Elevated serum S100B protein and neuron-specific enolase levels in carbon monoxide poisoning

Yardan, Türker; Çevik, Yunsur; Dönderici, Ömer; Kavalcı, Cemil; Yılmaz, Fatma Meriç; Yılmaz, Gülşen; Vural, Kubilay; Yüzbaşıoğlu, Yucel; Günaydın, Yahya Kemal; Sezer, Ahmet Ali

doi:10.1016/j.ajem.2008.04.016

Cited by 57 publications

(62 citation statements)

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“…8,10 The normal range of NSE in serum of a healthy individual is 4 to 12 lg/L, with females ranging from 2.9 to 9.6 lg/L (mean ¼ 5.3) and males with a slightly higher range of 3.4 to 11.7 lg/L (mean ¼ 6.3). 16 An individual with serum NSE higher than 12 lg/L is generally considered to be undergoing stress of neuronal and/or neuroendocrine cells.…”

Section: Discussionmentioning

confidence: 99%

“…Of the 14/46 (30.4 %) carriers with significantly elevated NSE levels (mean ¼ 75. 8 3 This implicates that mtDNA mutations are necessary but not sufficient to trigger optic neuropathy. 4 Both environmental and further genetic factors are believed to be relevant for disease expression.…”

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confidence: 99%

“…Neurons under stress of various types release NSE into the systemic circulation, making its assay a useful indicator of neuronal distress. 8,9 NSE levels have been used to predict neurological outcome in traumatic brain injury. 10 Retinal disease such as retinal detachment has also been shown to be sufficient to increase circulating serum NSE levels.…”

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confidence: 99%

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Neuron-Specific Enolase Is Elevated in Asymptomatic Carriers of Leber's Hereditary Optic Neuropathy

Yee

Ross‐Cisneros

Lee

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Neuron-specific enolase (NSE) is a biomarker for neuronal stress. Leber's hereditary optic neuropathy (LHON) is a mitochondrial disease affecting retinal ganglion cells (RGC). These RGCs and their axons in the retinal nerve fiber layer (RNFL) and optic nerve head may show subclinical pathology in unaffected mutation carriers, or undergo cell death in affected patients. We hypothesize that increased levels of blood NSE may characterize LHON carriers as a biomarker of ongoing RGC stress.METHODS. Serum was obtained from 74 members of a Brazilian pedigree with LHON carrying the homoplasmic 11778/ND4 mitochondrial DNA mutation. Classified by symptoms and psychophysical metrics, 46/74 patients were unaffected mutation ''carriers,'' 14/74 were ''affected,'' and 14/74 were ''off-pedigree'' controls. Serum NSE levels were determined by ELISA specific for the c subunit of NSE.RESULTS. Serum NSE concentrations in carriers (27.17 6 39.82 lg/L) were significantly higher than affected (5.66 6 4.19 lg/ L; P ¼ 0.050) and off-pedigree controls (6.20 6 2.35 lg/L; P ¼ 0.047). Of the 14/46 (30.4 %) carriers with significantly elevated NSE levels (mean ¼ 75.8 6 42.3 lg/L), 9/14 (64.3%) were male. Furthermore, NSE levels were nearly three times greater in asymptomatic male carriers (40.65 6 51.21 lg/L) than in asymptomatic female carriers (15.85 6 22.27 lg/L; P ¼ 0.034).CONCLUSIONS. Serum NSE levels are higher in LHON carriers compared with affected and off-pedigree individuals. A subgroup of mostly male carriers had significantly elevated serum NSE levels. Thus, male carriers are at higher risk for LHON-related neuronal stress. (Invest Ophthalmol Vis Sci.

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Section: Discussionmentioning

confidence: 99%

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Neuron-Specific Enolase Is Elevated in Asymptomatic Carriers of Leber's Hereditary Optic Neuropathy

Yee

Ross‐Cisneros

Lee

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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“…En revanche, dans l'étude de Cakir et al [28], la S-100β était significativement corrélée au score de Glasgow et diminuait dans le groupe OHB mais pas dans le groupe traité par O 2 normobare. Une autre étude montrait que les concentrations de S-100β étaient significativement plus élevées chez les patients inconscients en comparaison aux patients conscients [29]. De même, les concentrations initiales d'interleukine (IL)-6 [30] et de MBP [31] dans le LCR semblaient intéressantes pour prédire l'évolution vers un syndrome postintervallaire.…”

Section: Marqueurs Biologiquesunclassified

Intoxication au monoxyde de carbone et place de l’oxygénothérapie hyperbare

et al. 2011

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Le traitement par oxygénothérapie hyperbare (OHB) lors des intoxications au monoxyde de carbone est utilisé depuis plus de 50 ans. Néanmoins, le protocole à appliquer et le sous-groupe de patients pouvant bénéficier de l'OHB restent débattus. La physiopathologie de l'intoxication au monoxyde de carbone est complexe, expliquant la diversité des tableaux cliniques retrouvés neurologiques (troubles de la conscience et syndrome postintervallaire) mais aussi cardiaques (ischémie à coronaires saines notamment). La physiopathologie fait intervenir une hypoxie ané-mique par formation de carboxyhémoglobine mais aussi une hypoxie hypoxique par blocage de la chaîne respiratoire au niveau de la cytochrome oxydase, un stress oxydatif et des lésions d'ischémie-reperfusion. La carboxyhémoglobine (veineuse ou artérielle) n'est pas à prendre en compte pour le traitement ; le dosage de la troponine Ic au moindre doute est souhaitable. Les bases de traitement par l'OHB reposent d'abord sur des arguments physiopathologiques : détoxifica-tion plus rapide des protéines héminiques, effet antioxydant et amélioration de la physiologie cérébrale (diminution de la pression intracrânienne, diminution de l'oedème et préserva-tion de la zone de pénombre). Les autres arguments sont issus des essais thérapeutiques randomisés. Quatre des cinq études randomisées utilisant une OHB avec une pression supérieure à 2 ATA étaient positives. Deux études à 2 ATA étaient négatives. Ainsi, les recommandations européennes et américaines suggèrent l'utilisation d'OHB à 2,5 ATA au moins dans les situations à risque de séquelles neurologiques (tout signe neurologique objectif y compris perte de connaissance), en cas d'atteinte cardiaque ou de grossesse. Il faut insister sur un traitement par oxygénothérapie à fort débit pendant 8-12 heures en cas de non-indication de l'OHB. Pour citer cette revue : Réanimation 20 (2011). Mots clés Oxygénothérapie hyperbare · Intoxication au monoxyde de carboneAbstract Hyperbaric oxygen (HBO) is used since more than 50 years for carbon monoxide poisoning. However, HBO protocols and indications are still debated. Neurological (coma and delayed neuropsychological sequelae) and cardiac (ischemic changes with normal coronary arteries) clinical scenarios are explained by complex mechanisms. Carboxyhemoglobin formation, cytochrome oxydase inhibition, oxidative stress, as well as ischemia-reperfusion phenomenon are among these mechanisms. Venous and arterial carboxyhemoglobin levels are not correlated with the patient's final prognosis and thus not mandatory for indicating the treatment. Conversely, troponin IC measurement is strongly recommended if myocardial involvement is suspected. HBO treatment relies on mechanistic bases: earlier detoxification, anti-oxidant properties, and improvement in cerebral physiology (decrease in intracranial pressure and oedema, and ischemic penumbra preservation). Clinical basis is assessed by the results of the randomized clinical trials (RCTs). Four among the 5 RCTs using > 2 ATA OHB protocols were p...

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“…However, these factors have been reported to be unsatisfactory for the prediction of DNS. Although, biochemical markers are of great potential value in the assessment of the clinical status in CO poisoning [16,21], limited research has been conducted regarding the use of biochemical markers for the prediction of DNS.…”

Section: Introductionmentioning

confidence: 99%

Plasma copeptin as a predictor of intoxication severity and delayed neurological sequelae in acute carbon monoxide poisoning

Pang¹,

Wang²,

Wang³

et al. 2014

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Elevated serum S100B protein and neuron-specific enolase levels in carbon monoxide poisoning

Cited by 57 publications

References 17 publications

Neuron-Specific Enolase Is Elevated in Asymptomatic Carriers of Leber's Hereditary Optic Neuropathy

Neuron-Specific Enolase Is Elevated in Asymptomatic Carriers of Leber's Hereditary Optic Neuropathy

Intoxication au monoxyde de carbone et place de l’oxygénothérapie hyperbare

Plasma copeptin as a predictor of intoxication severity and delayed neurological sequelae in acute carbon monoxide poisoning

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