Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A role for lipopolysaccharides (endotoxins, LPS) in 7 the pathogenesis of Reye's syndrome (RS) has previously been suggested. Impairment of hepatic LPS clearance can lead to systemic endotoxemia as previous studies by this and other laboratories have suggested for several hepatic disorders including RS. Systemic LPS may mediate many of the clinical findings associated with RS by eliciting monokines such as tumor necrosis factor-alpha, interleukin-1, interleukin-6, and interleukin-8. Monoclonal antibody therapy directed at LPS, and monokines may represent a novel approach to the treatment of RS.
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PMID:Monoclonal antibody therapy in the treatment of Reye's syndrome. 147 50

It is estimated that more than 100 children die of influenza-associated encephalopathy (influenza encephalopathy) every year in Japan. Influenza encephalopathy is distinct from Reye's syndrome. Specifically, 20% of influenza encephalopathy patients exhibit bilateral thalamic necrosis on neuroimaging, a lesion referred to as acute necrotizing encephalopathy (ANE). Influenza encephalopathy may develop by the same pathogenetic mechanisms as ANE, possibly via vasoactive substances or a process leading to vasoconstriction in the central nervous system (CNS). A novel substitution at the receptor-binding site (Tyr 137 to Phe) was reported to be found exclusively in influenza type A (H3N2) viruses isolated from patients with influenza encephalopathy, suggesting that encephalopathy may be caused by a variant influenza type A (H3N2) virus. Recently, it has been reported that cytokines may mediate the disease and that a high plasma concentration of interleukin-6 could be an indicator of progression to encephalopathy. Although it is unknown whether influenza virus invades the CNS, amantadine therapy for influenza encephalopathy has been tried in Japan, in patients in whom influenza type A infection has been demonstrated by rapid antigen detection tests.
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PMID:Influenza-associated encephalopathy in Japan: pathogenesis and treatment. 1080 44

We addressed the incidence of influenza-associated acute encephalopathy, which is distinct from Reye syndrome, in children in Japan. Eighty-nine children with a mean age of 3.8 years were reported to have developed this disease during eight influenza seasons (December 1994-April 2002) in Hokkaido, Japan. None of them had received aspirin. Most of the patients rapidly became comatose with or without convulsions with a mean interval of 1.7 days from the onset of fever to the onset of central nervous system symptoms. Thirty-three (37.1%) patients died and 17 (19.1%) patients had neurological sequelae. A total of 53 (59.6%) cases were proved to have an influenza virus infection. Interleukin-6 and tumor necrosis factor-alpha were markedly elevated in serum and cerebrospinal fluid samples from two patients who died after a rapid, fulminant course. A post-mortem examination of one fatal case revealed vasogenic brain edema with generalized vasculopathy, suggesting that the generalized impairment of vascular endothelial cells caused by highly activated cytokines plays a central role in the pathophysiology of this disease. We conclude that influenza-associated acute encephalopathy may be an underestimated syndrome and is another reason to promote vaccination against influenza in infants and younger children.
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PMID:Influenza-associated acute encephalopathy in Japanese children in 1994-2002. 1516 92