The role of S100B protein, neuron-specific enolase, and glial fibrillary acidic protein in the evaluation of hypoxic brain injury in acute carbon monoxide poisoning

Akdemir, HU; Yardan, Türker; Katı, Celal; Duran, Latif; Alaçam, Hasan; Yılmaz, Yücel; Okuyucu, Ali

doi:10.1177/0960327114521049

Cited by 19 publications

(16 citation statements)

References 24 publications

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“…5,6 While the COHb level is easily and rapidly available at most institutions other biomarkers having been proposed to serve as better predictors of severity and prognosis in CO poisoning that include lactate and S100B but have yielded variable results. 7,8 The presence of microparticles in blood is also currently being explored as a potential biomarker for CO poisoning. 9 Many of these markers act as secondary measures of CO poisoning but do not directly measure the effects of CO.…”

Section: Introductionmentioning

confidence: 99%

A preliminary study in the alterations of mitochondrial respiration in patients with carbon monoxide poisoning measured in blood cells

Jang

Kelly

Hardy

et al. 2017

Clinical Toxicology

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Objectives Carbon monoxide (CO) is a colorless and odorless gas that is an important cause of poisoning mortality and morbidity in the United States. At this time there is no reliable method to predict severity of poisoning or clinical prognosis following CO exposure. Whole blood cells such as peripheral blood mononuclear cells (PBMCs) and platelets have been explored for their potential to act as sensitive biomarkers for mitochondrial dysfunction. Design The objective of this study was to measure mitochondrial respiration using intact cells obtained from patients exposed to CO as a potential biomarker for mitochondrial inhibition with results that can be obtained in a time frame useful for guiding clinical care. This was a prospective, observational pilot study performed from July 2015 to July 2016 at a single academic tertiary care center that is the location of the region’s only multi chamber hyperbaric. Measurements Clinical characteristics, patient demographics, mitochondrial respiration and outcomes were recorded. Main results There were 7 patients enrolled with a mean COHb level was (26.8+/−10) with a mean lactate of (1.1+/−0.4 mmol/L). All 7 CO exposures were related to heat generators used during winter months with two deaths. There was a positive correlation between maximal respiration and COHb levels with both a high maximal respiration and high spare respiratory capacity correlating with a high COHb level. There was a subset of PBMCs (n=4) that were analyzed for Complex IV (cytochrome c oxidase) activity. Conclusion In this pilot study, measurement can be performed in an appropriate timeline for clinical care with potential to serve as a prognostic marker. Further work is necessary to develop high-resolution respirometry as a clinical tool for assessing severity of illness and guiding therapy.

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Section: Introductionmentioning

confidence: 99%

A preliminary study in the alterations of mitochondrial respiration in patients with carbon monoxide poisoning measured in blood cells

Jang

Kelly

Hardy

et al. 2017

Clinical Toxicology

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“…Several studies have reported an association between increased serum NSE levels or cerebrospinal fluid (CSF) NSE levels and central nervous system (CNS) damage and neurological diseases [acute ischemic stroke , traumatic brain injury , Alzheimer's disease , delirium and epileptic seizures ]. In addition to cerebral injury, increased serum NSE levels have also been found to be associated with essential hypertension , lung cancer , acute carbon monoxide poisoning , pediatric cancer , renal cell carcinoma , diabetic peripheral neuropathy , and multiple myeloma .…”

Section: Introductionmentioning

confidence: 99%

Biological Variation and Reference Change Value Data for Serum Neuron‐Specific Enolase in a Turkish Population

Matyar

Öztürk

Karacor

et al. 2016

Clinical Laboratory Analysis

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“…In a study by Akdemir, where the roles of S100B, NSE, and GFAP in the assessment of hypoxic cerebral injury among patients with acute CO poisoning, S100B, NSE and GFAP's serum levels were significantly higher in the patient group than in the control group. 4 Akelma et al could not find any correlation between S100B protein level and Glasgow Coma Score (GCS) in children with CO poisoning. They detected that S100B protein level did not increase but NSE level increased.…”

Section: Discussionmentioning

confidence: 97%

“…Non-COHb biochemical markers have been investigated to predict CO poisoning, which is particularly neurotoxic and cardiotoxic. [3][4][5][6] Dogan et al reported that COHb levels are positively correlated with lactate levels in CO intoxication. 7 Netrins are important precursor proteins for neural and vascular development.…”

Section: Introductionmentioning

confidence: 99%

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Determination of netrin-1 levels and its relationship with neurotoxicity in carbon monoxide poisoning

Gedikli¹,

Emektar²,

Corbacioglu³

et al. 2019

Hum Exp Toxicol

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Objective: The aim of the study was to assess netrin-1 levels in carbon monoxide (CO) poisoning to determine its relationship with poisoning severity and neurotoxicity. Methods: This is a cross-sectional prospective study. The patients older than 18 years with CO poisoning were included. The patients were categorized into two groups on the basis of neurological involvement. Both the patient and the control groups were sampled for netrin-1 at 0th hour, and the patient group only was sampled for netrin-1 at 4th hour. Results: A total of 84 patients and 50 healthy controls were enrolled. The median 0th hour netrin-1 level of the patient group (765.1 pg/mL (619.8-983.1) was significantly higher than the control group (484 pg/mL (376-1031.6)) ( p < 0.001). There was also a significant difference between the 0th hour and 4th hour netrin-1 (888.9 pg/mL (700.3–1175.5)) levels in the patient group ( p < 0.001).There was no significant statistical difference between patients with and without neurological involvement ( p = 0.62) and between those who underwent hyperbaric oxygen therapy (HBOT) and those who did not ( p = 0.76) with respect to 4th hour netrin-1 levels. Conclusion: The significantly higher netrin-1 levels in patients with CO poisoning, suggests that netrin-1 is elevated as a stress marker. Although there is no significant difference in netrin-1 levels in patients with neurological impairment in CO poisonings, netrin-1 may show subclinically neurological effects. Hence, we believe that netrin-1 cannot be used as a marker of poisoning severity.

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The role of S100B protein, neuron-specific enolase, and glial fibrillary acidic protein in the evaluation of hypoxic brain injury in acute carbon monoxide poisoning

Cited by 19 publications

References 24 publications

A preliminary study in the alterations of mitochondrial respiration in patients with carbon monoxide poisoning measured in blood cells

A preliminary study in the alterations of mitochondrial respiration in patients with carbon monoxide poisoning measured in blood cells

Biological Variation and Reference Change Value Data for Serum Neuron‐Specific Enolase in a Turkish Population

Determination of netrin-1 levels and its relationship with neurotoxicity in carbon monoxide poisoning

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