Frequency of the TAFI – 438 G/A and factor XIIIA Val34Leu polymorphisms in patients with objectively proven pulmonary embolism
Summary Deep vein thrombosis (DVT) and pulmonary embolism (PE) are considered to be two forms of the same disease, however it is not fully understood what determines their clinical presentation. Proteins encoded by the FXIIIA and TAFI genes are involved in stabilizing the fibrin clot and in making i...
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| Veröffentlicht in: | Thrombosis and haemostasis 2003-09, Vol.90 (3), p.439-445 |
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| creator | Zidane, Majida de Visser, Marieke C. H. ten Wolde, Marije L.Vos, Hans de Monyé, Wouter Bertina, Rogier M. Huisman, Menno V. |
| description | Summary
Deep vein thrombosis (DVT) and pulmonary embolism (PE) are considered to be two forms of the same disease, however it is not fully understood what determines their clinical presentation.
Proteins encoded by the FXIIIA and TAFI genes are involved in stabilizing the fibrin clot and in making it more lysis resistant. The FXIIIA 34Leu and TAFI –438A alleles might protect against DVT. Information on such an association with PE is either contradictory or missing. We hypothesized that both polymorphisms might influence the formation and fate of emboli and accordingly the risk of PE. We determined the frequencies of both polymorphisms in patients with objectively demonstrated PE.
The frequency of FXIIIA Leu34Leu in PE patients and non-PE patients was 4.5% and 8.8%, [OR 0.5 (95% CI: 0.1 to 1.9)], respectively. For –438 A/A TAFI genotype the frequency was 1.5% and 8.1% [OR 0.1 (95% CI: 0.02 to 1.1)], respectively. |
| doi_str_mv | 10.1160/TH03-01-0035 |
| format | Article |
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Deep vein thrombosis (DVT) and pulmonary embolism (PE) are considered to be two forms of the same disease, however it is not fully understood what determines their clinical presentation.
Proteins encoded by the FXIIIA and TAFI genes are involved in stabilizing the fibrin clot and in making it more lysis resistant. The FXIIIA 34Leu and TAFI –438A alleles might protect against DVT. Information on such an association with PE is either contradictory or missing. We hypothesized that both polymorphisms might influence the formation and fate of emboli and accordingly the risk of PE. We determined the frequencies of both polymorphisms in patients with objectively demonstrated PE.
The frequency of FXIIIA Leu34Leu in PE patients and non-PE patients was 4.5% and 8.8%, [OR 0.5 (95% CI: 0.1 to 1.9)], respectively. For –438 A/A TAFI genotype the frequency was 1.5% and 8.1% [OR 0.1 (95% CI: 0.02 to 1.1)], respectively.</description><identifier>ISSN: 0340-6245</identifier><identifier>EISSN: 2567-689X</identifier><identifier>DOI: 10.1160/TH03-01-0035</identifier><identifier>PMID: 12958613</identifier><identifier>CODEN: THHADQ</identifier><language>eng</language><publisher>Stuttgart: Schattauer Verlag für Medizin und Naturwissenschaften</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Blood Coagulation, Fibrinolysis and Cellular Haemostasis ; Carboxypeptidase B2 - genetics ; Carboxypeptidase B2 - physiology ; Case-Control Studies ; DNA Mutational Analysis ; Factor XIII - genetics ; Factor XIII - physiology ; Female ; Gene Frequency ; Genetic Predisposition to Disease - genetics ; Hematologic and hematopoietic diseases ; Humans ; Male ; Medical sciences ; Middle Aged ; Mutation, Missense - physiology ; Odds Ratio ; Platelet diseases and coagulopathies ; Point Mutation - physiology ; Polymorphism, Genetic - physiology ; Pulmonary Embolism - blood ; Pulmonary Embolism - etiology ; Pulmonary Embolism - genetics ; Venous Thrombosis</subject><ispartof>Thrombosis and haemostasis, 2003-09, Vol.90 (3), p.439-445</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c543t-34649f053bd871b335fac6eacf2be415857e4a8a8a1bed6ff2f46df0b3deab3a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.thieme-connect.de/products/ejournals/pdf/10.1160/TH03-01-0035.pdf$$EPDF$$P50$$Gthieme$$H</linktopdf><linktohtml>$$Uhttps://www.thieme-connect.de/products/ejournals/html/10.1160/TH03-01-0035$$EHTML$$P50$$Gthieme$$H</linktohtml><link.rule.ids>314,780,784,3018,27924,27925,54559,54560</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15089216$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12958613$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zidane, Majida</creatorcontrib><creatorcontrib>de Visser, Marieke C. H.</creatorcontrib><creatorcontrib>ten Wolde, Marije</creatorcontrib><creatorcontrib>L.Vos, Hans</creatorcontrib><creatorcontrib>de Monyé, Wouter</creatorcontrib><creatorcontrib>Bertina, Rogier M.</creatorcontrib><creatorcontrib>Huisman, Menno V.</creatorcontrib><creatorcontrib>the Antelope study group</creatorcontrib><title>Frequency of the TAFI – 438 G/A and factor XIIIA Val34Leu polymorphisms in patients with objectively proven pulmonary embolism</title><title>Thrombosis and haemostasis</title><addtitle>Thromb Haemost</addtitle><description>Summary
Deep vein thrombosis (DVT) and pulmonary embolism (PE) are considered to be two forms of the same disease, however it is not fully understood what determines their clinical presentation.
Proteins encoded by the FXIIIA and TAFI genes are involved in stabilizing the fibrin clot and in making it more lysis resistant. The FXIIIA 34Leu and TAFI –438A alleles might protect against DVT. Information on such an association with PE is either contradictory or missing. We hypothesized that both polymorphisms might influence the formation and fate of emboli and accordingly the risk of PE. We determined the frequencies of both polymorphisms in patients with objectively demonstrated PE.
The frequency of FXIIIA Leu34Leu in PE patients and non-PE patients was 4.5% and 8.8%, [OR 0.5 (95% CI: 0.1 to 1.9)], respectively. For –438 A/A TAFI genotype the frequency was 1.5% and 8.1% [OR 0.1 (95% CI: 0.02 to 1.1)], respectively.</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Blood Coagulation, Fibrinolysis and Cellular Haemostasis</subject><subject>Carboxypeptidase B2 - genetics</subject><subject>Carboxypeptidase B2 - physiology</subject><subject>Case-Control Studies</subject><subject>DNA Mutational Analysis</subject><subject>Factor XIII - genetics</subject><subject>Factor XIII - physiology</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mutation, Missense - physiology</subject><subject>Odds Ratio</subject><subject>Platelet diseases and coagulopathies</subject><subject>Point Mutation - physiology</subject><subject>Polymorphism, Genetic - physiology</subject><subject>Pulmonary Embolism - blood</subject><subject>Pulmonary Embolism - etiology</subject><subject>Pulmonary Embolism - genetics</subject><subject>Venous Thrombosis</subject><issn>0340-6245</issn><issn>2567-689X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqtkc2KFDEUhQtRnHZ051qy0Y2Wk1R-unrZDPZMQ4ObVmYXUqkbKk2lUiapGXo37-Ab-iSm6MYBwZ1kEQJfzjn33KJ4S_BnQgS-2t9iWmJSYkz5s2JRcbEsRb26e14sMGW4FBXjF8WrGA8YE8FW_GVxQaoVrwWhi-JxE-DHBIM-Im9Q6gDt15st-vX4EzFao5urNVJDi4zSyQd0t91u1-i76inbwYRG3x-dD2Nno4vIDmhUycKQInqwqUO-OYBO9h76IxqDv4cMTL3zgwpHBK7xff73unhhVB_hzfm-LL5tvuyvb8vd15vt9XpXas5oKinL0Q3mtGnrJWko5TmSAKVN1QAjvOZLYKrOhzTQCmMqw0RrcENbUA1V9LL4cNLNSfLAMUlno4a-VwP4Kcol5YwxXmfw0wnUwccYwMgxWJcjS4Ll3LicG5eYyLnxjL87606Ng_YJPlecgfdnQEWtehPUoG184jiuVxURmft44lJnwYE8-CkMuZF_2eoTHXWnUlIThD-SqQs-txuzS96d7BQ4H5Oa39oPaV6QVEF3eTPSxjiBjCNoq3rp1DBFHeyYJOWkyi72P7osV-JvBxk7_yC75Hr6G8fg6Qo</recordid><startdate>20030901</startdate><enddate>20030901</enddate><creator>Zidane, Majida</creator><creator>de Visser, Marieke C. H.</creator><creator>ten Wolde, Marije</creator><creator>L.Vos, Hans</creator><creator>de Monyé, Wouter</creator><creator>Bertina, Rogier M.</creator><creator>Huisman, Menno V.</creator><general>Schattauer Verlag für Medizin und Naturwissenschaften</general><general>Schattauer GmbH</general><general>Schattauer</general><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>20030901</creationdate><title>Frequency of the TAFI – 438 G/A and factor XIIIA Val34Leu polymorphisms in patients with objectively proven pulmonary embolism</title><author>Zidane, Majida ; de Visser, Marieke C. H. ; ten Wolde, Marije ; L.Vos, Hans ; de Monyé, Wouter ; Bertina, Rogier M. ; Huisman, Menno V.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c543t-34649f053bd871b335fac6eacf2be415857e4a8a8a1bed6ff2f46df0b3deab3a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Blood Coagulation, Fibrinolysis and Cellular Haemostasis</topic><topic>Carboxypeptidase B2 - genetics</topic><topic>Carboxypeptidase B2 - physiology</topic><topic>Case-Control Studies</topic><topic>DNA Mutational Analysis</topic><topic>Factor XIII - genetics</topic><topic>Factor XIII - physiology</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mutation, Missense - physiology</topic><topic>Odds Ratio</topic><topic>Platelet diseases and coagulopathies</topic><topic>Point Mutation - physiology</topic><topic>Polymorphism, Genetic - physiology</topic><topic>Pulmonary Embolism - blood</topic><topic>Pulmonary Embolism - etiology</topic><topic>Pulmonary Embolism - genetics</topic><topic>Venous Thrombosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zidane, Majida</creatorcontrib><creatorcontrib>de Visser, Marieke C. H.</creatorcontrib><creatorcontrib>ten Wolde, Marije</creatorcontrib><creatorcontrib>L.Vos, Hans</creatorcontrib><creatorcontrib>de Monyé, Wouter</creatorcontrib><creatorcontrib>Bertina, Rogier M.</creatorcontrib><creatorcontrib>Huisman, Menno V.</creatorcontrib><creatorcontrib>the Antelope study group</creatorcontrib><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>Thrombosis and haemostasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zidane, Majida</au><au>de Visser, Marieke C. H.</au><au>ten Wolde, Marije</au><au>L.Vos, Hans</au><au>de Monyé, Wouter</au><au>Bertina, Rogier M.</au><au>Huisman, Menno V.</au><aucorp>the Antelope study group</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Frequency of the TAFI – 438 G/A and factor XIIIA Val34Leu polymorphisms in patients with objectively proven pulmonary embolism</atitle><jtitle>Thrombosis and haemostasis</jtitle><addtitle>Thromb Haemost</addtitle><date>2003-09-01</date><risdate>2003</risdate><volume>90</volume><issue>3</issue><spage>439</spage><epage>445</epage><pages>439-445</pages><issn>0340-6245</issn><eissn>2567-689X</eissn><coden>THHADQ</coden><abstract>Summary
Deep vein thrombosis (DVT) and pulmonary embolism (PE) are considered to be two forms of the same disease, however it is not fully understood what determines their clinical presentation.
Proteins encoded by the FXIIIA and TAFI genes are involved in stabilizing the fibrin clot and in making it more lysis resistant. The FXIIIA 34Leu and TAFI –438A alleles might protect against DVT. Information on such an association with PE is either contradictory or missing. We hypothesized that both polymorphisms might influence the formation and fate of emboli and accordingly the risk of PE. We determined the frequencies of both polymorphisms in patients with objectively demonstrated PE.
The frequency of FXIIIA Leu34Leu in PE patients and non-PE patients was 4.5% and 8.8%, [OR 0.5 (95% CI: 0.1 to 1.9)], respectively. For –438 A/A TAFI genotype the frequency was 1.5% and 8.1% [OR 0.1 (95% CI: 0.02 to 1.1)], respectively.</abstract><cop>Stuttgart</cop><pub>Schattauer Verlag für Medizin und Naturwissenschaften</pub><pmid>12958613</pmid><doi>10.1160/TH03-01-0035</doi><tpages>7</tpages></addata></record> |
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| ispartof | Thrombosis and haemostasis, 2003-09, Vol.90 (3), p.439-445 |
| issn | 0340-6245 2567-689X |
| language | eng |
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| source | MEDLINE; Thieme Connect Journals |
| subjects | Adult Aged Biological and medical sciences Blood Coagulation, Fibrinolysis and Cellular Haemostasis Carboxypeptidase B2 - genetics Carboxypeptidase B2 - physiology Case-Control Studies DNA Mutational Analysis Factor XIII - genetics Factor XIII - physiology Female Gene Frequency Genetic Predisposition to Disease - genetics Hematologic and hematopoietic diseases Humans Male Medical sciences Middle Aged Mutation, Missense - physiology Odds Ratio Platelet diseases and coagulopathies Point Mutation - physiology Polymorphism, Genetic - physiology Pulmonary Embolism - blood Pulmonary Embolism - etiology Pulmonary Embolism - genetics Venous Thrombosis |
| title | Frequency of the TAFI – 438 G/A and factor XIIIA Val34Leu polymorphisms in patients with objectively proven pulmonary embolism |
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