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

The patient was an 11-month-old boy who developed encephalopathy associated with respiratory syncytial virus bronchiolitis. Right hemispheric encephalopathy was indicated by left hemiparesis and a diffuse right hemispheric lesion detected with magnetic resonance imaging. Elevated levels of interleukin-6 in the cerebrospinal fluid during the acute phase suggested the involvement of increased production of one or more cytokines in the pathogenesis of viral related encephalopathy, similarly to that proposed for influenza encephalopathy.
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PMID:Elevated CSF IL-6 in a patient with respiratory syncytial virus encephalopathy. 1717 1

We studied the relation among serum cytokine levels, EEG changes, and mild neurological complications (delirium and febrile seizure) in children with influenza. The serum levels of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and soluble tumor necrosis factor receptor-1 (sTNFR-1) were measured in 27 children with proven influenza infection with mild neurological complications (10 patients with delirium and 17 with febrile seizures) and seven control children. EEG was recorded in 14 children with neurological complications. EEG showed focal slowing in four of nine patients with delirium and in four of five with febrile seizures. Generalized slowing was observed in one patient with delirium. The median serum IL-6 level was 31.2+/-15.1 pg/ml (range, 7.5-64.5 pg/ml) in the delirium group, 42.3+/-44.0 pg/ml (range, 8.0-196.0 pg/ml) in the febrile seizure group, and 15.4+/-7.0 pg/ml (range, 7.2-28.0 pg/ml) in the control group. Serum TNF-alpha and sTNFR-1 levels were not different among three groups. Mild neurological complications associated with influenza were related to the mildly abnormal serum IL-6 levels and EEG findings. The combination of these parameters will be useful for early diagnosis and differentiation of neurological complications in children with influenza. Further studies will be necessary for investigating that IL-6 has the diagnostic value for differentiation between severe encephalopathy and mild neurological complications in children with influenza.
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PMID:Serum levels of cytokines and EEG findings in children with influenza associated with mild neurological complications. 1728 1

We describe a rare case of clinically mild, influenza-associated encephalopathy with a reversible splenial lesion. A 12-year-old Japanese girl presented with fever and headache, followed by muscle weakness and somnolence. Magnetic resonance imaging on day 4 of her illness showed a solitary lesion of the splenium of the corpus callosum that was most prominently visualized on diffusion-weighted images. The patient was diagnosed with influenza B-associated encephalopathy. Her neurologic signs had completely recovered by day 6, and the splenial abnormalities disappeared on day 11. A review of the literature identified four additional pediatric cases of this type of influenza-associated encephalopathy: three and one were caused by influenza A and B viruses, respectively. Common features include prompt and complete recovery from clinical and radiologic abnormalities, a relatively older age (> or = 5 years), and a higher incidence among the Japanese. To better understand the pathophysiology of this encephalopathy, we examined interleukin-6, tumor necrosis factor-alpha, and soluble tumor necrosis factor receptor 1 levels in serum and cerebrospinal fluid from this patient. The results did not reveal any elevations of these cytokines in the sera or cerebrospinal fluid, suggesting that this condition is not mediated by augmented cytokine responses.
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PMID:Reversible splenial lesion in influenza virus encephalopathy. 1802 26

Enterohemorrhagic Escherichia coli (EHEC) induces hemorrhagic colitis and hemolytic uremic syndrome (HUS). Morbidity and mortality are increased in HUS patients with neurologic complications. To determine the pathogenesis of the central nervous system (CNS) involvement in HUS by EHEC, we determined the serum concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), soluble TNF receptor 1 (sTNFR1), IL-10, interferon-gamma (IFN-gamma), IL-2, IL-4, soluble E-selectin (sE-selectin), matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of metalloproteinase-1 (TIMP-1) during the acute stage in children with HUS with or without CNS involvement. Serum concentrations of IL-6, IL-10, sTNFR1, sE-selectin, MMP-9, and TIMP-1, but not TNF-alpha, IFN-gamma, IL-2, or IL-4, were significantly higher in patients with HUS with encephalopathy compared with controls. Serum IL-6, sTNFR1 and TIMP-1 concentrations were significantly higher in patients with HUS with encephalopathy compared with those with HUS without encephalopathy (P=0.031, P=0.005, and P=0.007, respectively) and those with acute colitis without HUS (P=0.011, P<0.001, and P=0.005, respectively). There were no significant differences in hemoglobin, platelet counts, leukocyte counts, or serum concentrations of IL-10, sE-selectin, MMP-9, aspartate aminotransferase, lactate dehydrogenase, blood urea nitrogen, creatinine, or C-reactive protein between the HUS patients with and without encephalopathy. Our preliminary study suggests that serum IL-6, sTNFR1 and TIMP-1 levels, particularly sTNFR1 and TIMP-1, are important for predicting neurological complications in patients with HUS.
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PMID:Soluble tumor necrosis factor receptor 1 and tissue inhibitor of metalloproteinase-1 in hemolytic uremic syndrome with encephalopathy. 1841 Sep 71

We describe a girl with sepsis-associated encephalopathy complicating biliary atresia. At 4 months of age, decreased consciousness and repetitive seizures of the left upper and lower extremities occurred in association with fever. Pseudomonas aeruginosa was cultured from blood, while bacterial culture was negative and cell counts were normal in cerebrospinal fluid. The interleukin-6 level in the cerebrospinal fluid was markedly elevated. MRI revealed unilateral subcortical white matter lesions in the right hemisphere. She was diagnosed as having sepsis-associated encephalopathy and was treated with dexamethasone and midazolam. She achieved normal psychomotor development until the last follow-up at 19 months of age, whereas mild atrophic changes were observed in the right hemisphere.
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PMID:Sepsis associated encephalopathy in an infant with biliary atresia. 1842 24

Nontyphoidal Salmonella (NTS) encephalopathy is characterized by rapidly progressive brain dysfunction that develops after NTS enteritis. The mechanism of central nervous system involvement remains unclear. We examined cerebrospinal fluids from 7 patients for cytokines and found elevated interleukin-6, interleukin-8, and monocyte chemotactic protein-1 concentrations in all the patients, suggesting that the proinflammatory cytokines are involved in the pathogenesis of NTS encephalopathy.
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PMID:Proinflammatory cytokines in cerebrospinal fluid from patients with nontyphoidal Salmonella encephalopathy. 1843 36

We present a 7-year-old boy diagnosed as having salmonella encephalopathy. He developed severe consciousness disturbance following enterocolitis. Electroencephalography showed diffuse and high-voltage slow activity but MR images of the brain were normal. Examination of inflammatory cytokines in serum and cerebrospinal fluid revealed high levels of interleukin-6, -8, and -10, and interferon gamma. Salmonella typhimurium was detected in a stool specimen. He was diagnosed as having salmonella-associated encephalopathy that had features of septic encephalopathy and quickly responded to high-dose methylpredonisolone therapy. High-dose methylpredonisolone was considered to be an effective treatment for hypercytokine-mediated S. encephalopathy.
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PMID:Salmonella encephalopathy successfully treated with high-dose methylpredonisolone therapy. 1921 41

Although neonatal hypoxic-ischemic encephalopathy is a common cause of childhood developmental disability, its timing, duration, and outcomes are poorly defined. Biomarkers serve as surrogates for disease injury, evolution, and outcome, but no tissue biomarker in routine clinical use can help predict outcomes in term newborn encephalopathy. We reviewed biomarkers in human term neonatal encephalopathy, to determine if current biomarkers are strong enough for clinical use as predictors of outcomes. A comprehensive search of databases identified 110 publications that met our inclusion criteria, i.e., (1) newborns at >36 weeks; (2) neonatal encephalopathy as defined by the American College of Obstetrics and Gynecology; (3) the use of a serum, urine, or cerebrospinal fluid biomarker; and (4) reported outcomes beyond age 12 months. Of those 110 publications, 22 reported outcomes beyond age 12 months. In single reports, urine lactate (P < 0.001), first urine S100 (P < 0.0001), cord-blood interleukin-6 (P = 0.02), serum nonprotein-bound iron (P < 0.001), serum CD14 cell NFkappaB activation (P = 0.014), serum interleukin-8 (P = 0.03), and serum ionized calcium (P = 0.001) were potential predictors of death or abnormal outcomes. A meta-analysis identified serum interleukin-1b (P = 0.04, n = 3), serum interleukin-6 (P = 0.04, n = 2), cerebrospinal fluid neuron-specific enolase (P = 0.03, n = 3), and cerebrospinal fluid interleukin-1b (P = 0.003, n = 2) as putative predictors of abnormal outcomes in survivors, when measured before age 96 hours. Several serum, urine, and cerebrospinal fluid biomarkers of term neonatal encephalopathy may provide important information regarding long-term outcomes. None, however, were studied extensively enough to warrant routine clinical use. Validation of these markers, either alone or in combination, is required in the development of viable therapeutic interventions.
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PMID:Systematic review of biomarkers of brain injury in term neonatal encephalopathy. 1921 35

It has been proposed that proinflammatory mechanisms are involved in the pathogenesis of brain edema in acute liver failure (ALF). The aim of this study was to assess the contribution of cerebral inflammation to the neurologic complications of ALF and to assess the antiinflammatory effect of mild hypothermia. Upregulation of CD11b/c immunoreactivity, consistent with microglial activation, was observed in the brains of ALF rats at coma stages of encephalopathy. Interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) mRNAs were increased two to threefold in the brains of ALF rats compared with that in sham-operated controls. The magnitude of increased expression of proinflammatory cytokines in the brain was correlated with the progression of encephalopathy and the onset of brain edema. Significant increases in IL-1beta, IL-6, and TNF-alpha levels were also found in the sera and cerebrospinal fluid (CSF) of these animals. Mild hypothermia delayed the onset of encephalopathy, prevented brain edema, and concomitantly attenuated plasma, brain, and CSF proinflammatory cytokines. These results show that experimental ALF leads to increases in brain production of proinflammatory cytokines, and afford the first direct evidence that central inflammatory mechanisms play a role in the pathogenesis of the cerebral complications of ALF. Antiinflammatory agents could be beneficial in the management of these complications.
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PMID:Direct evidence for central proinflammatory mechanisms in rats with experimental acute liver failure: protective effect of hypothermia. 1925 10

We reported a girl with HHV-6 infection associated with both acute encephalopathy with biphasic seizures and late reduced diffusion, and hemophagocytic syndrome. She had a prolonged convulsion after a one-day history of febrile illness. Cerebrospinal fluid or brain CT showed no abnormalities on admission and her consciousness was recovered on the next day. However, a prolonged seizure and deterioration of consciousness appeared on the sixth day of illness. Diffusion-weighted images revealed marked reduction of water diffusion in the bilateral frontal areas. HHV-6 infection was virologically proven by polymerase chain reaction. She was treated with gamma-globulin, steroid pulse therapy, and brain hypothermia. In addition, decrease in white blood cells and platelet counts, and elevation of liver enzymes and ferritin were noted on the fourth day of illness. Hemophagocytic macrophages were revealed by bone marrow aspiration on the sixth day. Her hematological and blood chemistry abnormalities recovered gradually after steroid pulse therapy. An elevation of interleukin-6, -8, and -10, and tumor necrosis factor in the serum and that of interleukin-4, -6, and-8 in the cerebrospinal fluid were observed at the onset of a late seizure. These facts suggested that hypercytokinemia will be related to the pathogenesis of acute encephalopathy of our patient.
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PMID:Acute encephalopathy with biphasic seizures and late reduced diffusion associated with hemophagocytic syndrome. 1955 82


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