Lupus-scleroderma syndrome induced by ethosuximide.

Teoh, P C; Chan, Hsiang-Sui

doi:10.1136/adc.50.8.658

Cited by 33 publications

(8 citation statements)

References 9 publications

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“…Central nervous system effects include drowsiness, dizziness, hiccups, fatigue, insomnia, tiredness, headache, and psychotic behaviors (Wallace 1996; Posner et al 2005). Ethosuximide has been also associated with a wide variety of idiosyncratic reactions, including allergic dermatitis, rash, Stevens‐Johnson syndrome, systemic lupus erythematosus, lupus‐like syndrome, serum sickness reaction, agranulocytosis, and aplastic anemia (Teoh and Chan 1975; Glauser 2000). Hematopoietic adverse effects include leukopenia, agranulocytosis, eosinophilia, and pancytopenia (Posner et al 2005).…”

Section: Safetymentioning

confidence: 99%

Ethosuximide: From Bench to Bedside

2007

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Ethosuximide, 2-ethyl-2-methylsuccinimide, has been used extensively for "petit mal" seizures and it is a valuable agent in studies of absence epilepsy. In the treatment of epilepsy, ethosuximide has a narrow therapeutic profile. It is the drug of choice in the monotherapy or combination therapy of children with generalized absence (petit mal) epilepsy. Commonly observed side effects of ethosuximide are dose dependent and involve the gastrointestinal tract and central nervous system. Ethosuximide has been associated with a wide variety of idiosyncratic reactions and with hematopoietic adverse effects. Typical absence seizures are generated as a result of complex interactions between the thalamus and the cerebral cortex. This thalamocortical circuitry is under the control of several specific inhibitory and excitatory systems arising from the forebrain and brainstem. Corticothalamic rhythms are believed to be involved in the generation of spike-and-wave discharges that are the characteristic electroencephalographic signs of absence seizures. The spontaneous pacemaker oscillatory activity of thalamocortical circuitry involves low threshold T-type Ca2+ currents in the thalamus, and ethosuximide is presumed to reduce these low threshold T-type Ca2+ currents in thalamic neurons. Ethosuximide also decreases the persistent Na+ and Ca2+ -activated K+ currents in thalamic and layer V cortical pyramidal neurons. In addition, there is evidence that in a genetic absence epilepsy rat model ethosuximide reduces cortical gamma-aminobutyric acid (GABA) levels. Also, elevated glutamate levels in the primary motor cortex of rats with absence epilepsy (but not in normal animals) are reduced by ethosuximide.

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Section: Safetymentioning

confidence: 99%

Ethosuximide: From Bench to Bedside

2007

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“…These include features of scleroderma, SLE, dermatomyositis and Stevens-Johnson syndrome (Dubois & Wallace 1987;Roberts & Marks 1983;Teoh & Chan 1975). These include features of scleroderma, SLE, dermatomyositis and Stevens-Johnson syndrome (Dubois & Wallace 1987;Roberts & Marks 1983;Teoh & Chan 1975).…”

Section: Anticonvulsantsmentioning

confidence: 99%

Drug-Related Lupus

Adams

Hess

1991

Drug Safety

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Adverse side effects to drugs and chemicals in which immune mechanisms may be responsible have been described in drug-related lupus (DRL). The spectrum of drugs that may elicit DRL includes such classes as the hydrazines, arylamines, and chemicals that can be metabolised to amines. The 2 major pathways of metabolism--acetylation and N-hydroxylation--are described in detail. The events leading to autoantibody production are not well understood; however, specific consideration of the genetic makeup of patients who are candidates for treatment with these drugs may help identify those at risk of developing DRL.

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“…Several case reports implicated ethosuximide (ESM) in this phenomenon (Teoh and Chan, 1975;Singsen et al, 1976), and a single documented case of primidone (PRM)-induced SLE has been published (Ahuja and Schumacher, 1966). The mechanisms by which these drugs produce SLE or unmask a diathesis toward it are unknown (AlarconSegovia and Palacios, 1981).…”

mentioning

confidence: 97%

Possible Induction of Systemic Lupus Erythematosus by Valproate

Bleck

Smith²

1990

Epilepsia

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Two patients developed clinical and laboratory evidence of systemic lupus erythematosus (SLE) during treatment with valproate (VPA) preparations. The first patient, a 47-year-old man, had fever, malaise, and thrombocytopenia 1 month after VPA was added to phenytoin (PHT) and primidone (PRM). He developed high titers of antinuclear antibodies (ANA) and anti-DNA antibodies, and hypocomplementemia. After discontinuation of PHT and VPA, steroid and immunoglobulin treatment was required for 4 weeks before his condition improved. The second patient, a 28-year-old woman, had been followed for idiopathic leukopenia for 3 years and had previously experienced fever and lymphadenopathy from PHT. After 4 months of divalproex therapy, she developed confusion, joint pain, and a dramatic increase in seizure frequency. She also developed high titers of ANA and anti-DNA antibodies and hypocomplementemia, along with a further decrease in white blood cell (WBC) count. These responded to steroid therapy and withdrawal of divalproex. Three months later, reintroduction of divalproex was followed by a return of ANA in low titer, which resolved after discontinuation. We believe that VPA may have caused true SLE in these patients, one of whom was probably predisposed.

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Lupus-scleroderma syndrome induced by ethosuximide.

Cited by 33 publications

References 9 publications

Ethosuximide: From Bench to Bedside

Ethosuximide: From Bench to Bedside

Drug-Related Lupus

Possible Induction of Systemic Lupus Erythematosus by Valproate

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