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OP0124 (2019)
Leyre Riancho-Zarrabeitia1, Victor Martinez Taboada2, Iñigo Rua-Figueroa3, Fernando Sánchez-Alonso4, María Galindo-Izquierdo5, Juan Ovalles6, Alejandro Olivé7, Antonio Fernandez-Nebro8, Jaime Calvo9, Raúl Menor-Almagro10, Eva Tomero Muriel11, Esther Uriarte Isacelaya12, Alina Boteanu13, Mariano Andres14, Mercedes Freire González15, Gregorio Santos Soler16, Esther Ruiz Lucea17, Mónica Ibañez Barceló18, Ivan Castellví19, Carles Galisteo20, Víctor Quevedo Vila21, Enrique Raya22, J. Narváez23, Lorena Expósito24, Josè A Hernandez Beriain25, Loreto Horcada26, Jose M Pego-Reigosa27
1H Sierrallana, Torrelavega, Spain
2HU Marques Valdecilla, Santander, Spain
3HU Doctor Negrin, Las Palmas de Gran Canaria, Spain
4Research Unit. SER, Madrid, Spain
5HU 12 Octubre, Madrid, Spain
6HGU Gregorio Marañon, Madrid, Spain
7HU Germans Trias i Pujol, Badalona, Spain
8HU Carlos Haya, Malaga, Spain
9HU Araba, Alava, Spain
10H Jerez, Jerez, Spain
11HU La Princesa, Madrid, Spain
12HU Donosti, San Sebastian, Spain
13HU Ramón y Cajal, Madrid, Spain
14HGU Alicante, Alicante, Spain
15HU Juan Canalejo, La Coruña, Spain
16H Marina Baixa, Villajoyosa, Spain
17HU Basurto, Bilbao, Spain
18HU Son Llatzer, Palma de Mallorca, Spain
19H Santa Creu i San Pau, Barcelona, Spain
20HU Parc Tauli, Sabadell, Spain
21H Monforte, Monforte, Spain
22HU San Cecilio, Granada, Spain
23HU Bellvitge, Hospitalet, Spain
24HU Canarias, Las Palmas de Gran Canaria, Spain
25HU Insular, Las Palmas de Gran Canaria, Spain
26CHU Navarra, Pamplona, Spain
27CHU Vigo, Vigo, Spain

Background: Antiphospholipid antibodies (aPL) have been associated with organ damage and certain features in SLE patients.

Objectives: To investigate the association between the different aPL and SLE manifestations as well as to elucidate the influence of the load of antibodies.

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

Results: Out of a total of 3651 SLE patients, 1368 were positive for aPL (44.9% of patients were positive for anticardiolipin (aCL) antibodies, 27.3% for anti b2glycoprotein I (aB2GPI) and 24% for lupus anticoagulant (LA)). Regarding the load of antibodies, 20.6%, 12.1% and 4.8% were positive for one, two and three antibodies, respectively. The association between the different aPL, the number of positive antibodies and antiphospholipid syndrome related manifestations is showed in Table 1 . Overall, all types of aPL were associated with classic APS manifestations, although LA, IgG isotypes, and patients with more than one aPL display a higher risk to develop clinical APS.

Regarding specific lupus manifestations, all aPL types showed a significant negative association with cutaneous manifestations. LA and aCL were associated with an increased risk of cardiac, respiratory and neuropsychiatric manifestations ( p <0.001). Furthermore, LA was also associated with an increased risk of renal disease ( p <0.001). aCL IgG was associated with a higher risk of specific lupus manifestations compared with aCL IgM. Interestingly, aB2GP IgG were only associated with an increased risk of seizures ( p < 0.001). When evaluating the influence of the load of antibodies, we found that the risk of neuropsychiatric manifestations ( p <0.001), as well as the cardiac ( p =0.003), and pulmonary manifestations ( p =0.001), significantly increased with a higher number of positive antibodies. Inversely, the risk of cutaneous symptoms decreased while the number of positive antibodies increased (OR 0.89, 95% CI 0.82-0.96, p =0.003).

Conclusion: There is a hierarchy for aPL and the risk of APS and lupus manifestations. aCL, and especially LA, confer a higher risk for major organ involvement in SLE patients. IgG isotypes and the load of aPL antibodies increase the risk for clinical APS and major lupus manifestations.

Disclosure of Interests: Leyre Riancho-Zarrabeitia Grant/research support from: Abbvie, Pfizer, UCB, MSD, GSK, Amgen, Roche travel grants, Victor Martinez Taboada: None declared, Iñigo Rua-Figueroa: None declared, Fernando Sánchez-Alonso: None declared, María Galindo-Izquierdo: None declared, Juan Ovalles: None declared, Alejandro Olivé Grant/research support from: ND, Consultant for: ND, Paid instructor for: ND, Speakers bureau: ND, Antonio Fernandez-Nebro: None declared, Jaime Calvo Consultant for: Bristol-Myers Squibb, Janssen, Celgene, Sanofi Genzyme, Speakers bureau: Bristol-Myers Squibb, Raúl Menor-Almagro: None declared, Eva Tomero Muriel: None declared, Esther Uriarte Isacelaya: None declared, Alina Boteanu: None declared, Mariano Andres: None declared, Mercedes Freire González: None declared, Gregorio Santos Soler: None declared, Esther Ruiz Lucea: None declared, Mónica Ibañez Barceló: None declared, Ivan Castellví Consultant for: I received fees less than 5000USD as a consultant for Kern and Actelion, Paid instructor for: I received fees less than 2000 USD as a instructor for Boehringer -Ingelheim, Novartis and Gebro, Speakers bureau: ND, Carles Galisteo: None declared, Víctor Quevedo Vila: None declared, Enrique Raya: None declared, J. Narváez Consultant for: Bristol-Myers Squibb, Lorena Expósito: None declared, José A Hernandez Beriain: None declared, Loreto Horcada: None declared, Jose M Pego-Reigosa: None declared

DOI: 10.1136/annrheumdis-2019-eular.2485

Citation: Ann Rheum Dis, volume 78, supplement 2, year 2019, page A136
Session: SLE, Sjogren and APS: systemic autoimmunity in the real life (Scientific Abstracts)