Serum Total and Lipid-Bound Sialic Acid Levels Following Acute Myocardial Infarction
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 incr...
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Veröffentlicht in: | Clinical chemistry and laboratory medicine 2000-12, Vol.38 (12), p.1249-1255 |
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description | 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 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 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. |
doi_str_mv | 10.1515/CCLM.2000.197 |
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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 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.</description><identifier>ISSN: 1434-6621</identifier><identifier>EISSN: 1437-4331</identifier><identifier>DOI: 10.1515/CCLM.2000.197</identifier><identifier>PMID: 11205689</identifier><language>eng</language><publisher>Berlin: Walter de Gruyter</publisher><subject>Age Factors ; Aged ; Aspartate Aminotransferases - blood ; Biological and medical sciences ; Cardiology. Vascular system ; Case-Control Studies ; Coronary heart disease ; Creatine Kinase - blood ; Female ; Heart ; Humans ; L-Lactate Dehydrogenase - blood ; Lipid Metabolism ; Lipids - blood ; Male ; Medical sciences ; Middle Aged ; Myocardial Infarction - blood ; N-Acetylneuraminic Acid - blood ; Neuraminidase - blood ; Thiobarbituric Acid Reactive Substances - metabolism ; Time Factors</subject><ispartof>Clinical chemistry and laboratory medicine, 2000-12, Vol.38 (12), p.1249-1255</ispartof><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-e744a66292eb68dd890484cd6a8aebb02f2d5ff478ba5310286041ebe832fdca3</citedby><cites>FETCH-LOGICAL-c494t-e744a66292eb68dd890484cd6a8aebb02f2d5ff478ba5310286041ebe832fdca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=944219$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11205689$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GÖKMEN, Selma Süer</creatorcontrib><creatorcontrib>KILICLI, Gülseven</creatorcontrib><creatorcontrib>ÖZCELIK, Fatih</creatorcontrib><creatorcontrib>GÜLEN, Sendogan</creatorcontrib><title>Serum Total and Lipid-Bound Sialic Acid Levels Following Acute Myocardial Infarction</title><title>Clinical chemistry and laboratory medicine</title><addtitle>Clinical Chemistry and Laboratory Medicine</addtitle><description>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 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 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.</description><subject>Age Factors</subject><subject>Aged</subject><subject>Aspartate Aminotransferases - blood</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Case-Control Studies</subject><subject>Coronary heart disease</subject><subject>Creatine Kinase - blood</subject><subject>Female</subject><subject>Heart</subject><subject>Humans</subject><subject>L-Lactate Dehydrogenase - blood</subject><subject>Lipid Metabolism</subject><subject>Lipids - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - blood</subject><subject>N-Acetylneuraminic Acid - blood</subject><subject>Neuraminidase - blood</subject><subject>Thiobarbituric Acid Reactive Substances - metabolism</subject><subject>Time Factors</subject><issn>1434-6621</issn><issn>1437-4331</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEtP3DAQgC1UxLNHrlWkSr2F2o7tOEdYsRQpiMcuvVoT20Eu3nixkwL_vt6ygtO8Ps2MPoROCD4lnPCfs1l7fUoxzmVT76ADwqq6ZFVFvvzPWSkEJfvoMKU_GBPOWb2H9gmhmAvZHKDlwsZpVSzDCL6AwRStWztTnocp5wsH3uniTLvct3-tT8U8eB9e3PCYu9Noi-u3oCGaDBZXQw9Rjy4Mx2i3B5_s1208Qg_zi-XsV9neXF7NztpSs4aNpa0Zg_xeQ20npDGywUwybQRIsF2HaU8N73tWyw54RTCVAjNiOysr2hsN1RH68b53HcPzZNOoVi5p6z0MNkxJ1ZQzKijNYPkO6hhSirZX6-hWEN8UwWqjUW00qo1GlTVm_tt28dStrPmkt94y8H0LQNLg-wiDdumDaxijpPk869JoXz-mEJ-UqKuaq7slU3hx18r730LdVv8AAf2IbA</recordid><startdate>20001201</startdate><enddate>20001201</enddate><creator>GÖKMEN, Selma Süer</creator><creator>KILICLI, Gülseven</creator><creator>ÖZCELIK, Fatih</creator><creator>GÜLEN, Sendogan</creator><general>Walter de Gruyter</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20001201</creationdate><title>Serum Total and Lipid-Bound Sialic Acid Levels Following Acute Myocardial Infarction</title><author>GÖKMEN, Selma Süer ; KILICLI, Gülseven ; ÖZCELIK, Fatih ; GÜLEN, Sendogan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-e744a66292eb68dd890484cd6a8aebb02f2d5ff478ba5310286041ebe832fdca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Age Factors</topic><topic>Aged</topic><topic>Aspartate Aminotransferases - blood</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Case-Control Studies</topic><topic>Coronary heart disease</topic><topic>Creatine Kinase - blood</topic><topic>Female</topic><topic>Heart</topic><topic>Humans</topic><topic>L-Lactate Dehydrogenase - blood</topic><topic>Lipid Metabolism</topic><topic>Lipids - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - blood</topic><topic>N-Acetylneuraminic Acid - blood</topic><topic>Neuraminidase - blood</topic><topic>Thiobarbituric Acid Reactive Substances - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GÖKMEN, Selma Süer</creatorcontrib><creatorcontrib>KILICLI, Gülseven</creatorcontrib><creatorcontrib>ÖZCELIK, Fatih</creatorcontrib><creatorcontrib>GÜLEN, Sendogan</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical chemistry and laboratory medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GÖKMEN, Selma Süer</au><au>KILICLI, Gülseven</au><au>ÖZCELIK, Fatih</au><au>GÜLEN, Sendogan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serum Total and Lipid-Bound Sialic Acid Levels Following Acute Myocardial Infarction</atitle><jtitle>Clinical chemistry and laboratory medicine</jtitle><addtitle>Clinical Chemistry and Laboratory Medicine</addtitle><date>2000-12-01</date><risdate>2000</risdate><volume>38</volume><issue>12</issue><spage>1249</spage><epage>1255</epage><pages>1249-1255</pages><issn>1434-6621</issn><eissn>1437-4331</eissn><abstract>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 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 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.</abstract><cop>Berlin</cop><cop>New York, NY</cop><pub>Walter de Gruyter</pub><pmid>11205689</pmid><doi>10.1515/CCLM.2000.197</doi><tpages>7</tpages></addata></record> |
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subjects | Age Factors Aged Aspartate Aminotransferases - blood Biological and medical sciences Cardiology. Vascular system Case-Control Studies Coronary heart disease Creatine Kinase - blood Female Heart Humans L-Lactate Dehydrogenase - blood Lipid Metabolism Lipids - blood Male Medical sciences Middle Aged Myocardial Infarction - blood N-Acetylneuraminic Acid - blood Neuraminidase - blood Thiobarbituric Acid Reactive Substances - metabolism Time Factors |
title | Serum Total and Lipid-Bound Sialic Acid Levels Following Acute Myocardial Infarction |
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