Classic Thrombophilias and Thrombotic Risk Among Middle‐Aged and Older Adults: A Population‐Based Cohort Study
Background Five classic thrombophilias have been recognized: factor V Leiden (rs6025), the prothrombin G20210A variant (rs1799963), and protein C, protein S, and antithrombin deficiencies. This study aimed to determine the thrombotic risk of classic thrombophilias in a cohort of middle-aged and olde...
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| Published in | Journal of the American Heart Association Vol. 11; no. 4; p. e023018 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley and Sons Inc
15.02.2022
Wiley |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2047-9980 2047-9980 |
| DOI | 10.1161/JAHA.121.023018 |
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| Abstract | Background Five classic thrombophilias have been recognized: factor V Leiden (rs6025), the prothrombin G20210A variant (rs1799963), and protein C, protein S, and antithrombin deficiencies. This study aimed to determine the thrombotic risk of classic thrombophilias in a cohort of middle-aged and older adults. Methods and Results Factor V Leiden, prothrombin G20210A and protein-coding variants in the
(protein C),
(protein S), and
(antithrombin) anticoagulant genes were determined in 29 387 subjects (born 1923-1950, 60% women) who participated in the Malmö Diet and Cancer study (1991-1996). The Human Gene Mutation Database was used to define 68 disease-causing mutations. Patients were followed up from baseline until the first event of venous thromboembolism (VTE), death, or Dec 31, 2018. Carriership (n=908, 3.1%) for disease-causing mutations in the
,
, and
genes was associated with incident VTE: Hazard ratio (HR) was 1.6 (95% CI, 1.3-1.9). Variants not in Human Gene Mutation Database were not linked to VTE (HR, 1.1; 95% CI, 0.8-1.5). Heterozygosity for rs6025 and rs1799963 was associated with incident VTE: HR, 1.8 (95% CI, 1.6-2.0) and HR, 1.6 (95% CI, 1.3-2.0), respectively. The HR for carrying 1 classical thrombophilia variant was 1.7 (95% CI, 1.6-1.9). HR was 3.9 (95% CI, 3.1-5.0) for carriers of ≥2 thrombophilia variants. Conclusions The 5 classic thrombophilias are associated with a dose-graded risk of VTE in middle-aged and older adults. Disease-causing variants in the
,
, and
genes were more common than the rs1799963 variant but the conferred genetic risk was comparable with the rs6025 and rs1799963 variants. |
|---|---|
| AbstractList | Background Five classic thrombophilias have been recognized: factor V Leiden (rs6025), the prothrombin G20210A variant (rs1799963), and protein C, protein S, and antithrombin deficiencies. This study aimed to determine the thrombotic risk of classic thrombophilias in a cohort of middle-aged and older adults. Methods and Results Factor V Leiden, prothrombin G20210A and protein-coding variants in the PROC (protein C), PROS1 (protein S), and SERPINC1 (antithrombin) anticoagulant genes were determined in 29 387 subjects (born 1923-1950, 60% women) who participated in the Malmö Diet and Cancer study (1991-1996). The Human Gene Mutation Database was used to define 68 disease-causing mutations. Patients were followed up from baseline until the first event of venous thromboembolism (VTE), death, or Dec 31, 2018. Carriership (n=908, 3.1%) for disease-causing mutations in the PROC, PROS1, and SERPINC1 genes was associated with incident VTE: Hazard ratio (HR) was 1.6 (95% CI, 1.3-1.9). Variants not in Human Gene Mutation Database were not linked to VTE (HR, 1.1; 95% CI, 0.8-1.5). Heterozygosity for rs6025 and rs1799963 was associated with incident VTE: HR, 1.8 (95% CI, 1.6-2.0) and HR, 1.6 (95% CI, 1.3-2.0), respectively. The HR for carrying 1 classical thrombophilia variant was 1.7 (95% CI, 1.6-1.9). HR was 3.9 (95% CI, 3.1-5.0) for carriers of ≥2 thrombophilia variants. Conclusions The 5 classic thrombophilias are associated with a dose-graded risk of VTE in middle-aged and older adults. Disease-causing variants in the PROC, PROS1, and SERPINC1 genes were more common than the rs1799963 variant but the conferred genetic risk was comparable with the rs6025 and rs1799963 variants.Background Five classic thrombophilias have been recognized: factor V Leiden (rs6025), the prothrombin G20210A variant (rs1799963), and protein C, protein S, and antithrombin deficiencies. This study aimed to determine the thrombotic risk of classic thrombophilias in a cohort of middle-aged and older adults. Methods and Results Factor V Leiden, prothrombin G20210A and protein-coding variants in the PROC (protein C), PROS1 (protein S), and SERPINC1 (antithrombin) anticoagulant genes were determined in 29 387 subjects (born 1923-1950, 60% women) who participated in the Malmö Diet and Cancer study (1991-1996). The Human Gene Mutation Database was used to define 68 disease-causing mutations. Patients were followed up from baseline until the first event of venous thromboembolism (VTE), death, or Dec 31, 2018. Carriership (n=908, 3.1%) for disease-causing mutations in the PROC, PROS1, and SERPINC1 genes was associated with incident VTE: Hazard ratio (HR) was 1.6 (95% CI, 1.3-1.9). Variants not in Human Gene Mutation Database were not linked to VTE (HR, 1.1; 95% CI, 0.8-1.5). Heterozygosity for rs6025 and rs1799963 was associated with incident VTE: HR, 1.8 (95% CI, 1.6-2.0) and HR, 1.6 (95% CI, 1.3-2.0), respectively. The HR for carrying 1 classical thrombophilia variant was 1.7 (95% CI, 1.6-1.9). HR was 3.9 (95% CI, 3.1-5.0) for carriers of ≥2 thrombophilia variants. Conclusions The 5 classic thrombophilias are associated with a dose-graded risk of VTE in middle-aged and older adults. Disease-causing variants in the PROC, PROS1, and SERPINC1 genes were more common than the rs1799963 variant but the conferred genetic risk was comparable with the rs6025 and rs1799963 variants. BACKGROUND: Five classic thrombophilias have been recognized: factor V Leiden (rs6025), the prothrombin G20210A variant (rs1799963), and protein C, protein S, and antithrombin deficiencies. This study aimed to determine the thrombotic risk of classic thrombophilias in a cohort of middle-aged and older adults. METHODS AND RESULTS: Factor V Leiden, prothrombin G20210A and protein-coding variants in the PROC (protein C), PROS1 (protein S), and SERPINC1 (antithrombin) anticoagulant genes were determined in 29 387 subjects (born 1923–1950, 60% women) who participated in the Malmö Diet and Cancer study (1991–1996). The Human Gene Mutation Database was used to define 68 disease-causing mutations. Patients were followed up from baseline until the first event of venous thromboembolism (VTE), death, or Dec 31, 2018. Carriership (n=908, 3.1%) for disease-causing mutations in the PROC, PROS1, and SERPINC1 genes was associated with incident VTE: Hazard ratio (HR) was 1.6 (95% CI, 1.3–1.9). Variants not in Human Gene Mutation Database were not linked to VTE (HR, 1.1; 95% CI, 0.8–1.5). Heterozygosity for rs6025 and rs1799963 was associated with incident VTE: HR, 1.8 (95% CI, 1.6–2.0) and HR, 1.6 (95% CI, 1.3–2.0), respectively. The HR for carrying 1 classical thrombophilia variant was 1.7 (95% CI, 1.6–1.9). HR was 3.9 (95% CI, 3.1–5.0) for carriers of ≥2 thrombophilia variants. CONCLUSIONS: The 5 classic thrombophilias are associated with a dose-graded risk of VTE in middle-aged and older adults. Disease-causing variants in the PROC, PROS1, and SERPINC1 genes were more common than the rs1799963 variant but the conferred genetic risk was comparable with the rs6025 and rs1799963 variants. Background Five classic thrombophilias have been recognized: factor V Leiden (rs6025), the prothrombin G20210A variant (rs1799963), and protein C, protein S, and antithrombin deficiencies. This study aimed to determine the thrombotic risk of classic thrombophilias in a cohort of middle‐aged and older adults. Methods and Results Factor V Leiden, prothrombin G20210A and protein‐coding variants in the PROC (protein C), PROS1 (protein S), and SERPINC1 (antithrombin) anticoagulant genes were determined in 29 387 subjects (born 1923–1950, 60% women) who participated in the Malmö Diet and Cancer study (1991–1996). The Human Gene Mutation Database was used to define 68 disease‐causing mutations. Patients were followed up from baseline until the first event of venous thromboembolism (VTE), death, or Dec 31, 2018. Carriership (n=908, 3.1%) for disease‐causing mutations in the PROC, PROS1, and SERPINC1 genes was associated with incident VTE: Hazard ratio (HR) was 1.6 (95% CI, 1.3–1.9). Variants not in Human Gene Mutation Database were not linked to VTE (HR, 1.1; 95% CI, 0.8–1.5). Heterozygosity for rs6025 and rs1799963 was associated with incident VTE: HR, 1.8 (95% CI, 1.6–2.0) and HR, 1.6 (95% CI, 1.3–2.0), respectively. The HR for carrying 1 classical thrombophilia variant was 1.7 (95% CI, 1.6–1.9). HR was 3.9 (95% CI, 3.1–5.0) for carriers of ≥2 thrombophilia variants. Conclusions The 5 classic thrombophilias are associated with a dose‐graded risk of VTE in middle‐aged and older adults. Disease‐causing variants in the PROC, PROS1, and SERPINC1 genes were more common than the rs1799963 variant but the conferred genetic risk was comparable with the rs6025 and rs1799963 variants. BACKGROUND: Five classic thrombophilias have been recognized: factor V Leiden (rs6025), the prothrombin G20210A variant (rs1799963), and protein C, protein S, and antithrombin deficiencies. This study aimed to determine the thrombotic risk of classic thrombophilias in a cohort of middle-aged and older adults. METHODS AND RESULTS: Factor V Leiden, prothrombin G20210A and protein-coding variants in the PROC (protein C), PROS1 (protein S), and SERPINC1 (antithrombin) anticoagulant genes were determined in 29 387 subjects (born 1923–1950, 60% women) who participated in the Malmö Diet and Cancer study (1991–1996). The Human Gene Mutation Database was used to define 68 disease-causing mutations. Patients were followed up from baseline until the first event of venous thromboembolism (VTE), death, or Dec 31, 2018. Carriership (n=908, 3.1%) for disease-causing mutations in the PROC, PROS1, and SERPINC1 genes was associated with incident VTE: Hazard ratio (HR) was 1.6 (95% CI, 1.3–1.9). Variants not in Human Gene Mutation Database were not linked to VTE (HR, 1.1; 95% CI, 0.8–1.5). Heterozygosity for rs6025 and rs1799963 was associated with incident VTE: HR, 1.8 (95% CI, 1.6–2.0) and HR, 1.6 (95% CI, 1.3–2.0), respectively. The HR for carrying 1 classical thrombophilia variant was 1.7 (95% CI, 1.6–1.9). HR was 3.9 (95% CI, 3.1–5.0) for carriers of ≥2 thrombophilia variants. CONCLUSIONS: The 5 classic thrombophilias are associated with a dose-graded risk of VTE in middle-aged and older adults. Disease-causing variants in the PROC, PROS1, and SERPINC1 genes were more common than the rs1799963 variant but the conferred genetic risk was comparable with the rs6025 and rs1799963 variants. Background Five classic thrombophilias have been recognized: factor V Leiden (rs6025), the prothrombin G20210A variant (rs1799963), and protein C, protein S, and antithrombin deficiencies. This study aimed to determine the thrombotic risk of classic thrombophilias in a cohort of middle-aged and older adults. Methods and Results Factor V Leiden, prothrombin G20210A and protein-coding variants in the (protein C), (protein S), and (antithrombin) anticoagulant genes were determined in 29 387 subjects (born 1923-1950, 60% women) who participated in the Malmö Diet and Cancer study (1991-1996). The Human Gene Mutation Database was used to define 68 disease-causing mutations. Patients were followed up from baseline until the first event of venous thromboembolism (VTE), death, or Dec 31, 2018. Carriership (n=908, 3.1%) for disease-causing mutations in the , , and genes was associated with incident VTE: Hazard ratio (HR) was 1.6 (95% CI, 1.3-1.9). Variants not in Human Gene Mutation Database were not linked to VTE (HR, 1.1; 95% CI, 0.8-1.5). Heterozygosity for rs6025 and rs1799963 was associated with incident VTE: HR, 1.8 (95% CI, 1.6-2.0) and HR, 1.6 (95% CI, 1.3-2.0), respectively. The HR for carrying 1 classical thrombophilia variant was 1.7 (95% CI, 1.6-1.9). HR was 3.9 (95% CI, 3.1-5.0) for carriers of ≥2 thrombophilia variants. Conclusions The 5 classic thrombophilias are associated with a dose-graded risk of VTE in middle-aged and older adults. Disease-causing variants in the , , and genes were more common than the rs1799963 variant but the conferred genetic risk was comparable with the rs6025 and rs1799963 variants. |
| Author | Manderstedt, Eric Khalid, Shareef Staples, Jeffrey C Shuldiner, Alan Engström, Gunnar Mitnaul, Lyndon J Melander, Olle Lattari, Michael Manoochehri, Kia Widom, Louis Salerno, William Lopez, Alexander Hawes, Alicia Blumenfeld, Andrew Beechert, Christina Padilla, Maria Sotiropoulos Krasheninina, Olga Baras, Aris Habegger, Lukas Halldén, Christer Reid, Jeffrey G Mighty, Jason Nafde, Mrunali Lind‐Halldén, Christina Polanco, Tommy Gu, Zhenhua O’Keeffe, Sean Pradhan, Manasi Abecasis, Goncalo Overton, John D Lotta, Luca A. Coppola, Giovanni Forsythe, Caitlin Schleicher, Thomas D Cantor, Michael Bai, Xiaodong Balasubramanian, Suganthi Dahlbäck, Björn Panea, Razvan Rasool, Ayesha Elf, Johan Economides, Aris Ulloa, Ricardo H Lanche, Rouel Maxwell, Evan K Boutkov, Boris Eom, Gisu Mansfield, Adam J Orelus, Max Lotta, Luca A Zöller, Bengt Svensson, Peter J. Jones, Marcus B Fuller, Erin D Wolf, Sarah E |
| AuthorAffiliation | 3 Department of Translational Medicine Lund University Skåne University Hospital Malmö Sweden 4 Regeneron Genetics Center Tarrytown NY 2 Department of Clinical Sciences Lund University Skåne University Hospital Malmö Sweden 5 Center for Primary Health Care Research Lund University and Region Skåne Malmö Sweden 1 Department of Environmental Science and Bioscience Kristianstad University Kristianstad Sweden |
| AuthorAffiliation_xml | – name: 4 Regeneron Genetics Center Tarrytown NY – name: 3 Department of Translational Medicine Lund University Skåne University Hospital Malmö Sweden – name: 2 Department of Clinical Sciences Lund University Skåne University Hospital Malmö Sweden – name: 5 Center for Primary Health Care Research Lund University and Region Skåne Malmö Sweden – name: 1 Department of Environmental Science and Bioscience Kristianstad University Kristianstad Sweden |
| Author_xml | – sequence: 1 givenname: Eric surname: Manderstedt fullname: Manderstedt, Eric organization: Department of Environmental Science and Bioscience Kristianstad University Kristianstad Sweden – sequence: 2 givenname: Christina surname: Lind‐Halldén fullname: Lind‐Halldén, Christina organization: Department of Environmental Science and Bioscience Kristianstad University Kristianstad Sweden – sequence: 3 givenname: Christer orcidid: 0000-0002-9355-3901 surname: Halldén fullname: Halldén, Christer organization: Department of Environmental Science and Bioscience Kristianstad University Kristianstad Sweden – sequence: 4 givenname: Johan surname: Elf fullname: Elf, Johan organization: Department of Clinical Sciences Lund UniversitySkåne University Hospital Malmö Sweden – sequence: 5 givenname: Peter J. orcidid: 0000-0003-2901-6877 surname: Svensson fullname: Svensson, Peter J. organization: Department of Clinical Sciences Lund UniversitySkåne University Hospital Malmö Sweden – sequence: 6 givenname: Björn surname: Dahlbäck fullname: Dahlbäck, Björn organization: Department of Translational Medicine Lund UniversitySkåne University Hospital Malmö Sweden – sequence: 7 givenname: Gunnar orcidid: 0000-0002-8618-9152 surname: Engström fullname: Engström, Gunnar organization: Department of Clinical Sciences Lund UniversitySkåne University Hospital Malmö Sweden – sequence: 8 givenname: Olle surname: Melander fullname: Melander, Olle organization: Department of Clinical Sciences Lund UniversitySkåne University Hospital Malmö Sweden – sequence: 9 givenname: Aris surname: Baras fullname: Baras, Aris organization: Regeneron Genetics Center Tarrytown NY – sequence: 10 givenname: Luca A. surname: Lotta fullname: Lotta, Luca A. organization: Regeneron Genetics Center Tarrytown NY – sequence: 11 givenname: Bengt orcidid: 0000-0002-8250-5613 surname: Zöller fullname: Zöller, Bengt organization: Center for Primary Health Care Research Lund University and Region Skåne Malmö Sweden – sequence: 12 givenname: Goncalo surname: Abecasis fullname: Abecasis, Goncalo – sequence: 13 givenname: Aris surname: Baras fullname: Baras, Aris – sequence: 14 givenname: Michael surname: Cantor fullname: Cantor, Michael – sequence: 15 givenname: Giovanni surname: Coppola fullname: Coppola, Giovanni – sequence: 16 givenname: Aris surname: Economides fullname: Economides, Aris – sequence: 17 givenname: Luca A surname: Lotta fullname: Lotta, Luca A – sequence: 18 givenname: John D surname: Overton fullname: Overton, John D – sequence: 19 givenname: Jeffrey G surname: Reid fullname: Reid, Jeffrey G – sequence: 20 givenname: Alan surname: Shuldiner fullname: Shuldiner, Alan – sequence: 21 givenname: Christina surname: Beechert fullname: Beechert, Christina – sequence: 22 givenname: Caitlin surname: Forsythe fullname: Forsythe, Caitlin – sequence: 23 givenname: Erin D surname: Fuller fullname: Fuller, Erin D – sequence: 24 givenname: Zhenhua surname: Gu fullname: Gu, Zhenhua – sequence: 25 givenname: Michael surname: Lattari fullname: Lattari, Michael – sequence: 26 givenname: Alexander surname: Lopez fullname: Lopez, Alexander – sequence: 27 givenname: Thomas D surname: Schleicher fullname: Schleicher, Thomas D – sequence: 28 givenname: Maria Sotiropoulos surname: Padilla fullname: Padilla, Maria Sotiropoulos – sequence: 29 givenname: Louis surname: Widom fullname: Widom, Louis – sequence: 30 givenname: Sarah E surname: Wolf fullname: Wolf, Sarah E – sequence: 31 givenname: Manasi surname: Pradhan fullname: Pradhan, Manasi – sequence: 32 givenname: Kia surname: Manoochehri fullname: Manoochehri, Kia – sequence: 33 givenname: Ricardo H surname: Ulloa fullname: Ulloa, Ricardo H – sequence: 34 givenname: Xiaodong surname: Bai fullname: Bai, Xiaodong – sequence: 35 givenname: Suganthi surname: Balasubramanian fullname: Balasubramanian, Suganthi – sequence: 36 givenname: Andrew surname: Blumenfeld fullname: Blumenfeld, Andrew – sequence: 37 givenname: Boris surname: Boutkov fullname: Boutkov, Boris – sequence: 38 givenname: Gisu surname: Eom fullname: Eom, Gisu – sequence: 39 givenname: Lukas surname: Habegger fullname: Habegger, Lukas – sequence: 40 givenname: Alicia surname: Hawes fullname: Hawes, Alicia – sequence: 41 givenname: Shareef surname: Khalid fullname: Khalid, Shareef – sequence: 42 givenname: Olga surname: Krasheninina fullname: Krasheninina, Olga – sequence: 43 givenname: Rouel surname: Lanche fullname: Lanche, Rouel – sequence: 44 givenname: Adam J surname: Mansfield fullname: Mansfield, Adam J – sequence: 45 givenname: Evan K surname: Maxwell fullname: Maxwell, Evan K – sequence: 46 givenname: Mrunali surname: Nafde fullname: Nafde, Mrunali – sequence: 47 givenname: Sean surname: O’Keeffe fullname: O’Keeffe, Sean – sequence: 48 givenname: Max surname: Orelus fullname: Orelus, Max – sequence: 49 givenname: Razvan surname: Panea fullname: Panea, Razvan – sequence: 50 givenname: Tommy surname: Polanco fullname: Polanco, Tommy – sequence: 51 givenname: Ayesha surname: Rasool fullname: Rasool, Ayesha – sequence: 52 givenname: William surname: Salerno fullname: Salerno, William – sequence: 53 givenname: Jeffrey C surname: Staples fullname: Staples, Jeffrey C – sequence: 54 givenname: Marcus B surname: Jones fullname: Jones, Marcus B – sequence: 55 givenname: Jason surname: Mighty fullname: Mighty, Jason – sequence: 56 givenname: Lyndon J surname: Mitnaul fullname: Mitnaul, Lyndon J |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35112923$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Contributor | Khalid, Shareef Staples, Jeffrey C Polanco, Tommy Gu, Zhenhua Pradhan, Manasi Abecasis, Goncalo Overton, John D O'Keeffe, Sean Coppola, Giovanni Shuldiner, Alan Forsythe, Caitlin Schleicher, Thomas D Cantor, Michael Bai, Xiaodong Mitnaul, Lyndon J Lattari, Michael Balasubramanian, Suganthi Manoochehri, Kia Widom, Louis Salerno, William Panea, Razvan Lopez, Alexander Hawes, Alicia Blumenfeld, Andrew Rasool, Ayesha Beechert, Christina Padilla, Maria Sotiropoulos Krasheninina, Olga Baras, Aris Economides, Aris Ulloa, Ricardo H Lanche, Rouel Maxwell, Evan K Boutkov, Boris Eom, Gisu Habegger, Lukas Mansfield, Adam J Orelus, Max Reid, Jeffrey G Lotta, Luca A Mighty, Jason Nafde, Mrunali Jones, Marcus B Fuller, Erin D Wolf, Sarah E |
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| Copyright | 2022 The Authors and Regeneron Genetics Center. Published on behalf of the American Heart Association, Inc., by Wiley. |
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| Snippet | Background Five classic thrombophilias have been recognized: factor V Leiden (rs6025), the prothrombin G20210A variant (rs1799963), and protein C, protein S,... BACKGROUND: Five classic thrombophilias have been recognized: factor V Leiden (rs6025), the prothrombin G20210A variant (rs1799963), and protein C, protein S,... |
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| SubjectTerms | Aged Anticoagulants Antithrombins Cardiology and Cardiovascular Disease Clinical Medicine Cohort Studies epidemiology Factor V - genetics Female genetics Humans Kardiologi och kardiovaskulära sjukdomar Klinisk medicin Male Medical and Health Sciences Medicin och hälsovetenskap Middle Aged Mutation natural anticoagulants Original Research Protein C - genetics Protein S - genetics Prothrombin Risk Factors thrombophilia Thrombophilia - complications Thrombosis - complications Thrombosis - epidemiology Thrombosis - genetics venous thromboembolism Venous Thromboembolism - diagnosis Venous Thromboembolism - epidemiology Venous Thromboembolism - genetics |
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| Title | Classic Thrombophilias and Thrombotic Risk Among Middle‐Aged and Older Adults: A Population‐Based Cohort Study |
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