Risk of venous thromboembolism associated with single and combined effects of Factor V Leiden, Prothrombin 20210A and Methylenetethraydrofolate reductase C677T: ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-07-31

AUTHORS

Benedetto Simone, Valerio De Stefano, Emanuele Leoncini, Jeppe Zacho, Ida Martinelli, Joseph Emmerich, Elena Rossi, Aaron R. Folsom, Wassim Y. Almawi, Pierre Y. Scarabin, Martin den Heijer, Mary Cushman, Silvana Penco, Amparo Vaya, Pantep Angchaisuksiri, Gulfer Okumus, Donato Gemmati, Simona Cima, Nejat Akar, Kivilcim I. Oguzulgen, Véronique Ducros, Christoph Lichy, Consuelo Fernandez-Miranda, Andrzej Szczeklik, José A. Nieto, Jose Domingo Torres, Véronique Le Cam-Duchez, Petar Ivanov, Carlos Cantu-Brito, Veronika M. Shmeleva, Mojka Stegnar, Dotun Ogunyemi, Suhair S. Eid, Nicola Nicolotti, Emma De Feo, Walter Ricciardi, Stefania Boccia

ABSTRACT

Genetic and environmental factors interact in determining the risk of venous thromboembolism (VTE). The risk associated with the polymorphic variants G1691A of factor V (Factor V Leiden, FVL), G20210A of prothrombin (PT20210A) and C677T of methylentetrahydrofolate reductase (C677T MTHFR) genes has been investigated in many studies. We performed a pooled analysis of case–control and cohort studies investigating in adults the association between each variant and VTE, published on Pubmed, Embase or Google through January 2010. Authors of eligible papers, were invited to provide all available individual data for the pooling. The Odds Ratio (OR) for first VTE associated with each variant, individually and combined with the others, were calculated with a random effect model, in heterozygotes and homozygotes (dominant model for FVL and PT20210A; recessive for C677T MTHFR). We analysed 31 databases, including 11,239 cases and 21,521 controls. No significant association with VTE was found for homozygous C677T MTHFR (OR: 1.38; 95 % confidence intervals [CI]: 0.98–1.93), whereas the risk was increased in carriers of either heterozygous FVL or PT20210 (OR = 4.22; 95 % CI: 3.35–5.32; and OR = 2.79;95 % CI: 2.25–3.46, respectively), in double heterozygotes (OR = 3.42; 95 %CI 1.64-7.13), and in homozygous FVL or PT20210A (OR = 11.45; 95 %CI: 6.79-19.29; and OR: 6.74 (CI 95 % 2.19–20.72), respectively). The stratified analyses showed a stronger effect of FVL on individuals ≤ 45 years (p value for interaction = 0.036) and of PT20210A in women using oral contraceptives (p-value for interaction = 0.045). In this large pooled analysis, inclusive of large studies like MEGA, no effect was found for C677T MTHFR on VTE; FVL and PT20210A were confirmed to be moderate risk factors. Notably, double carriers of the two genetic variants produced an impact on VTE risk significantly increased but weaker than previously thought. More... »

PAGES

621-647

References to SciGraph publications

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  • Journal

    TITLE

    European Journal of Epidemiology

    ISSUE

    8

    VOLUME

    28

    Author Affiliations

  • Institute of Public Health - Section of Hygiene, Department of Public Health, Università Cattolica del Sacro Cuore, L.go F.Vito 1, 00168, Rome, Italy
  • Institute of Hematology, Università Cattolica del Sacro Cuore, Rome, Italy
  • Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, Herlev, Denmark
  • A. Bianchi Bonomi Hemophilia and Thrombosis Center, Department of Internal Medicine and Medical Specialties, Fondazione IRCCS Ca’ Granda - Ospedale Maggiore Policlinico, Milan, Italy
  • Hôpital Européen Georges Pompidou, Service de Médecine Vasculaire, Centre Claude Bernard et Laboratoire d’Hémostase, Paris, France
  • Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN, USA
  • Department of Medical Biochemistry, Arabian Gulf University, Manama, Bahrain
  • INSERM, UMRS 1018, Villejuif, France
  • Department of Internal Medicine, VU Medical Center, PO-box 7057, 1007 MB, Amsterdam, The Netherlands
  • Department of Medicine, University of Vermont, 05446, Burlington, VT, USA
  • Medical Genetics, Clinical Chemistry and Clinical Pathology Laboratory, Niguarda Ca’ Granda Hospital, Piazza Ospedale Maggiore 3, 20100, Milan, Italy
  • Thrombosis and Hemostasis Unit, Department of Clinical Pathology, La Fe University Hospital, Valencia, Spain
  • Department of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand
  • Department of Pulmonary Diseases, Istanbul Medical Faculty, Istanbul University, Capa-Istanbul, Turkey
  • Centre for the Study of Haemostasis and Thrombosis Institute of Human Anatomy, The University of Ferrara, Ferrara, Italy
  • Department of Pediatric Molecular Genetics, Ankara University, Ankara, Turkey
  • Department of Pulmonary Medicine, Gazi University School of Medicine, Ankara, Turkey
  • Département de Biochimie, Toxicologie et Pharmacologie, Centre Hospitalier Universitaire, BP 217, 38043, Grenoble, France
  • Department of Neurology, Klinikum Memmingen, Bismarckstrasse 23, 87700, Memmingen, Germany
  • Servicio de Medicina Interna, Hospital Universitario, 12 de Octubre, Madrid, Spain
  • Department of Medicine, Jagiellonian University School of Medicine, Cracow, Poland
  • Department of of Internal Medicine, Virgen de la Luz Hospital, Cuenca, Spain
  • Grupo de Investigación en Trombosis, Hospital Universitario San Vicente de Paúl, Universidad de Antioquia, Medellín, Colombia
  • Department of Biochemistry, Toxicology and Pharmacology, Grenoble Universitary Hospital, BP 217, 38043 Grenoble, France
  • Department of Biochemistry, University of Medicine, Pleven, Bulgaria
  • Stroke Clinic, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico, Mexico
  • Russian Institute of Haematology and Transfusion, 2-nd Sovietskaya 16, St. Petersburg, Russia
  • Department of Vascular Diseases, University Medical Centre Ljubljana, Ljubljana, Slovenia
  • Perinatology Unit, Morristown Memorial Hospital, Morristown, NJ, USA
  • King Hussein Medical Center, Princess Iman Research Center for Laboratory Sciences, Amman, Jordan
  • IRCCS S. Raffaele Pisana, Rome, Italy
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s10654-013-9825-8

    DOI

    http://dx.doi.org/10.1007/s10654-013-9825-8

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1044337961

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/23900608


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    24 schema:description Genetic and environmental factors interact in determining the risk of venous thromboembolism (VTE). The risk associated with the polymorphic variants G1691A of factor V (Factor V Leiden, FVL), G20210A of prothrombin (PT20210A) and C677T of methylentetrahydrofolate reductase (C677T MTHFR) genes has been investigated in many studies. We performed a pooled analysis of case–control and cohort studies investigating in adults the association between each variant and VTE, published on Pubmed, Embase or Google through January 2010. Authors of eligible papers, were invited to provide all available individual data for the pooling. The Odds Ratio (OR) for first VTE associated with each variant, individually and combined with the others, were calculated with a random effect model, in heterozygotes and homozygotes (dominant model for FVL and PT20210A; recessive for C677T MTHFR). We analysed 31 databases, including 11,239 cases and 21,521 controls. No significant association with VTE was found for homozygous C677T MTHFR (OR: 1.38; 95 % confidence intervals [CI]: 0.98–1.93), whereas the risk was increased in carriers of either heterozygous FVL or PT20210 (OR = 4.22; 95 % CI: 3.35–5.32; and OR = 2.79;95 % CI: 2.25–3.46, respectively), in double heterozygotes (OR = 3.42; 95 %CI 1.64-7.13), and in homozygous FVL or PT20210A (OR = 11.45; 95 %CI: 6.79-19.29; and OR: 6.74 (CI 95 % 2.19–20.72), respectively). The stratified analyses showed a stronger effect of FVL on individuals ≤ 45 years (p value for interaction = 0.036) and of PT20210A in women using oral contraceptives (p-value for interaction = 0.045). In this large pooled analysis, inclusive of large studies like MEGA, no effect was found for C677T MTHFR on VTE; FVL and PT20210A were confirmed to be moderate risk factors. Notably, double carriers of the two genetic variants produced an impact on VTE risk significantly increased but weaker than previously thought.
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