Castellvi19 and
  20. Jose Maria Pego Reigosa20
  1. 1Hospital Sierrallana
  2. 2Hospital Universitario Marqués de Valdecilla
  3. 3Hospital de Gran Canaria dr. Negrín
  4. 4Sociedad Española de Reumatología
  5. 5Hospital Universitario 12 De Octubre
  6. 6Hospital General Universitario Gregorio Marañón
  7. 7Hospital German Trias i Pujol
  8. 8UGC de Reumatología, Instituto de Investigación Biomédica de Málaga (IBIMA) Hospital Regional Universitario de Málaga, Spain
  9. 9Hospital Universitario Araba
  10. 10Hospital de Bellvitge
  11. 11Hospital De La Princesa
  12. 12Hospital De Donostia
  13. 13Hospital Ramón y Cajal
  14. 14Hospital General Universitario Alicante
  15. 15Hospital Juan Canalejo A Coruña (CHUAC)
  16. 16Hospital Marina Baixa
  17. 17Hospital De Basurto
  18. 18Hospital Son Llàtzer De Palma De Mallorca
  19. 19Hospital Santa Creu i Sant Pau
  20. 20Complexo hospitalario Universitario Vigo


Background Antiphospholipid antibodies (aPL) have been associated with organ damage and certain features in systemic lupus erythematosus (SLE) patients. Our aim was to investigate the differences between SLE patients according to the presence of aPL and/or clinical antiphospholipid syndrome (APS).

Methods Patients from the RELESSER-T registry were included. RELESSER-T is a multicenter, hospital-based registry, with retrospective cross-sectional collection of data from a large representative sample of adult non-selected patients with SLE attending Spanish rheumatology services from the public national health system.

Results We included 3651 SLE patients and 1368 were positive for aPL (44.9% of patients were positive for anticardiolipin antibodies, 27.3% showed positivity for anti b2glycoprotein I and 24% for lupus anticoagulant). Overall 2283 patients were classified as SLE no aPL, 528 as SLE-APS and 840 as SLE-aPL. Demographic data, clinical and laboratory features in the different groups are showed in table 1. Regarding cardiovascular risk factors, SLE-APS patients had higher rates of hypertension, dyslipidemia and diabetes than SLE-aPL and SLE no aPL patients (p<0.001, p<0.001 and p=0,022, respectively). SLE-APS patients showed a lower prevalence of photosensitivity and higher frequencies of serositis, proteinuria (>0.5 grs), urinary cell casts, seizures and psychosis (p0.001). Overall, SLE-APS patients showed a lower rate of cutaneous manifestations and higher rates of neuropsychiatric, cardiac, pulmonary, renal, joint and ophthalmological manifestations (table 1). In accordance with a more severe clinical profile, higher frequency of anti-DNA antibodies and hypocomplementemia were observed in the SLE-APS group (p<0.001). In addition to a higher disease activity (SLEDAI), SLE APS patients presented more damage accrual with higher values in SLICC (1.9±2.2 in SLE APS, 0.9±1.4 in SLE aPL and 1.1±1.6, p<0.001) and Katz indexes (3±1.8 in SLE APS, 2.7±1.7 in SLE aPL and 2.6±1.6 in SLE no aPL, p<0.001).

Abstract 81 Table 1

Main demographic data, clinical and laboratory features in the studied groups

Conclusions SLE-APS patients show a more severe clinical profile with higher frequency of major organ involvement and more damage accrual than SLE-aPL and SLE no APL.

Funding Source(s): None

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