RESUMO
BACKGROUND AND PURPOSE: Although the causes of multiple sclerosis (MS) remain partially unknown, environmental and genetic factors are thought to play a role in its aetiopathogenesis. Hypovitaminosis D, Epstein-Barr virus (EBV) and human herpesvirus 6 (HHV-6) infections have been described as possible MS triggers. Our aim was to analyse the possible link between 25-hydroxyvitamin D [25(OH)D] and viruses in patients with MS. METHODS: We included 482 patients with MS in a 2-year study. Serum samples were collected to analyse 25(OH)D levels and, according to sample availability, antibody titres against EBV and HHV-6 by enzyme-linked immunosorbent assay. DNA was extracted from blood in order to analyse EBV and HHV-6 viral load by quantitative real-time polymerase chain reaction and to genotype MS-related single nucleotide polymorphisms (rs3135388, rs2248359 and rs12368653) when possible. RESULTS: The 25(OH)D levels were significantly higher in the first semester of the year than in the second. Carriers of the risk allele rs2248359-C showed lower 25(OH)D levels than non-carriers. For EBV, viral load was significantly higher when 25(OH)D levels were low, demonstrating an inverse correlation between 25(OH)D levels and EBV load. CONCLUSIONS: The 25(OH)D levels could be involved in the regulation of EBV replication/reactivation in patients with MS.
Assuntos
Infecções por Herpesviridae/sangue , Herpesvirus Humano 4/isolamento & purificação , Herpesvirus Humano 6/isolamento & purificação , Esclerose Múltipla/sangue , Esclerose Múltipla/virologia , Vitamina D/análogos & derivados , Adulto , Calcifediol , Feminino , Infecções por Herpesviridae/virologia , Humanos , Masculino , Carga Viral , Vitamina D/sangue , Adulto JovemRESUMO
OBJECTIVE: Previous epidemiologic studies have shown that around 5% of the population will suffer a tonic clonic seizure during their life. The aim of this study is to know how many and which of these people will suffer a second seizure and become epileptic. PATIENTS AND METHODS: 175 patients seen in the emergency department of the Vall d Hebron Hospital were included. They were divided in three groups according to the clinical suspicion of having had a seizure. Only the patients with low clinical suspicion and also normal EEG standard and EEG in sleep deprivation were excluded (16). The patients with previous episodes of lost of consciousness, previous episodes of possible mioclonias or absence were not excluded. RESULTS: After a first tonic clonic seizure the patients who did not receive treatment present a risk of relapse of 66% followed two years and the patients treated 46%. The difference between two groups was statistically significant. Dividing the patients according to the type of seizure: primary generalised, partial or nor localised we did not find differences in the risk of relapse. Dividing the patients according to their etiology we found that the group of patients with provoked seizures was different from the rest groups: symptomatic, genetic or cryptogenic and idiopathic, who had equal risk of recurrence. We found that the presence of previous episodes of lost of consciousness, the clinical suspicion and, probably (we obtained nearly statistical signification) de EEG and the presence of previous mioclonias or absences were risk factors. Other factor like age at the moment of the first episode, febrile seizures, familiar history, antecedents of stroke, encephalitis, neurosurgery and dementia were not related with the risk of relapse. CONCLUSIONS: With the exception of provoked seizures the rest of first tonic clonic seizures have a high risk of relapse (around 60 70%) and if they go with abnormal EEG, previous episodes of absences or mioclonias starting treatment must be considered.