Coagulation and Fibrinolysis in Inflammatory Bowel Disease and in Giant Cell Arteritis
Background: In inflammatory bowel disease (IBD), gut microvascular thrombosis as well as thromboembolic complications have repeatedly been observed. We examined the long-term course of markers of coagulation and fibrinolysis in relation to clinical disease activity. Materials and Methods: In a prosp...
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| Veröffentlicht in: | Pathophysiology of haemostasis and thrombosis 2003-01, Vol.33 (2), p.75-83 |
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| creator | Vrij, Anton A. Rijken, Joop van Wersch, Jan W.J. Stockbrügger, Reinhold W. |
| description | Background: In inflammatory bowel disease (IBD), gut microvascular thrombosis as well as thromboembolic complications have repeatedly been observed. We examined the long-term course of markers of coagulation and fibrinolysis in relation to clinical disease activity. Materials and Methods: In a prospective study, prothrombin fragment 1 and 2 (F1.2), thrombin-antithrombin complex (TAT), antithrombin, D-dimer, plasmin-α 2 -antiplasmin complex (PAP) and plasminogen activator inhibitor-1 (PAI-1) were measured in 20 patients with Crohn’s disease (CD), 18 with ulcerative colitis (UC), and 19 with giant cell arteritis during active and inactive disease, as well as in 51 controls without inflammation. Results: Levels of F1.2, TAT, D-dimer, PAP and PAI-1 were significantly higher in active versus inactive CD and UC. However, even after 12 months of follow-up, in CD and UC the mean levels of F1.2, D-dimer and PAP were significantly higher than the levels of the controls. Conclusions: Levels of F1.2, D-dimer and PAP were markedly raised for a long time in clinically inactive IBD, underlining a chronic state of hypercoagulation and enhanced fibrinolysis. |
| doi_str_mv | 10.1159/000073850 |
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We examined the long-term course of markers of coagulation and fibrinolysis in relation to clinical disease activity. Materials and Methods: In a prospective study, prothrombin fragment 1 and 2 (F1.2), thrombin-antithrombin complex (TAT), antithrombin, D-dimer, plasmin-α 2 -antiplasmin complex (PAP) and plasminogen activator inhibitor-1 (PAI-1) were measured in 20 patients with Crohn’s disease (CD), 18 with ulcerative colitis (UC), and 19 with giant cell arteritis during active and inactive disease, as well as in 51 controls without inflammation. Results: Levels of F1.2, TAT, D-dimer, PAP and PAI-1 were significantly higher in active versus inactive CD and UC. However, even after 12 months of follow-up, in CD and UC the mean levels of F1.2, D-dimer and PAP were significantly higher than the levels of the controls. Conclusions: Levels of F1.2, D-dimer and PAP were markedly raised for a long time in clinically inactive IBD, underlining a chronic state of hypercoagulation and enhanced fibrinolysis.</description><identifier>ISSN: 1424-8832</identifier><identifier>EISSN: 1424-8840</identifier><identifier>DOI: 10.1159/000073850</identifier><identifier>PMID: 14624048</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Biomarkers - blood ; Blood Coagulation ; Blood Sedimentation ; C-Reactive Protein - analysis ; Case-Control Studies ; Colitis, Ulcerative - blood ; Crohn Disease - blood ; Female ; Fibrinolysis ; Gastroenterology. Liver. Pancreas. Abdomen ; Giant Cell Arteritis - blood ; Hematologic and hematopoietic diseases ; Humans ; Inflammatory Bowel Diseases - blood ; Male ; Medical sciences ; Middle Aged ; Original Paper ; Other diseases. Semiology ; Platelet diseases and coagulopathies ; Prospective Studies ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Thrombophilia</subject><ispartof>Pathophysiology of haemostasis and thrombosis, 2003-01, Vol.33 (2), p.75-83</ispartof><rights>2003 S. Karger AG, Basel</rights><rights>2004 INIST-CNRS</rights><rights>Copyright 2003 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-fa49139475b2468e9065b5007cfba23f0dd515600d7c2e1548ea0a6adbc6df2d3</citedby><cites>FETCH-LOGICAL-c459t-fa49139475b2468e9065b5007cfba23f0dd515600d7c2e1548ea0a6adbc6df2d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2429,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15303919$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14624048$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vrij, Anton A.</creatorcontrib><creatorcontrib>Rijken, Joop</creatorcontrib><creatorcontrib>van Wersch, Jan W.J.</creatorcontrib><creatorcontrib>Stockbrügger, Reinhold W.</creatorcontrib><title>Coagulation and Fibrinolysis in Inflammatory Bowel Disease and in Giant Cell Arteritis</title><title>Pathophysiology of haemostasis and thrombosis</title><addtitle>Pathophysiol Haemos Thromb</addtitle><description>Background: In inflammatory bowel disease (IBD), gut microvascular thrombosis as well as thromboembolic complications have repeatedly been observed. We examined the long-term course of markers of coagulation and fibrinolysis in relation to clinical disease activity. Materials and Methods: In a prospective study, prothrombin fragment 1 and 2 (F1.2), thrombin-antithrombin complex (TAT), antithrombin, D-dimer, plasmin-α 2 -antiplasmin complex (PAP) and plasminogen activator inhibitor-1 (PAI-1) were measured in 20 patients with Crohn’s disease (CD), 18 with ulcerative colitis (UC), and 19 with giant cell arteritis during active and inactive disease, as well as in 51 controls without inflammation. Results: Levels of F1.2, TAT, D-dimer, PAP and PAI-1 were significantly higher in active versus inactive CD and UC. However, even after 12 months of follow-up, in CD and UC the mean levels of F1.2, D-dimer and PAP were significantly higher than the levels of the controls. Conclusions: Levels of F1.2, D-dimer and PAP were markedly raised for a long time in clinically inactive IBD, underlining a chronic state of hypercoagulation and enhanced fibrinolysis.</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Blood Coagulation</subject><subject>Blood Sedimentation</subject><subject>C-Reactive Protein - analysis</subject><subject>Case-Control Studies</subject><subject>Colitis, Ulcerative - blood</subject><subject>Crohn Disease - blood</subject><subject>Female</subject><subject>Fibrinolysis</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Giant Cell Arteritis - blood</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Inflammatory Bowel Diseases - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Original Paper</subject><subject>Other diseases. Semiology</subject><subject>Platelet diseases and coagulopathies</subject><subject>Prospective Studies</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Thrombophilia</subject><issn>1424-8832</issn><issn>1424-8840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpt0ElLAzEUB_Agiq3Vg2dBBkHBw2jWWY612gUKeqhehzeTpERnqckU6bc3dkp7MZeXw4-3_BG6JPiBEJE-Yv9ilgh8hPqEUx4mCcfH-z-jPXTm3CfGHqfsFPUIjyjHPOmjj1EDy3UJrWnqAGoZjE1uTd2UG2dcYOpgVusSqgraxm6Cp-ZHlcGzcQqc2nIvJgbqNhipsgyGtlXWtMadoxMNpVMXuzpA7-OXxWgazl8ns9FwHhZcpG2ogaeEpTwWOeVRolIciVz4YwqdA2UaSymIiDCWcUEVETxRgCECmReR1FSyAbrr-q5s871Wrs0q4wq_CtSqWbssJiyOKBUe3newsI1zVulsZU0FdpMRnP2FmO1D9PZ613SdV0oe5C41D253AFwBpbZQF8YdnGCYpST17qZzX2CXyu7B23SxnZStpPbo6l_U7fIL2rONJg</recordid><startdate>20030101</startdate><enddate>20030101</enddate><creator>Vrij, Anton A.</creator><creator>Rijken, Joop</creator><creator>van Wersch, Jan W.J.</creator><creator>Stockbrügger, Reinhold W.</creator><general>Karger</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>20030101</creationdate><title>Coagulation and Fibrinolysis in Inflammatory Bowel Disease and in Giant Cell Arteritis</title><author>Vrij, Anton A. ; Rijken, Joop ; van Wersch, Jan W.J. ; Stockbrügger, Reinhold W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-fa49139475b2468e9065b5007cfba23f0dd515600d7c2e1548ea0a6adbc6df2d3</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>Biomarkers - blood</topic><topic>Blood Coagulation</topic><topic>Blood Sedimentation</topic><topic>C-Reactive Protein - analysis</topic><topic>Case-Control Studies</topic><topic>Colitis, Ulcerative - blood</topic><topic>Crohn Disease - blood</topic><topic>Female</topic><topic>Fibrinolysis</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Giant Cell Arteritis - blood</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Inflammatory Bowel Diseases - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Original Paper</topic><topic>Other diseases. Semiology</topic><topic>Platelet diseases and coagulopathies</topic><topic>Prospective Studies</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Thrombophilia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vrij, Anton A.</creatorcontrib><creatorcontrib>Rijken, Joop</creatorcontrib><creatorcontrib>van Wersch, Jan W.J.</creatorcontrib><creatorcontrib>Stockbrügger, Reinhold W.</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>Pathophysiology of haemostasis and thrombosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vrij, Anton A.</au><au>Rijken, Joop</au><au>van Wersch, Jan W.J.</au><au>Stockbrügger, Reinhold W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Coagulation and Fibrinolysis in Inflammatory Bowel Disease and in Giant Cell Arteritis</atitle><jtitle>Pathophysiology of haemostasis and thrombosis</jtitle><addtitle>Pathophysiol Haemos Thromb</addtitle><date>2003-01-01</date><risdate>2003</risdate><volume>33</volume><issue>2</issue><spage>75</spage><epage>83</epage><pages>75-83</pages><issn>1424-8832</issn><eissn>1424-8840</eissn><abstract>Background: In inflammatory bowel disease (IBD), gut microvascular thrombosis as well as thromboembolic complications have repeatedly been observed. We examined the long-term course of markers of coagulation and fibrinolysis in relation to clinical disease activity. Materials and Methods: In a prospective study, prothrombin fragment 1 and 2 (F1.2), thrombin-antithrombin complex (TAT), antithrombin, D-dimer, plasmin-α 2 -antiplasmin complex (PAP) and plasminogen activator inhibitor-1 (PAI-1) were measured in 20 patients with Crohn’s disease (CD), 18 with ulcerative colitis (UC), and 19 with giant cell arteritis during active and inactive disease, as well as in 51 controls without inflammation. Results: Levels of F1.2, TAT, D-dimer, PAP and PAI-1 were significantly higher in active versus inactive CD and UC. However, even after 12 months of follow-up, in CD and UC the mean levels of F1.2, D-dimer and PAP were significantly higher than the levels of the controls. Conclusions: Levels of F1.2, D-dimer and PAP were markedly raised for a long time in clinically inactive IBD, underlining a chronic state of hypercoagulation and enhanced fibrinolysis.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>14624048</pmid><doi>10.1159/000073850</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Biological and medical sciences Biomarkers - blood Blood Coagulation Blood Sedimentation C-Reactive Protein - analysis Case-Control Studies Colitis, Ulcerative - blood Crohn Disease - blood Female Fibrinolysis Gastroenterology. Liver. Pancreas. Abdomen Giant Cell Arteritis - blood Hematologic and hematopoietic diseases Humans Inflammatory Bowel Diseases - blood Male Medical sciences Middle Aged Original Paper Other diseases. Semiology Platelet diseases and coagulopathies Prospective Studies Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Thrombophilia |
| title | Coagulation and Fibrinolysis in Inflammatory Bowel Disease and in Giant Cell Arteritis |
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