Serum total and lipid-bound sialic acid levels following acute myocardial infarction

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dc.contributor.authorGökmen, SS
dc.contributor.authorKiliçli, G
dc.contributor.authorÖzçelik, F
dc.contributor.authorGülen, S
dc.date.accessioned2024-06-12T11:16:31Z
dc.date.available2024-06-12T11:16:31Z
dc.date.issued2000
dc.departmentTrakya Üniversitesien_US
dc.description.abstractAlthough serum total sialic acid has been shown to be a cardiovascular risk factor, with elevated levers associated with increased cardiovascular mortality and also with cerebrovascular disease, the reason for the elevation in serum sialic acid content remains obscure. It has been shown that an increased output of serum proteins by the liver due to some type of acute phase reaction may be one of the possible sources of an increased serum sialic acid concentration in patients with myocardial infarction. An increase in the activity of sialidase, which cleaves the terminal sialic acid residues from oligosaccharides, glycoproteins and gangliosides, may also play an important role in the elevation of serum total sialic acid in myocardial infarction. Elevated serum total sialic acid in the blood might result either from the shedding or secreting of sialic acid from the cell membrane surface, or releasing of cellular sialic acid from the cell into the bloodstream due to cell damage after myocardial infarction. The purpose of the present study is to investigate serum total and lipid-bound sialic acid and the enzymes serum lactate dehydrogenase, creatine kinase and aspartate aminotransferase in patients with acute myocardial infarction, at 24 h post-infarction (day 1), 48 h post-infarction (day 2) and 72 h post-infarction (day 3). A possible role of cell damage in the elevation of serum total and lipid-bound sialic acid levels in these patients was also evaluated. In this study, 40 patients with myocardial infarction ranging in age from 42 to 68 years, and 26 healthy volunteers ranging in age from 45 to 71 years were included. Serum total sialic acid determination was carried out by the thiobarbituric acid method of Warren and lipid-bound sialic acid by the method of Katopodis. Our data shows that a) there is a gradual increase in the levels of serum total sialic acid and lipid-bound sialic acid during the first three days after the acute myocardial infarction and b) the elevation in serum total sialic acid revels correlates with the elevation in lactate dehydrogenase activity only on day 1 following infarction. Therefore, either the shedding or secreting of sialic acid from the cell or cell membrane surface may be partly responsible for an increased serum sialic acid concentration especially on day 1 following myocardial infarction.en_US
dc.identifier.doi10.1515/CCLM.2000.197
dc.identifier.endpage1255en_US
dc.identifier.issn1434-6621
dc.identifier.issn1437-4331
dc.identifier.issue12en_US
dc.identifier.pmid11205689en_US
dc.identifier.scopus2-s2.0-0034507234en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage1249en_US
dc.identifier.urihttps://doi.org/10.1515/CCLM.2000.197
dc.identifier.urihttps://hdl.handle.net/20.500.14551/24351
dc.identifier.volume38en_US
dc.identifier.wosWOS:000166975600006en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWalter De Gruyter Gmbhen_US
dc.relation.ispartofClinical Chemistry And Laboratory Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectTotal Sialic Aciden_US
dc.subjectLipid-Bound Sialic Aciden_US
dc.subjectLactate Dehydrogenaseen_US
dc.subjectCreatine Kinaseen_US
dc.subjectAspartate Aminotransferaseen_US
dc.subjectAcute Myocardial Infarctionen_US
dc.subjectLow-Density-Lipoproteinen_US
dc.titleSerum total and lipid-bound sialic acid levels following acute myocardial infarctionen_US
dc.typeArticleen_US

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