RESUMEN
OBJECTIVE: To elucidate the incidence and risk factors for paradoxical effects (i.e., increased seizure frequency, increased seizure severity, or onset of new seizure types) of levetiracetam (LEV) in people with epilepsy (PWE) and identify the usefulness of electroencephalography (EEG) in predicting these effects. METHODS: We examined data for consecutive PWE treated with LEV. All PWE underwent EEG and magnetic resonance imaging (MRI) before LEV administration. We also evaluated the incidence of paradoxical LEV effects and conducted multivariate logistic regression analyses to identify the associated factors. RESULTS: In total, 210 (66.2%) of 317 PWEs treated in our department had a history of LEV use. The incidence of paradoxical LEV effects was 5.2% (n = 11) and was significantly associated with a high LEV dose (p = 0.029), high seizure frequency (p = 0.005), temporal lobe epilepsy (p = 0.004), focal awareness seizure (p = 0.004), focal impaired awareness seizure (p = 0.007), spike (p = 0.015), rhythmic epileptiform discharges (REDs; p = 0.003), and MRI-identified focal cortical dysplasia (FCD; p < 0.0001). Multivariate analyses revealed that REDs (odds ratio [OR] = 5.35, p = 0.048, 95% confidence interval [CI]: 1.01-28.21) were independently associated with paradoxical LEV effects. CONCLUSIONS: Paradoxical LEV effects occurred in PWE, particularly in those with drug-resistant focal epilepsy. Furthermore, the occurrence of REDs in EEG was an independent factor associated with the paradoxical effects of LEV in PWE.
Asunto(s)
Epilepsia Refractaria , Epilepsias Parciales , Epilepsia , Humanos , Levetiracetam/efectos adversos , Epilepsia/complicaciones , Epilepsia/tratamiento farmacológico , Epilepsia/inducido químicamente , Convulsiones/tratamiento farmacológico , Convulsiones/inducido químicamente , Epilepsias Parciales/tratamiento farmacológico , Electroencefalografía , Epilepsia Refractaria/tratamiento farmacológico , Anticonvulsivantes/efectos adversos , Resultado del TratamientoRESUMEN
We report the case of a 42-year-old man with chronic hepatitis B virus infection who developed weakness and paresthesia in the extremities 2 months after administration of pegylated interferon (Peg-IFN)α-2a. Nerve conduction studies conducted 6 months after onset showed abnormal temporal dispersions in both tibial nerves. We diagnosed chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) resulting from treatment with Peg-IFNα-2a. Neurological symptoms were prolonged despite suspension of the treatment. Subsequent treatment with intravenous immunoglobulin improved both clinical symptoms and temporal dispersion. IFNα-induced CIDP is rare, but can reportedly progress even after interruption of IFN-α without immunotherapy. Patients presenting with polyneuropathy after initiation of IFN-α thus require close attention.
Asunto(s)
Síndrome de Guillain-Barré/inducido químicamente , Síndrome de Guillain-Barré/dietoterapia , Hepatitis B Crónica/tratamiento farmacológico , Inmunoglobulinas Intravenosas/uso terapéutico , Interferón-alfa/efectos adversos , Polietilenglicoles/efectos adversos , Adulto , Enfermedad Crónica , Síndrome de Guillain-Barré/tratamiento farmacológico , Humanos , Interferón-alfa/administración & dosificación , Masculino , Polietilenglicoles/administración & dosificación , Proteínas Recombinantes/administración & dosificación , Proteínas Recombinantes/efectos adversos , Resultado del TratamientoRESUMEN
From the whole herb of Leucas cephalotes SPRENG., new labdane-, norlabdane- and abietane-type diterpenes named leucasdins A (1), B (2) and C (3), respectively, and two protostane-type triterpenes named leucastrins A (4) and B (5) were isolated, together with a known triterpene, oleanolic acid, five sterols, 7-oxositosterol, 7-oxostigmasterol, 7alpha-hydroxysitosterol, 7alpha-hydroxystigmasterol and stigmasterol, and eight flavones, 5-hydroxy-7,4'-dimethoxyflavone, pillion, gonzalitosin I, tricin, cosmosin, apigenin 7-O-beta-D-(6-O-p-coumaroyl)glucopyranoside, anisofolin A and luteolin 4'-O-beta-D-glucuronopyranoside. The structures of 1--5 were determined as (3S,6R,8R,9R,13S,16S)-9,13,15,16-bisepoxy-3,16-diacetoxy-6-formyloxylabdane, (3S,6R)-3-acetoxy-6-formyloxy-iso-ambreinolide, (4R,9S,12R,13R)-12,13-dihydroxyabiet-7-en-18-oic acid, (3S,17S,20S,24S)-3,20-dihydroxy-24-methylprotost-25-en, and (3S,17S,20S,24S)-3,20,24-trihydroxyprotost-25-en respectively, based on spectral and chemical data.