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Examination of IL-1β, IL-6, and TNF α levels in serum and cerebrospinal fluid of patients with spontaneous subarachnoid hemorrhage and their relationship with systemic inflamatory response syndrome and multiple organ dysfunction syndrome / 中国医师杂志
Journal of Chinese Physician ; (12): 1466-1469, 2013.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-440300
Biblioteca responsável: WPRO
ABSTRACT
Objective To explore the levels of IL-1β,IL-6 and tumor necrosis factor α (TNF α) in serum and cerebrospinal fluid of patients with spontaneous subarachnoid hemorrhage and their relationship with systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS).Methods The levels of interleukin-1β(IL-1β),interleukin-6(IL-6),and TNF α in serum and cerebrospinal fluid of patients with spontaneous subarachnoid hemorrhage were measured with enzyme-linked immunosorbent assay (ELISA).Results The levels of IL-1β,IL-6,and TNFα in serum and cerebrospinal fluid of patients with spontaneous subarachnoid hemorrhage were significantly higher than those of control group (P < 0.05),but the increased time of these cytokines was different.Three cytokines in serum and the cerebrospinal fluid levels of IL-1β and IL-6 but not TNFα were significantly related to SIRS and MODS.Condusions The increased cytokine levels in serum and cerebrospinal fluid of patients with spontaneous subarachnoid hemorrhage may be related to SIRS and MODS,and the measurement of IL-1β,IL-6,and TNFαin serum,and IL-1β and IL-6 in cerebrospinal fluid of patients with spontaneous subarachnoid hemorrhage can be useful to predict and treat SIRS and MODS.

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo prognóstico Idioma: Chinês Revista: Journal of Chinese Physician Ano de publicação: 2013 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Tipo de estudo: Estudo prognóstico Idioma: Chinês Revista: Journal of Chinese Physician Ano de publicação: 2013 Tipo de documento: Artigo
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