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)

This study determined the concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), soluble TNF receptor 1 (sTNFR1) and soluble E-selectin (sE-selectin) in cerebrospinal fluid (CSF) and serum from 15 children with influenza virus-associated encephalopathy to determine the role of cytokines in the pathogenesis. Cytokines and sTNFR1 were measured by enzyme-linked immunosorbent assay. The CSF IL-6, TNF-alpha and sTNFR1 concentrations were elevated in 9, 4 and 4 of 12 children, respectively. The serum concentrations of IL-6, TNF-alpha, sTNFR1 and sE-selectin were elevated in 10, 2, 5 and 7 of 13 children, respectively. Four children with elevated TNF-alpha and sTNFR1 levels in the CSF had neurological sequelae. The results suggested that cytokines not only in serum but also in CSF play a pivotal role in influenza virus-associated encephalopathy, and that the CSF TNF-alpha and sTNFR1 levels may be important for predicting neurological sequelae.
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PMID:Cerebrospinal fluid and serum levels of cytokines and soluble tumor necrosis factor receptor in influenza virus-associated encephalopathy. 1268 86

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

We present a case report of encephalopathy associated with Salmonella urbana infection in a child. A 5-year-old boy was admitted to our clinic with convulsions and coma. Cerebrospinal fluid (CSF) interleukin-6 (IL-6) and IL-8 were elevated at onset and were decreased within normal limit on the fifth day. Residual neurological deficits included severe mental deficits and spastic tetraplegia. High levels of CSF proinflammatory cytokines might be related to central nervous system (CNS) disease activity. Although encephalopathy is a rare complication of non-typhi Salmonella infection, it should be borne in mind as an occasionally serious and potentially lethal disease.
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PMID:Cerebrospinal fluid cytokines in Salmonella urbana encephalopathy. 1521 48

The aim of this study was to define the predictive values of serum and cerebrospinal fluid concentrations of interleukin-6 and neuron-specific enolase and urinary uric acid/creatinine ratio for outcome in term infants with perinatal asphyxia. All biochemical markers were measured simultaneously within the 24-72 hours of life in 21 infants. The infants were monitored with a standardized neurologic and developmental evaluation protocol over the 2 years of life. The overall outcome at 2 years of age was categorized as "favorable" or "adverse". According to Sarnat and Sarnat classification, 12 infants had mild encephalopathy and 9 infants had moderate to severe encephalopathy. Seven of 9 (78%) infants with moderate to severe encephalopathy had adverse outcome. However, all infants with mild encephalopathy had favorable outcome. Interleukin-6 and neuron specific enolase levels in cerebrospinal fluid and serum interleukin-6 levels were significantly correlated with the degree of encephalopathy, as well as the outcome. Interleukin-6 in cerebrospinal fluid (cutoff value, 25.9 pg/mL) had the highest predictive value among the biochemical markers. The predictive factors identified in this study should be examined for their ability in a fresh clinical sample in the neonatal intensive care unit before these markers can be applied to the routine clinical of infants with perinatal asphyxia.
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PMID:Value of biochemical markers for outcome in term infants with asphyxia. 1551 13

The role of cytokines in the pathogenesis of brain injury and their relation to neurological outcomes of asphyxiated neonates is not fully defined. We hypothesize that interleukin-1 beta (IL-1beta), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in cerebrospinal fluid (CSF) correlate with the severity of brain injury and can predict neurological deficits in infants who suffered from hypoxic ischemic encephalopathy (HIE). A prospective study was conducted on 24 term infants diagnosed with HIE and 13 controls. HIE was clinically classified into mild, moderate and severe according to Sarnat and Sarnat grading. Blood and CSF samples were obtained from all infants in the first 24h of life as part of routine investigations for suspected meningitis and/or sepsis. Neurological examination and Denver Developmental Screening Test II (DDST II) were performed at 6 and 12 months of life. IL-1beta, IL-6 and TNF-alpha were all significantly increased in HIE infants when compared to control. IL-1beta in the CSF correlated with the severity of HIE (r=0.61, P=0.001) more than IL-6 (r=0.45, P=0.004) or TNF-alpha (r=0.47, P=0.003). IL-1beta exhibited the highest CSF/serum ratio among the three studied cytokines suggesting its local release in the brain after the initial hypoxic injury. Abnormal neurological findings and/or abnormal DDST II at 6 and 12 months were best predicted by IL-1beta in the CSF (sensitivity=88% and specificity=80%). This study confirms the role of IL-1beta in the ongoing neuronal injury that occurs in the latent phase following the original HIE insult.
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PMID:IL-1beta, IL-6 and TNF-alpha and outcomes of neonatal hypoxic ischemic encephalopathy. 1618 55

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-alpha), 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-alpha, 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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PMID:Laboratory characteristics of acute encephalopathy with multiple organ dysfunctions. 1619 4

The aim of this study was to assess the validity of serum and CSF oxidative status of patients with IE in their initial stage through the d-ROM (Diacron-Reactive Oxygen Metabolites, Italy) test, compared to those with other neurological diseases. The study was conducted on the following four groups: (1) influenza virus-associated encephalopathy (IE, n = 8), including four patients showing neurological sequelae or mortal; (2) influenza virus-associated febrile seizures (IFS, n = 11); (3) febrile convulsion (FC, n = 10): (4) enterovirus-associated encephalopathy (EE, n = 4), including one patient with neurological sequelae. The CSF d-ROM levels in the IE group were significantly higher than those in the IFS and the FC groups but not in the EE group. In addition, general laboratory findings such as leukocytes, platelets, C-reactive protein, aspartate aminotransferase, creatinine, creatinine kinase and LDH, including interleukin-6 (IL-6), were analyzed in each group. The CSF d-ROM levels in the IE group were significantly higher than those in the IFS and FC groups but not in the EE group. As for the serum d-ROM levels and general laboratory findings, with the exception of CSF IL-6 levels in IE, no significant differences were detected compared with the other groups. In patients with IE, the CSF d-ROM levels could be a valid predictive biomarker of the severity, and oxidative stress may be related to the pathogenesis of IE.
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PMID:Diagnostic and predictive value of CSF d-ROM level in influenza virus-associated encephalopathy. 1641 81

We describe a 10-month-old girl who developed convulsive status during febrile illness. Human herpesvirus 6 DNA was detected in both the serum and the cerebrospinal fluid by polymerase chain reaction. Interleukin-6 was increased in the serum. The patient improved after a commencement of steroids pulse therapy. This case suggests that proinflammatory cytokines are responsible for the pathogenesis of the encephalopathy.
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PMID:Steroid therapy in an infant with human herpesvirus 6 encephalopathy. 1663 89

A 7-year-old female suddenly exhibited high fever and convulsions, and entered a semi-coma. She also had thrombocytopenia, elevated aminotransferase, prolonged prothrombin time and activated partial thromboplastin time, and hemophagocytes in the bone marrow. The brain magnetic resonance imaging revealed multiple low-intensity areas on the T1-weighted images, and high-intensity areas on the T2-weighted images bilaterally in the thalamus, the dorsal part of the pons, and the cerebellar white matter. The patient was diagnosed as having both acute necrotizing encephalopathy and hemophagocytic syndrome. Serum and cerebrospinal fluid interleukin-6 and tumor necrosis factor-alpha were elevated to the same high levels (serum:cerebrospinal fluid interleukin-6, 103:101 pg/mL; tumor necrosis factor-alpha 753:753 pg/mL). The clinical symptoms and the magnetic resonance imaging findings improved immediately after the administration of dexamethasone. These results suggest that the hypercytokinemia and the hyperpermeability of both the blood-brain barrier and the capillary walls of the central nervous system might be essential in the pathogenesis of acute necrotizing encephalopathy, and that early steroid therapy might be effective in these conditions.
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PMID:Acute necrotizing encephalopathy associated with hemophagocytic syndrome. 1663 10

Exercise-associated hyponatremia (EAH) has emerged in recent years as a life-threatening complication of endurance sports that may lead to fatal cerebral and pulmonary edema. Defined as a serum sodium concentration <135 mEq/L (1 mEq/L = 1 mmol/L), symptomatic EAH is a dilutional hyponatremia with abnormal fluid retention mediated by decreased urine production, which is a variant of the syndrome of inappropriate antidiuretic hormone secretion. Strategies for prevention and treatment must take into account the pathophysiology underlying this dominant clinical paradigm. Beyond educating runners to drink moderately, monitoring changes in body weight during endurance sports may facilitate the early detection of positive fluid balance characteristic of symptomatic cases. Rapid diagnosis by point-of-care testing indicates the need for fluid restriction in mild cases and emergent treatment with hypertonic (3%) NaCl to reverse acute hypotonic encephalopathy. The efficacy of arginine vasopressin V(2) receptor antagonists warrants study as an alternative treatment to loop diuretics for volume overload in these patients. Nonosmotic stimulation of arginine vasopressin secretion may be mediated in part by enhanced release of muscle-derived interleukin-6 during glycogen depletion, linking exertional rhabdomyolysis to the pathogenesis of EAH.
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PMID:Exercise-associated hyponatremia: role of cytokines. 1684 89


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