Anticardiolipin antibodies in childhood rheumatic disorders

Anticardiolipin antibodies (aCL) have been reported to occur in a wide vari ety of autoimmune and non-autoimmune disorders in adults. Our objective was to investigate the prevalence and isotype distribution of aCL and its relationship with the features of antiphospholipid syndrome (A PS) in childhood rheumatic disorders. Between November 1995 and May 1996, all patients who visited our paediatric rheumatology clinic whose guardians signed a consent form participated in the study. The study population included 106 patients (36 systemic lupus er ythematosus (SLE), 28 juvenile rheumatoid arthritis (JRA), 11 fibromyalgia, 7 sarcoidosis, 5 dermatomyositis, 3 rheumatic fever (RF), 3 vasculitis, 2 scleroderma, and 11 miscellaneous). aCL measurements were performed by enzy me linked immunoabsorbent assay (ELISA). All patients were carefully evalua ted for symptoms and signs of APS. Eighteen of the 106 patients (17%) were tested positive for one or more of the three aCL isotypes. In SLE, aCL were found positive in 13 of 36 (37%); in JRA 2 of 28 (7%); in sarcoidosis 2 of 7; and in RF 1 of 3. aCL of IgG is otype were found positive in 16 patients (1 1 SLE, 2 sarcoidosis, 2 JRA, an d 1 RF). This isotype was usually detected at low titers (16-24 GPL). aCL o f IgM isotype were found positive in five patients (2 sarcoidosis, 2 SLE, 1 JRA), and aCL of IgA isotype were found positive in only three patients (2 SLE, I sarcoidosis). Clinical features of APS were rarely seen in our SLE population and were not associated with the presence of aCL. None of the pa tients in the other groups exhibited any clinical manifestations of APS. In conclusion, aCL were found in 37% of our childhood SLE patients as compa red with only 7% in JRA. These were mostly aCL of IgG isotype of low titers and therefore were not associated with the main features of APS. Prospecti ve studies with a larger sample size may be needed to ascertain the exact p revalence and clinical significance of aCL in childhood-onset SLE.