Systemic Lupus Erythematosus Associated with Use of Valproate

Abstract

A 30-year-old man with long-standing localization-related epilepsy and mental retardation had seizures that were partially controlled with valproate (VPA) 500 mg four times daily. Routine examination showed severe thrombocytopenia with mild leukopenia and chronic low-grade hemolytic anemia. Pertinent laboratory results included positive ANA, rheumatoid factor, anti-NIA, circulating immune complexes, and antihistone antibody. The patient was treated with high dosage prednisone with partial improvement, but continued to have exacerbations at lower dosages. Fourteen months later, VPA was discontinued, and rapid improvement ensued. Prednisone was subsequently discontinued, and the patient has now maintained normal platelet counts for 18 months.

Hypermethylation of the TSLC1/IGSF4 promoter is associated with tobacco smoking and a poor prognosis in primary nonsmall cell lung carcinoma

“…Subject UB1 was taking phenytoin, which is associated with a low risk of drug‐induced lupus (30), whereas subject UB2 initially received phenytoin, but it was replaced with sodium valproate/oxcarbazepine and subsequently with levetiracetam. Sodium valproate is associated only anecdotally with drug‐induced lupus (36, 38–40), and the anti–Ro 60 autoantibodies persisted after sodium valproate was replaced by oxcarbazepine and levetiracetam, neither of which is associated with drug‐induced lupus (41). Since the lupus‐like syndrome and autoantibody production did not abate when the anticonvulsant regimen was altered, and since the autoantibodies classically associated with drug‐induced lupus (anti‐ssDNA and antichromatin) (30) were not detected, whereas subjects UB1 and UB2 both produced autoantibodies (anti‐RNP, anti–Ro 60) not associated with drug‐induced lupus, we conclude that subjects UB1 and UB2 did not have drug‐induced lupus.…”

Lupus‐like disease and high interferon levels corresponding to trisomy of the type I interferon cluster on chromosome 9p

“…Subject UB1 was taking phenytoin, which is associated with a low risk of drug-induced lupus (30), whereas subject UB2 initially received phenytoin, but it was replaced with sodium valproate/oxcarbazepine and subsequently with levetiracetam. Sodium valproate is associated only anecdotally with drug-induced lupus (36,(38)(39)(40), and the anti-Ro 60 autoantibodies persisted after sodium valproate was replaced by oxcarbazepine and levetiracetam, neither of which is associated with drug-induced lupus (41). Since the lupus-like syndrome and autoantibody production did not abate when the anticonvulsant regimen was altered, and since the autoantibodies classically associated with drug-induced lupus (anti-ssDNA and antichromatin) (30) were not detected, whereas subjects UB1 and UB2 both produced autoantibodies (anti-RNP, anti-Ro 60) not associated with druginduced lupus, we conclude that subjects UB1 and UB2 did not have drug-induced lupus.…”

No association of anti-GM1 and anti-GAD antibodies with juvenile myoclonic epilepsy: A pilot study

“…Immune responses in patients with epilepsy may present a genetic coupling to epilepsy phenotype or may occur as consequence of long-term anti-epileptic treatment. VPA, the drug of choice for JME, may cause immunological problems like development of drug-induced systemic lupus erythematosus (SLE) [19][20][21] and lupus anti-coagulant. 22 We could not demonstrate any association of the AEDs with anti-GAD as well as anti-GM1 positivity in our pilot study.…”