Approximately 10% of patients with
systemic lupus erythematosus (SLE) develop epileptic
seizures. When occurring before the onset of generalized SLE, the
seizures are mainly primary generalized. Accordingly, long-term treatment with anti-epileptic drugs may precipitate SLE, or
epilepsy and SLE may both occur as manifestations of a genetically determined predisposition. Some patients develop
IgA deficiency during
phenytoin treatment. This condition is reversible and
IgA becomes normalized when
phenytoin is withdrawn (
drug-induced
IgA deficiency). Some epileptic patients have a
drug-independent
IgA deficiency. Patients with
drug-induced
IgA deficiency are usually
HLA-A2, while those with
drug-independent
IgA deficiency are HLA-A1,B8. The gene coding for
IgA deficiency seems to be located in the HLA complex on chromosome 6. The gene locus for juvenile
myoclonus epilepsy and related disorders is also on chromosome 6 and in close relation to the gene locus for the HLA system.
Juvenile myoclonic epilepsy may be accompanied by
drug-induced
IgA deficiency, but there are also cases with other sometimes less-defined
epilepsies, associated with this anomaly. It is possible that the relationship between
epilepsy and immune disturbances is related to a common genetically determined susceptibility.