Increased Lipoprotein(a) Is an Important Risk Factor for Venous Thromboembolism in Childhood
Background —Serum levels of lipoprotein(a) [Lp(a)] are determined largely by genetic variation in the gene encoding for apolipoprotein(a) [apo(a)], the specific protein component of Lp(a) that is very homologous to plasminogen. High plasma levels of Lp(a) increase the risk for premature atherosclero...
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| Published in | Circulation (New York, N.Y.) Vol. 100; no. 7; pp. 743 - 748 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
17.08.1999
American Heart Association, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0009-7322 1524-4539 1524-4539 |
| DOI | 10.1161/01.CIR.100.7.743 |
Cover
| Abstract | Background
—Serum levels of lipoprotein(a) [Lp(a)] are determined largely by genetic variation in the gene encoding for apolipoprotein(a) [apo(a)], the specific protein component of Lp(a) that is very homologous to plasminogen. High plasma levels of Lp(a) increase the risk for premature atherosclerotic vessel diseases. We investigated the little-characterized role of Lp(a) as a risk factor for venous thromboembolic diseases, alone and in conjunction with established thrombophilic risk factors of proteins regulating blood coagulation and fibrinolysis.
Methods and Results
—Serum levels of Lp(a) and lipids, protein C, protein S, and antithrombin, as well as the size of apo(a) isoforms and the presence of the factor V:Q
506
mutation, were determined in 186 consecutively admitted children from neonates to 18 years old with a history of venous thrombosis and in 186 age- and disease-matched control subjects. Children with a history of venous thrombosis had a significantly higher median Lp(a) level (19 versus 4.4 mg/dL) than control subjects. The risk for thromboembolic events in children with Lp(a) levels in the upper quartile, ie, >30 mg/dL, was 7.2 (95% CI, 3.7 to 14.5). The size of apo(a) isoforms was inversely related to Lp(a) levels and to the risk for thromboembolic events. Compared with the highest quartile of the apo(a) size distribution, the lowest quartile was associated with a risk of 8.2. In addition, multivariate statistical analysis gives evidence that the factor V:Q
506
mutation (OR/CI, 2.8/1.6 to 4.9), protein C (OR/CI, 6.5/2.1 to 19), and antithrombin deficiency (OR/CI, 10.4/1.2 to 90) were independent risk factors of childhood venous thrombosis. Coincidence of elevated Lp(a) with factor V:Q
506
mutation or deficiencies of protein C or antithrombin further increased the risk for thromboembolic events to 8.4.
Conclusions
—Lp(a) >30 mg/dL is a risk factor for venous thromboembolism in childhood. Lp(a) measurements should be included in the screening of causal factors in children with venous thromboembolic events. |
|---|---|
| AbstractList | BACKGROUND: Serum levels of lipoprotein(a) [Lp(a)] are determined largely by genetic variation in the gene encoding for apolipoprotein(a) [apo(a)], the specific protein component of Lp(a) that is very homologous to plasminogen. High plasma levels of Lp(a) increase the risk for premature atherosclerotic vessel diseases. We investigated the little-characterized role of Lp(a) as a risk factor for venous thromboembolic diseases, alone and in conjunction with established thrombophilic risk factors of proteins regulating blood coagulation and fibrinolysis. METHODS AND RESULTS: Serum levels of Lp(a) and lipids, protein C, protein S, and antithrombin, as well as the size of apo(a) isoforms and the presence of the factor V:Q(506) mutation, were determined in 186 consecutively admitted children from neonates to 18 years old with a history of venous thrombosis and in 186 age- and disease-matched control subjects. Children with a history of venous thrombosis had a significantly higher median Lp(a) level (19 versus 4.4 mg/dL) than control subjects. The risk for thromboembolic events in children with Lp(a) levels in the upper quartile, ie, >30 mg/dL, was 7.2 (95% CI, 3.7 to 14.5). The size of apo(a) isoforms was inversely related to Lp(a) levels and to the risk for thromboembolic events. Compared with the highest quartile of the apo(a) size distribution, the lowest quartile was associated with a risk of 8.2. In addition, multivariate statistical analysis gives evidence that the factor V:Q(506) mutation (OR/CI, 2.8/1.6 to 4.9), protein C (OR/CI, 6.5/2.1 to 19), and antithrombin deficiency (OR/CI, 10.4/1.2 to 90) were independent risk factors of childhood venous thrombosis. Coincidence of elevated Lp(a) with factor V:Q(506) mutation or deficiencies of protein C or antithrombin further increased the risk for thromboembolic events to 8.4. CONCLUSIONS: Lp(a) >30 mg/dL is a risk factor for venous thromboembolism in childhood. Lp(a) measurements should be included in the screening of causal factors in children with venous thromboembolic events. Serum levels of lipoprotein(a) [Lp(a)] are determined largely by genetic variation in the gene encoding for apolipoprotein(a) [apo(a)], the specific protein component of Lp(a) that is very homologous to plasminogen. High plasma levels of Lp(a) increase the risk for premature atherosclerotic vessel diseases. We investigated the little-characterized role of Lp(a) as a risk factor for venous thromboembolic diseases, alone and in conjunction with established thrombophilic risk factors of proteins regulating blood coagulation and fibrinolysis.BACKGROUNDSerum levels of lipoprotein(a) [Lp(a)] are determined largely by genetic variation in the gene encoding for apolipoprotein(a) [apo(a)], the specific protein component of Lp(a) that is very homologous to plasminogen. High plasma levels of Lp(a) increase the risk for premature atherosclerotic vessel diseases. We investigated the little-characterized role of Lp(a) as a risk factor for venous thromboembolic diseases, alone and in conjunction with established thrombophilic risk factors of proteins regulating blood coagulation and fibrinolysis.Serum levels of Lp(a) and lipids, protein C, protein S, and antithrombin, as well as the size of apo(a) isoforms and the presence of the factor V:Q(506) mutation, were determined in 186 consecutively admitted children from neonates to 18 years old with a history of venous thrombosis and in 186 age- and disease-matched control subjects. Children with a history of venous thrombosis had a significantly higher median Lp(a) level (19 versus 4.4 mg/dL) than control subjects. The risk for thromboembolic events in children with Lp(a) levels in the upper quartile, ie, >30 mg/dL, was 7.2 (95% CI, 3.7 to 14.5). The size of apo(a) isoforms was inversely related to Lp(a) levels and to the risk for thromboembolic events. Compared with the highest quartile of the apo(a) size distribution, the lowest quartile was associated with a risk of 8.2. In addition, multivariate statistical analysis gives evidence that the factor V:Q(506) mutation (OR/CI, 2.8/1.6 to 4.9), protein C (OR/CI, 6.5/2.1 to 19), and antithrombin deficiency (OR/CI, 10.4/1.2 to 90) were independent risk factors of childhood venous thrombosis. Coincidence of elevated Lp(a) with factor V:Q(506) mutation or deficiencies of protein C or antithrombin further increased the risk for thromboembolic events to 8.4.METHODS AND RESULTSSerum levels of Lp(a) and lipids, protein C, protein S, and antithrombin, as well as the size of apo(a) isoforms and the presence of the factor V:Q(506) mutation, were determined in 186 consecutively admitted children from neonates to 18 years old with a history of venous thrombosis and in 186 age- and disease-matched control subjects. Children with a history of venous thrombosis had a significantly higher median Lp(a) level (19 versus 4.4 mg/dL) than control subjects. The risk for thromboembolic events in children with Lp(a) levels in the upper quartile, ie, >30 mg/dL, was 7.2 (95% CI, 3.7 to 14.5). The size of apo(a) isoforms was inversely related to Lp(a) levels and to the risk for thromboembolic events. Compared with the highest quartile of the apo(a) size distribution, the lowest quartile was associated with a risk of 8.2. In addition, multivariate statistical analysis gives evidence that the factor V:Q(506) mutation (OR/CI, 2.8/1.6 to 4.9), protein C (OR/CI, 6.5/2.1 to 19), and antithrombin deficiency (OR/CI, 10.4/1.2 to 90) were independent risk factors of childhood venous thrombosis. Coincidence of elevated Lp(a) with factor V:Q(506) mutation or deficiencies of protein C or antithrombin further increased the risk for thromboembolic events to 8.4.Lp(a) >30 mg/dL is a risk factor for venous thromboembolism in childhood. Lp(a) measurements should be included in the screening of causal factors in children with venous thromboembolic events.CONCLUSIONSLp(a) >30 mg/dL is a risk factor for venous thromboembolism in childhood. Lp(a) measurements should be included in the screening of causal factors in children with venous thromboembolic events. Serum levels of lipoprotein(a) [Lp(a)] are determined largely by genetic variation in the gene encoding for apolipoprotein(a) [apo(a)], the specific protein component of Lp(a) that is very homologous to plasminogen. High plasma levels of Lp(a) increase the risk for premature atherosclerotic vessel diseases. We investigated the little-characterized role of Lp(a) as a risk factor for venous thromboembolic diseases, alone and in conjunction with established thrombophilic risk factors of proteins regulating blood coagulation and fibrinolysis. Serum levels of Lp(a) and lipids, protein C, protein S, and antithrombin, as well as the size of apo(a) isoforms and the presence of the factor V:Q(506) mutation, were determined in 186 consecutively admitted children from neonates to 18 years old with a history of venous thrombosis and in 186 age- and disease-matched control subjects. Children with a history of venous thrombosis had a significantly higher median Lp(a) level (19 versus 4.4 mg/dL) than control subjects. The risk for thromboembolic events in children with Lp(a) levels in the upper quartile, ie, >30 mg/dL, was 7.2 (95% CI, 3.7 to 14.5). The size of apo(a) isoforms was inversely related to Lp(a) levels and to the risk for thromboembolic events. Compared with the highest quartile of the apo(a) size distribution, the lowest quartile was associated with a risk of 8.2. In addition, multivariate statistical analysis gives evidence that the factor V:Q(506) mutation (OR/CI, 2.8/1.6 to 4.9), protein C (OR/CI, 6.5/2.1 to 19), and antithrombin deficiency (OR/CI, 10.4/1.2 to 90) were independent risk factors of childhood venous thrombosis. Coincidence of elevated Lp(a) with factor V:Q(506) mutation or deficiencies of protein C or antithrombin further increased the risk for thromboembolic events to 8.4. Lp(a) >30 mg/dL is a risk factor for venous thromboembolism in childhood. Lp(a) measurements should be included in the screening of causal factors in children with venous thromboembolic events. Background —Serum levels of lipoprotein(a) [Lp(a)] are determined largely by genetic variation in the gene encoding for apolipoprotein(a) [apo(a)], the specific protein component of Lp(a) that is very homologous to plasminogen. High plasma levels of Lp(a) increase the risk for premature atherosclerotic vessel diseases. We investigated the little-characterized role of Lp(a) as a risk factor for venous thromboembolic diseases, alone and in conjunction with established thrombophilic risk factors of proteins regulating blood coagulation and fibrinolysis. Methods and Results —Serum levels of Lp(a) and lipids, protein C, protein S, and antithrombin, as well as the size of apo(a) isoforms and the presence of the factor V:Q 506 mutation, were determined in 186 consecutively admitted children from neonates to 18 years old with a history of venous thrombosis and in 186 age- and disease-matched control subjects. Children with a history of venous thrombosis had a significantly higher median Lp(a) level (19 versus 4.4 mg/dL) than control subjects. The risk for thromboembolic events in children with Lp(a) levels in the upper quartile, ie, >30 mg/dL, was 7.2 (95% CI, 3.7 to 14.5). The size of apo(a) isoforms was inversely related to Lp(a) levels and to the risk for thromboembolic events. Compared with the highest quartile of the apo(a) size distribution, the lowest quartile was associated with a risk of 8.2. In addition, multivariate statistical analysis gives evidence that the factor V:Q 506 mutation (OR/CI, 2.8/1.6 to 4.9), protein C (OR/CI, 6.5/2.1 to 19), and antithrombin deficiency (OR/CI, 10.4/1.2 to 90) were independent risk factors of childhood venous thrombosis. Coincidence of elevated Lp(a) with factor V:Q 506 mutation or deficiencies of protein C or antithrombin further increased the risk for thromboembolic events to 8.4. Conclusions —Lp(a) >30 mg/dL is a risk factor for venous thromboembolism in childhood. Lp(a) measurements should be included in the screening of causal factors in children with venous thromboembolic events. |
| Author | Münchow, Nicole Assmann, Gerd Junker, Ralf Koch, Hans-Georg von Eckardstein, Arnold Hartmeier, Marion Nowak-Göttl, Ulrike |
| Author_xml | – sequence: 1 givenname: Ulrike surname: Nowak-Göttl fullname: Nowak-Göttl, Ulrike organization: From the Department of Pediatrics (U.N.-G., M.H., H.-G.K., N.M.), the Department of Clinical Chemistry and Laboratory Medicine (R.J., G.A., A.v.E.), and the Department of Arteriosclerosis Research (R.J., G.A., A.v.E.), Westfälische Wilhelms-Universität, Münster, and the University of Hamburg (N.M.), Germany – sequence: 2 givenname: Ralf surname: Junker fullname: Junker, Ralf organization: From the Department of Pediatrics (U.N.-G., M.H., H.-G.K., N.M.), the Department of Clinical Chemistry and Laboratory Medicine (R.J., G.A., A.v.E.), and the Department of Arteriosclerosis Research (R.J., G.A., A.v.E.), Westfälische Wilhelms-Universität, Münster, and the University of Hamburg (N.M.), Germany – sequence: 3 givenname: Marion surname: Hartmeier fullname: Hartmeier, Marion organization: From the Department of Pediatrics (U.N.-G., M.H., H.-G.K., N.M.), the Department of Clinical Chemistry and Laboratory Medicine (R.J., G.A., A.v.E.), and the Department of Arteriosclerosis Research (R.J., G.A., A.v.E.), Westfälische Wilhelms-Universität, Münster, and the University of Hamburg (N.M.), Germany – sequence: 4 givenname: Hans-Georg surname: Koch fullname: Koch, Hans-Georg organization: From the Department of Pediatrics (U.N.-G., M.H., H.-G.K., N.M.), the Department of Clinical Chemistry and Laboratory Medicine (R.J., G.A., A.v.E.), and the Department of Arteriosclerosis Research (R.J., G.A., A.v.E.), Westfälische Wilhelms-Universität, Münster, and the University of Hamburg (N.M.), Germany – sequence: 5 givenname: Nicole surname: Münchow fullname: Münchow, Nicole organization: From the Department of Pediatrics (U.N.-G., M.H., H.-G.K., N.M.), the Department of Clinical Chemistry and Laboratory Medicine (R.J., G.A., A.v.E.), and the Department of Arteriosclerosis Research (R.J., G.A., A.v.E.), Westfälische Wilhelms-Universität, Münster, and the University of Hamburg (N.M.), Germany – sequence: 6 givenname: Gerd surname: Assmann fullname: Assmann, Gerd organization: From the Department of Pediatrics (U.N.-G., M.H., H.-G.K., N.M.), the Department of Clinical Chemistry and Laboratory Medicine (R.J., G.A., A.v.E.), and the Department of Arteriosclerosis Research (R.J., G.A., A.v.E.), Westfälische Wilhelms-Universität, Münster, and the University of Hamburg (N.M.), Germany – sequence: 7 givenname: Arnold surname: von Eckardstein fullname: von Eckardstein, Arnold organization: From the Department of Pediatrics (U.N.-G., M.H., H.-G.K., N.M.), the Department of Clinical Chemistry and Laboratory Medicine (R.J., G.A., A.v.E.), and the Department of Arteriosclerosis Research (R.J., G.A., A.v.E.), Westfälische Wilhelms-Universität, Münster, and the University of Hamburg (N.M.), Germany |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1929509$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/10449697$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 1999 INIST-CNRS Copyright American Heart Association, Inc. Aug 17, 1999 |
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| Keywords | Human Vascular disease Risk factor Cardiovascular disease Exploration Thromboembolism Vein Child Lipoprotein a |
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—Serum levels of lipoprotein(a) [Lp(a)] are determined largely by genetic variation in the gene encoding for apolipoprotein(a) [apo(a)], the... Serum levels of lipoprotein(a) [Lp(a)] are determined largely by genetic variation in the gene encoding for apolipoprotein(a) [apo(a)], the specific protein... BACKGROUND: Serum levels of lipoprotein(a) [Lp(a)] are determined largely by genetic variation in the gene encoding for apolipoprotein(a) [apo(a)], the... |
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| SubjectTerms | Activated Protein C Resistance - epidemiology Adolescent Antithrombins - deficiency Apolipoproteins A - genetics Bacterial Infections - blood Bacterial Infections - epidemiology Biological and medical sciences Blood and lymphatic vessels Blood Proteins - analysis Cardiology. Vascular system Case-Control Studies Child Child, Preschool Comorbidity Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Factor V - genetics Female Genetic Predisposition to Disease Germany - epidemiology Heart Diseases - blood Heart Diseases - epidemiology Humans Infant, Newborn Lipids - blood Lipoprotein(a) - blood Lipoproteins - blood Male Medical sciences Multivariate Analysis Neoplasms - blood Neoplasms - epidemiology Rheumatic Diseases - blood Rheumatic Diseases - epidemiology Risk Factors Thromboembolism - blood Thromboembolism - epidemiology Thromboembolism - genetics Thrombophilia - blood Thrombophilia - epidemiology Thrombophilia - genetics Venous Thrombosis - blood Venous Thrombosis - epidemiology Venous Thrombosis - genetics |
| Title | Increased Lipoprotein(a) Is an Important Risk Factor for Venous Thromboembolism in Childhood |
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