RESUMO
Primary non-Hodgkin lymphoma of the central nervous system is rare in pediatric AIDS patients. We report a seven-year-old HIV-infected boy, in stage C3 of the disease, who developed non-Hodgkin lymphoma in the central nervous system with a leptomeningeal location. The patient started with signs and symptoms of increased intracranial pressure, impaired consciousness and then became blind. The diagnosis was based on brain biopsy, immunophenotypic studies of B cells, and Epstein-Barr virus serology of the cerebrospinal fluid. The boy was treated with intrathecal and systemic chemotherapy. Fifteen months after diagnosis he had clinically improved, but he then relapsed with a thalamic tumor. He was treated with radiotherapy and he died four months later. In the present article, we discuss diagnostic difficulties, evolution, treatment, and the association of this neoplasm with the Epstein-Barr virus.
Assuntos
Síndrome da Imunodeficiência Adquirida/complicações , Linfoma não Hodgkin/etiologia , Neoplasias Meníngeas/etiologia , Síndrome da Imunodeficiência Adquirida/líquido cefalorraquidiano , Síndrome da Imunodeficiência Adquirida/patologia , Antígenos CD/líquido cefalorraquidiano , Criança , Citometria de Fluxo/métodos , Humanos , Linfoma não Hodgkin/líquido cefalorraquidiano , Linfoma não Hodgkin/patologia , Imageamento por Ressonância Magnética/métodos , Masculino , Neoplasias Meníngeas/líquido cefalorraquidiano , Neoplasias Meníngeas/patologiaRESUMO
Cellular and molecular mechanisms involved in the generation of seizures and the magnitude of neural cells injury are not fully understood. We evaluated astrocyte and/or neuronal injury in rats in the pentylenetetrazol model of acute seizures by measuring S100B and NSE levels in cerebrospinal fluid. Additionally, we determined ADP and GDP hydrolysis by soluble nucleoside triphosphate diphosphohydrolase in the cerebrospinal fluid, and the concentration of nucleosides adenosine, inosine and guanosine as putative markers of brain injury. After pentylenetetrazol-induced seizures: (i) S100B values increased from 10 to 30 min, returning to control levels at 24 h; NSE levels presented a biphasic increase: an increase at 10 to 30 min returning to control levels, and again at 240 min followed by a decline at 24 h; (ii) nucleotidase activities increased from 10 min, returning to control levels at 240 min; (iii) guanosine and inosine levels increased exclusively after 30 min. In summary, this study showed biochemical changes in the cerebrospinal fluid occurring after seizures induced by pentylenetetrazol. Such events may have a modulating effect upon seizure expression, particularly nucleoside triphosphate diphosphohydrolase activities and nucleoside concentrations, but are nevertheless followed by neural death as evidenced by the increase in NSE and S100B levels.
Assuntos
Encéfalo/metabolismo , Degeneração Neural/líquido cefalorraquidiano , Proteínas do Tecido Nervoso/líquido cefalorraquidiano , Purinas/líquido cefalorraquidiano , Convulsões/líquido cefalorraquidiano , Adenosina/líquido cefalorraquidiano , Difosfato de Adenosina/metabolismo , Animais , Antígenos CD/líquido cefalorraquidiano , Apirase/líquido cefalorraquidiano , Biomarcadores/líquido cefalorraquidiano , Encéfalo/fisiopatologia , Convulsivantes , Modelos Animais de Doenças , Feminino , Guanosina/farmacologia , Guanosina Difosfato/metabolismo , Hidrólise , Inosina/farmacologia , Degeneração Neural/diagnóstico , Degeneração Neural/fisiopatologia , Fatores de Crescimento Neural/líquido cefalorraquidiano , Pentilenotetrazol , Fosfopiruvato Hidratase/líquido cefalorraquidiano , Ratos , Ratos Wistar , Subunidade beta da Proteína Ligante de Cálcio S100 , Proteínas S100/líquido cefalorraquidiano , Convulsões/induzido quimicamente , Convulsões/fisiopatologia , Fatores de Tempo , Regulação para Cima/efeitos dos fármacos , Regulação para Cima/fisiologiaRESUMO
INTRODUCTION: Alzheimer s disease (AD) is a progressive degenerative disease affecting a significant proportion of the elderly population. The disease is characterized clinically by a progressive loss of memory function and mental impairment associated with the presence of degenerative well known pathological lesions. Although, the pathogenesis of AD is unclear; several reports indicate the involvement of immune factors. PATIENTS AND METHODS: This paper evaluates some cerebrospinal fluid immune markers from 21 patients with early and late AD and 20 age matched non-demented subjects. The analytical method included the evaluation of T cell subpopulations (using AcMc CD2, CD4, CD8) and activated T cells (AcMc HLA-DR and CD25) from CSF and peripheral blood by immunocytochemical techniques on a fixed cell slide as described by Bernd. The lymphocyte phenotype expressed as a percentage of positively stained cells for each cell surface marker evaluated. RESULTS: Some significant differences were observed for T cell subpopulations from different compartments, between the different AD groups and the controls (p< 0.05). Nevertheless, the most significant differences were found in the activated T cells from cerebrospinal fluid between AD groups and controls (p< 0.01). CONCLUSIONS: These results support the theory of neuroimmune dysregulation, probably involved in the progressive neurodegeneration and dementia in some AD.