RESUMO
OBJECTIVES: Multiple sclerosis is an inflammatory condition of the central nervous system whose etiology is influenced by immunologic, genetic, and environmental factors. Aim of the present study was to determine if any relation exists between IL-18 -137C/G and -607C/A gene promoter polymorphisms on the individual susceptibility of multiple sclerosis and also to investigate the possible effect of IL-18 activity regarding this kind of polymorphism and MS. PATIENTS AND METHODS: 113 patients with clinically definite MS and 135 ethnically-matched controls were participated in this study. IL-18 -137C/G and -607C/A gene promoter polymorphisms were analyzed by Sequence Specific Polymerase Chain Reaction (SS-PCR), while levels of serum IL-18 were measured by Enzyme Linked Immunoassay Assay (ELISA) in patients with MS and healthy controls. RESULTS: Our results showed that the IL-18 -607AA genotype indicated 6 times higher risk in the development of MS (OR=6.883; 3.17-14.96; p<0.001). According to our findings, smoking seems to be an important confounding factor in MS patients with carrying IL-18 -607 AA and CA+AA genotypes. However, no meaningful association was found with IL-18 -137C/G gene promoter polymorphism. CONCLUSION: In conclusion, we suggest that IL-18 -607C/A gene promoter polymorphism is a major genetic factor for determining individual susceptibility to MS, where smoking status also increases the risk of MS.
Assuntos
Interleucina-18/sangue , Interleucina-18/genética , Esclerose Múltipla/sangue , Esclerose Múltipla/genética , Adulto , Feminino , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Polimorfismo Genético , Regiões Promotoras Genéticas , Risco , Fumar/efeitos adversos , Fumar/genéticaRESUMO
Stroke is a multifactorial disease caused by the combination of certain risk factors and genetic factors. There are possible risk factors having important role in the pathogenesis of stroke. The most important environmental factors are cigarette smoking and oxidative stress which have different sources. GST (M1, T1, P1) have major roles in detoxification of the products of oxidative stress and they are polymorphic. DNA damages can also be repaired by repair enzymes such as OGG1 and XRCC1 which are highly polymorphic and have pivotal roles in repair systems. In the present study, we investigated that polymorphisms in genes involved in detoxification and DNA-repair pathways might modify the individual's risk for ischemic stroke. Furthermore, the products of oxidative stress and antioxidant capacity were measured and the impact of gene polymorphism on them was evaluated. Our data showed that OGG1 Ser326Cys and XRCC1 Arg399Gln gene polymorphisms had impacts on the development of stroke.
Assuntos
DNA Glicosilases/genética , Proteínas de Ligação a DNA/genética , Estresse Oxidativo/genética , Polimorfismo de Nucleotídeo Único/genética , Espécies Reativas de Oxigênio/sangue , Acidente Vascular Cerebral/genética , Antioxidantes/metabolismo , Isquemia Encefálica/complicações , Estudos de Casos e Controles , Análise Mutacional de DNA , Proteínas de Ligação a DNA/metabolismo , Ensaio de Imunoadsorção Enzimática , Feminino , Genótipo , Glutationa Transferase/genética , Humanos , Hidroxiquinolinas/sangue , Masculino , Fatores de Risco , Estatísticas não Paramétricas , Acidente Vascular Cerebral/etiologia , Acidente Vascular Cerebral/fisiopatologia , Turquia , Proteína 1 Complementadora Cruzada de Reparo de Raio-XRESUMO
Alterations in blink reflex excitability may occur in the contralateral side (CLS) and in the symptomatic side after peripheral facial palsy (PFP). In this study, the alterations of blink reflex in CLS were evaluated in cases with PFP who showed "three different types" of recovery. For this purpose, the R2 response area and recovery curve of the blink reflex were evaluated. The study included 51 patients suffering from PFP and 20 age- and sex-matched healthy controls. Cases with PFP were divided into three groups: patients with PFP with partially cured and accompanied by synkinesis (postfacial syndrome), patients with PFP with residual weakness, and patients who suffered from recurrent PFP. All three groups' R2 values of CLS were compared with the values of controls and patients who had synkinesis. The CLS of all three groups' R2 area values were found to be significantly higher when compared with controls. These values were found to be highest in patients who suffered from recurrent PFP. Hyperexcitability occurs in CLS after PFP and this is highest in patients who suffer from recurrent PFP. It suggested that the contralateral reorganization caused by peripheral nerve damage correlates with the severity of the lesion and the recurrence of axon damage enhances the excitability of the reflex cycle, which affects the contralateral facial nucleus.
