Avaliação dos perfis imunológico e inflamatório nos pacientes com Narcolepsia, segundo o seu nível de Hipocretina-1

Detalhes bibliográficos
Ano de defesa: 2009
Autor(a) principal: Coelho, Fernando Morgadinho Santos [UNIFESP]
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Tese
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: http://repositorio.unifesp.br/handle/11600/9113
Resumo: Introduction: The pathophysiology of narcolepsy is still unknown. The genetic markers of histocompatibility complex, as well as, the decreasing of Hypocretin- 1 propose a confirmation of immunological theory. There are few studies considering the differences between immunological presence and absence of allele HLA-DQB1*0602, as well comparing the groups of patients with Hypocretin-1 levels. Objectives: To measure the subpopulations of the Total, CD2, CD3, T (CD4 and CD8), B (CD19) and Natural Killer (CD56), beyond the serum levels of the IL-6, TNF and CD40L, with and without the presence of the HLA-DBQ1*0602 allele and in the groups with above and below 110pg/ml of Hipocretina-1 in the spinal fluid. Methodology: After obtaining a sample of cerebral spinal fluid for Hipocretina-1 analysis, the narcoleptic patients and healthy volunteers were evaluated concerning the sleep and the daytime sleepiness by a polysomnography and the Multiple Sleepiness Latency Test (MSLT). Epworth Sleepiness Scale (ESS), Beck Depressions Inventory, Anxiety-State Questionnaire (Idate) and Body Mass Index (BMI) were applied as well. Blood samples were collected and analyzed for Total, CD2, CD3, TCD4, TCD8, CD56 and CD19 lymphocytes; Interleukin -6; Tumoral Necrosis Factor, CD40L and HLA-DB1* 0602 allele. Results: The average of the ESS was higher in the patients with narcolepsy (17.7 ± 0.7 vs7.7 ± 0.7; p<0.0001). The sleep latency of the narcoleptic patients was shorter than in the control group. The average of the latencies of the MSLT was smaller and the amount of the SOREM was higher in the narcoleptic patients group. In these patients the counting of total lymphocytes (2446 ± 123.2 vs 2000.3 + 513.7; p=0.01), CD2 (2028 ± 106.5 vs 1612.1 + 431.6 p=.006), CD3 (1892 ± 102.1 vs 1485.5 + 425.8; p=0.005) and TCD4 (1238 ± 85,9 vs 945 + 247.1; p=0.007) were decreased in comparison to the control group. There were no differences among the other groups. Conclusions: The T and TCD4 lymphopenia observed in the narcoleptic patients could have been caused by the low production by the lymphoid organs, the increase of the peripheral destruction or lower activation by the antigen presenting cells. The T and TCD4 lymphopenia associated to the reduction of the CDL40 observed in the narcoleptic patients could promote to the dysfunction of the antigen presenting cell. A decreased production of the CD40L could reduce the amplification of the immunological reaction already studied in others self immunes models.