PEDIATRICS Vol. 92 No. 6 December 1993, pp. 849-853
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Childhood-Onset Systemic Lupus Erythematosus: Antiphospholipid Antibodies in 37 Patients and Their First-Degree Relatives

Charles Molta MD1, Olivier Meyer MD2, Christine Dosquet MD3, Marcela Montes de Oca MD4, Marie-Claude Babron PhD4, Françoise Danon MD5, Cécile Kaplan MD6, Sylvie Clémenceau 6, Françoise Castellano 6, and Micheline Levy MD4

1 From the Division of Rheumatology Kaiser Permanente, Cleveland, OH
2 From the Service de Rhumatolologie, Hôpital Universitaire Bichat, Paris, France
3 From the Laboratoire d'Immunologie, Hôpital Universitaire Lariboisiére, Paris
4 From the Unité de Recherches d'Epidémiologie Génétique, INSERM U 155, Paris
5 From Laboratoire d'Immunologie et d'Histocompatibilité, Hôpital Universitaire Saint-Louis, Paris
6 From the Service d'Immunologie Leuco-plaquettaire, Institut National de Transfusion Sanguine, Paris

Objective. Antiphospholipid antibodies (aPL) are noted with increased frequency in patients with systemic lupus erythematosus (SLE). The main manifestations found to be associated with aPL are arterial and venous thrombotic events, thrombocytopenia, and recurrent pregnancy loss This study is an attempt to define the incidence of aPL in patients with childhood-onset SLE and in their relatives and to correlate their presence with clinical manifestations, and especially, to evaluate the risk of thrombosis in aPL-positive subjects.

Methodology. We studied 37 unrelated patients and 107 of their first-degree relatives. VDRL, IgG and IgM anticardiolipin, and IgG antiphosphatidylethanolamine antibodies were studied in all probands during periods of clinical remission and in first-degree relatives at the time of interview. Lupus anticoagulant had only been studied in probands during an SLE flare-up.

Results. Thirty-eight percent of probands and 19% of relatives were positive for at least one aPL, with little over-lap between the different aPL studied. -No aPL-negative proband developed thrombosis. Two of the aPL-positive probands had thrombotic events before testing, and a third one showed thrombosis after testing. Only two probands had high levels of IgG aCL and showed thrombosis. The occurrence of aPL positivity in relatives was not always related to its presence in probands. None of the aPL-positive relatives had hadthrombosis, but recurrent fetal loss was noted in one aPL-positive mother with SLE. Although there was a high frequency of SLE, SLE-like disease, auto-immune disorders or positive serological findings for lupus in first-degree relatives, many of these relativew did not test positive for aPL.

Conclusion. The high levels of IgG aCL may be considered a risk factor for thrombosis. Findings in relatives suggest a multifactorial origin for autoimmune disease and antibody production.

Key Words: systemic lupus erythematosus • antiphospholipid antibodies • anticardiolipin • lupus anticoagulant • VDRL test • relatives

Submitted on September 1, 1992
Accepted on July 23, 1993




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