Antinuclear Antibodies and Lupus-like Syndromes in Children Receiving Anticonvulsants

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Abstract
Drug-induced systemic lupus erythematosus (SLE)-like syndromes in children are most commonly associated with the administration of ethosuximide, diphenylhydantoin and trimethadione. Five children receiving ethosuximide, who presented with syndromes suggestive of SLE, were studied. Each had fever, malar rash, arthritis and lymphadenopathy. Two children had pleural effusions, and another developed myocarditis and pericarditis. Three patients had anti-DNA antibodies associated with low serum C3 [the 3rd complement component]. In 4 of 5 children, symptoms disappeared with the discontinuation of ethosuximide; 2 of these continue to have antinuclear antibodies (ANA). One child continues to have active SLE with nephritis. A group of 101 children from a seizure clinic were tested for the presence of ANA. ANA were found in 14 of 70 children receiving ethosuximide and/or diphenylhydantoin; 2 of 14 had anti-DNA antibodies. Serum ANA titers in the drug-induced SLE group did not differ significantly from those of the asymptomatic seizure patients. ANA were also present in 5 of 23 children receiving phenobarbital only. The induction of ANA by phenobarbital is a possible hypothesis. Quantitative Ig and C3 were not significantly altered in the asymptomatic children with ANA. Follow-up studies at 10 mo. showed no asymptomatic child with ANA to have developed clinical evidence of SLE. Asymptomatic children who develop ANA probably should have careful observation, but need not have their anticonvulsants discontinued.