ab17_3

Clinical significance of anticardiolipin antibodies in juvenile idiopathic arthritis

C.R.B. Serra, S.H. Rodrigues, N.P. Silva, F.R. Sztajnbok¹, L.E.C. Andrade

Escola Paulista de Medicina, Rheumatology Division, Universidade Federal de São Paulo, São Paulo; ¹Pediatric Rheumatology Division, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.

ABSTRACT
Objective
Anticardiolipin antibodies (aCL) have been demonstrated in a large spectrum of autoimmune diseases. However, its occurrence in childhood, in particular in juvenile idiopathic arthritis (JIA), is not well established. The present study addressed the frequency and clinical significance of aCL in a group of JIA patients.

Methods
aCL (IgG and IgM isotypes), antinuclear antibodies (ANA), and rheumatoid factor (RF) were determined in 86 children with JIA (33 systemic, 31 polyarticular and 22 oligoarticular onset type). Thirty-two juvenile systemic erythematosus lupus patients (JSLE) and 52 healthy children formed the control groups. The disease activity and functional status of the JIA patients were scored to study their possible associations with the presence of aCL.

Results
Serum aCL levels above the normal range were detected in 28/86 JIA patients (32.5%), 12/32 JSLE patients (37.5%), and 3/52 healthy children (6%). Positive aCL levels were slightly or moderately elevated (usually below 30 GPL and 20 MPL). The presence of aCL was not associated with the presence of ANA or RF. Associations between aCL and clinical parameters, such as disease onset, duration, activity or severity could not be established. No JIA patient had vascular thrombosis, thrombocytopenia or "livedo reticularis".

Conclusion
aCL occurred in low titers in JIA children, in a similar frequency to that observed in JSLE. No association with JIA clinical parameters or the clinical features classically linked to the antiphospholipid antibody syndrome were observed.

Key words
Juvenile idiopathic arthritis, anticardiolipin antibodies, antiphospholipid antibodies, autoantibodies.

This work was partially supported by funds from the Council for Scientific and Technological Development (CNPq) and the Brazilian Society of Rheumatology. C.R.B. Serra was supported by a grant from the National Agency for Development of Superior Teaching Personnel (CAPES).

Please address correspondence and reprint requests to: Luís E.C. Andrade, MD, Escola Paulista de Medicina - UNIFESP, Rheumatology Division, Rua Botucatu 740, São Paulo SP 04023-062, Brazil.