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Laboratory characteristics of acute encephalopathy with multiple organ dysfunctions

      Abstract

      To clarify the laboratory characteristics and deduce the pathogenesis of acute encephalopathy associated with multiple organ dysfunctions in Japan. We measured cytokine levels [tumor necrosis factor alpha (TNF-α), soluble tumor necrosis factor-receptor 1 (sTNF-R1), and interleukin-6 (IL-6)] in serum and cerebrospinal fluid (CSF) as well as general laboratory examinations in 27 patients with acute encephalopathy. Urea nitrogen (UN), creatinine (Cr), aspartate aminotransferase (AST), lactic dehydrogenase (LDH), and C-reactive protein (CRP) levels in blood, and CSF protein levels at the initial stage were significantly higher in patients with an unfavorable outcome. TNF-α, sTNF-R1, and IL-6 levels at the initial stage were higher in the serum than in the CSF of patients with acute encephalopathy. Serum cytokine levels correlated well with patient outcome. The high CSF protein level and the high UN, Cr, AST, LDH, and CRP levels in the blood represent the severity of vascular leakage through the blood–brain barrier and multiple organ dysfunctions, respectively, and thus suggest an unfavorable prognosis. The high serum inflammatory cytokine levels at the initial stage and the good correlation of those levels with the outcome suggest that intravascular inflammation has a significant role in vascular leakage and multiple organ dysfunctions in acute encephalopathy.

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      References

        • Trost L.C.
        • Lemasters J.J.
        The mitochondrial permeability transition: a new pathophysiological mechanism for Reye's syndrome and toxic injury.
        J Pharmacol Exp Ther. 1996; 278: 1000-1005
        • Lemasters J.J.
        • Nieminen A.-L.
        • Qian T.
        • Trost L.C.
        • Elmore S.P.
        • Nishimura Y.
        • et al.
        The mitochondrial permeability transition in cell death: a common mechanism in necrosis. Apoptosis and autophagy.
        Biochim Biophys Acta. 1998; 1366: 177-196
        • Kasai T.
        • Togashi T.
        • Morishima T.
        Encephalopathy associated with influenza epidemics.
        Lancet. 2000; 355: 1558-1559
        • Morishima T.
        • Togashi T.
        • Yokota S.
        • Okuno Y.
        • Miyazaki C.
        • Tashiro M.
        • et al.
        Encephalitis and encephalopathy associated with an influenza epidemic in Japan.
        Clin Infect Dis. 2002; 35: 512-517
        • Ito Y.
        • Ichiyama T.
        • Kimura H.
        • Shibata M.
        • Ishiwada N.
        • Kuroki H.
        • et al.
        Detection of influenza virus RNA by reverse transcription-PCR and proinflammatory cytokines in influenza-virus-associated encephalopathy.
        J Med Virol. 1999; 58: 420-425
        • Ichiyama T.
        • Nishikawa M.
        • Yoshitomi T.
        • Hayashi T.
        • Furukawa S.
        Tumor necrosis factor-α, interleukin-1β, and interleukin-6 in cerebrospinal fluid from children with prolonged febrile seizures: comparison with acute encephalitis/encephalopathy.
        Neurology. 1998; 50: 407-411
        • Kawada J.
        • Kimura H.
        • Ito Y.
        • Hara S.
        • Iriyama M.
        • Yoshikawa T.
        • et al.
        Systemic cytokine responses in patients with influenza-associated encephalopathy.
        J Infect Dis. 2003; 188: 690-698
        • Waage A.
        • Halstensen A.
        • Shalaby R.
        • Brandzaeg P.
        • Kierulf P.
        • Espevik T.
        Local production of tumor necrosis factor-α, interleukin 1, and interleukin 6 in meningococcal meningitis.
        J Exp Med. 1989; 170: 1859-1867
        • Mustafa M.M.
        • Lbel M.H.
        • Ramilo O.
        • Olsen K.D.
        • Reisch J.S.
        • Beutler B.
        • et al.
        Correlation of interleukin-1β and cachectin concentrations in cerebrospinal fluid and outcome from bacterial meningitis.
        J Pediatr. 1989; 115: 208-213
        • Tokunaga Y.
        • Kira R.
        • Takemoto M.
        • Gondo K.
        • Ishioka H.
        • Mihara F.
        • et al.
        Diagnostic usefulness of diffusion-weighted magnetic resonance imaging in influenza-associated acute encephalopathy or encephalitis.
        Brain Dev. 2000; 22: 451-453
        • Sato N.
        • Goto T.
        • Haranaka K.
        • Satomi N.
        • Nariuchi H.
        • Mano-Hirano Y.
        • et al.
        Actions of tumor necrosis factor on cultured vascular endothelial cells: morphologic modulation, growth inhibition, and cytotoxicity.
        J Natl Cancer Inst. 1986; 76: 1113-1121
        • Movat H.Z.
        Tumor necrosis factor and interleukin-1: role in acute inflammation and microvascular injury.
        J Lab Clin Med. 1987; 110: 668-681
        • Bevilacqua M.P.
        • Stengelin S.
        • Gimbrone Jr, M.A.
        • Seed B.
        Endothelial leukocyte adhesion molecule 1: an inducible receptor of neutrophils related to complement regulatory proteins and lectins.
        Science. 1989; 243: 1160-1165
        • Munakata M.
        • Kato R.
        • Yokoyama H.
        • Haginoya K.
        • Tanaka Y.
        • Kayaba J.
        • et al.
        Combined therapy with hypothermia and anticytokine agents in influenza A encephalopathy.
        Brain Dev. 2000; 22: 373-377