RESUMO
Platelet-activating factor (PAF) is a phospholipid mediator of inflammation with a wide range of biological activities, including the alteration of barrier function of endothelium. A biological assay combined with high pressure liquid chromatography-tandem mass spectrometry showed that plasma and cerebral spinal fluid (CSF) PAF levels in 20 patients with relapsing/remitting or secondary progressive multiple sclerosis (MS) studied by magnetic resonance imaging (MRI) were significantly higher than in healthy controls (plasma: 3.29+/-4.52 vs. 0.48+/-0.36 ng/ml, p < 0.002; CSF: 4.95+/-6.22 ng/ml vs. 0.01+/-0.04 ng/ml, p < 0.0001). Values were also significantly higher in relapsing/remitting than in secondary progressive (plasma: 5.10+/-4.97 vs. 0.52+/-0.85 ng/ml, p < 0.005; CSF: 8.59+/-6.39 vs. 0.55+/-0.68 ng/ml, p < 0.002). It was also found that both plasma (R2: 0.65) and CSF (R2:0.72) levels were correlated with the MRI number of gadolinium enhancing lesions, which are markers of blood-brain barrier (BBB) injury, whereas their peaks were not correlated with the MRI number of white matter lesions, nor with the expanded disability status score (EDSS) according to Kurtze [Kurtze, J.F., 1983. Rating neurological impairment in multiple sclerosis: an expanded disability scale (EDSS). Neurology 33, 1444-1452]. Both plasma and CSF in patients with relapsing/remitting MS and marked gadolinium enhancement contained the two major molecular species of PAF: 1-0-hexadecyl- (C16:O) and 1-0-octadecyl-sn-glycero-3-phosphocholine (C18:O). The ratio of the two molecular species was different in the two biological fluids, being PAF C18:0 more abundant in CSF and PAF C16:0 in plasma, indicating a different cellular origin of PAF or different enzymatic processing. These findings suggest that PAF is a significant mediator of BBB injury in the early stages of MS, rather than a marker of its progression and severity.
Assuntos
Anti-Hipertensivos/líquido cefalorraquidiano , Barreira Hematoencefálica/imunologia , Esclerose Múltipla/sangue , Esclerose Múltipla/líquido cefalorraquidiano , Fator de Ativação de Plaquetas/análogos & derivados , Adolescente , Adulto , Idoso , Anti-Hipertensivos/análise , Capilares/imunologia , Capilares/metabolismo , Criança , Progressão da Doença , Feminino , Gadolínio , Cromatografia Gasosa-Espectrometria de Massas , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Esclerose Múltipla/diagnóstico , Fator de Ativação de Plaquetas/análise , Fator de Ativação de Plaquetas/líquido cefalorraquidiano , Fator de Ativação de Plaquetas/genética , RecidivaAssuntos
Etambutol/efeitos adversos , Glomerulonefrite/complicações , Mielite Transversa/induzido quimicamente , Neurite Óptica/induzido quimicamente , Doenças do Sistema Nervoso Periférico/induzido quimicamente , Tuberculose Pulmonar/tratamento farmacológico , Uremia/complicações , Adulto , Etambutol/administração & dosagem , Seguimentos , Humanos , Masculino , Exame Neurológico , Parestesia/induzido quimicamente , Acuidade Visual/efeitos dos fármacosRESUMO
4 cases of ataxic hemiparesis syndrome are supported by CT proof of a lesion confined to the posterior and superior part of the internal capsule, near the corona radiata. The site of lesion is usually held to be the basis pontis and rostral midbrain. We intend to furnish further evidence in support of an old hypothesis incriminating the corona radiata-internal capsule.