How much apoptosis does carbon monoxide poisoning cause? Primary clinical soluble TWEAK protein level study

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dc.contributor.authorBadem, N. Dindar
dc.contributor.authorComertpay, E.
dc.contributor.authorCoskun, F.
dc.date.accessioned2020-06-25T18:30:47Z
dc.date.available2020-06-25T18:30:47Z
dc.date.issued2019
dc.departmentKırıkkale Üniversitesi
dc.descriptionDINDAR BADEM, NERMIN/0000-0002-5095-7818
dc.description.abstractCarbon monoxide (CO) is an important cause of deaths via poisoning. CO poisoning causes inhibition of O-2 transport and development of tissue hypoxia, which then causes cell apoptosis. A significant indicator of cell apoptosis, soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) protein, is important for the stimulation of apoptosis. The primary purpose of this study is to determine whether apoptosis occurs during acute CO poisoning and to show that sTWEAK protein is an indicator of apoptosis that can be analyzed as a marker in the peripheral blood sample. The secondary aim is to determine the diagnostic and prognostic values of sTWEAK protein. The study was performed prospectively on 43 patients with CO poisoning and 30 healthy volunteer control individuals. The anamneses were taken from all patients, who also underwent physical examination. Complete blood count, biochemical markers, cardiac enzymes, and arterial blood gas measurements were analyzed. All the patients' sTWEAK protein levels were also analyzed. The sTWEAK protein level of patients with CO poisoning was 2278 pg/mL (1197-7234), while the level of the control group was 1609 pg/mL (310-3721). The patients' sTWEAK levels were significantly higher than the controls (area under the curve: 0.77 (0.66-0.89); p < 0.001), and the cutoff value was determined as 1895.50 pg/mL. The cutoff level had a sensitivity of 74.4%, a specificity of 76.7%, a positive predictive value of 82.0%, and a negative predictive value of 67.6%. sTWEAK is a significant indicator of apoptosis in CO poisoning that can be analyzed in the peripheral blood. However, further clinical trials are needed in terms of prognostic criteria.en_US
dc.description.sponsorshipKirikkale University Scientific Research Projects UnitKirikkale University [2015/019]en_US
dc.description.sponsorshipThe author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was funded by Kirikkale University Scientific Research Projects Unit, project number 2015/019.en_US
dc.identifier.doi10.1177/0960327119845038
dc.identifier.endpage982en_US
dc.identifier.issn0960-3271
dc.identifier.issn1477-0903
dc.identifier.issue8en_US
dc.identifier.pmid31030571
dc.identifier.scopus2-s2.0-85065250045
dc.identifier.scopusqualityQ2
dc.identifier.startpage974en_US
dc.identifier.urihttps://doi.org/10.1177/0960327119845038
dc.identifier.urihttps://hdl.handle.net/20.500.12587/7723
dc.identifier.volume38en_US
dc.identifier.wosWOS:000476722600009
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSage Publications Ltden_US
dc.relation.ispartofHuman & Experimental Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCO poisoningen_US
dc.subjectsTWEAK proteinen_US
dc.subjectapoptosisen_US
dc.subjectCOHb levelen_US
dc.titleHow much apoptosis does carbon monoxide poisoning cause? Primary clinical soluble TWEAK protein level studyen_US
dc.typeArticle

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