| Serum total and lipid-bound sialic acid levels following acute myocardial infarction. | |
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MedLine Citation:
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PMID: 11205689 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Although serum total sialic acid has been shown to be a cardiovascular risk factor, with elevated levels 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 acfd 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 levels 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. |
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Authors:
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S S Gökmen; G Kiliçli; F Ozçelik; S Gülen |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Clinical chemistry and laboratory medicine : CCLM / FESCC Volume: 38 ISSN: 1434-6621 ISO Abbreviation: Clin. Chem. Lab. Med. Publication Date: 2000 Dec |
Date Detail:
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Created Date: 2001-02-05 Completed Date: 2001-04-05 Revised Date: 2005-11-17 |
Medline Journal Info:
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Nlm Unique ID: 9806306 Medline TA: Clin Chem Lab Med Country: Germany |
Other Details:
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Languages: eng Pagination: 1249-55 Citation Subset: IM |
Affiliation:
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Biochemistry Department, Trakya University, School of Medicine, Edirne, Turkey. Oner@Turk.net |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Age Factors Aged Aspartate Aminotransferases / blood Case-Control Studies Creatine Kinase / blood Female Humans L-Lactate Dehydrogenase / blood Lipid Metabolism* Lipids / blood Male Middle Aged Myocardial Infarction / blood* N-Acetylneuraminic Acid / blood* Neuraminidase / blood Thiobarbituric Acid Reactive Substances / metabolism Time Factors |
| Chemical | |
Reg. No./Substance:
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0/Lipids; 0/Thiobarbituric Acid Reactive Substances; 131-48-6/N-Acetylneuraminic Acid; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 2.6.1.1/Aspartate Aminotransferases; EC 2.7.3.2/Creatine Kinase; EC 3.2.1.18/Neuraminidase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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