Prevalence of the prothrombin gene variant 20210 G→A among patients with myocardial infarction

被引:44
作者
Arruda, VR
Siquiera, LH
Chiaparini, LC
Coelho, OR
Mansur, AP
Ramires, A
Annichino-Bizzacchi, JM
机构
[1] Univ Estadual Campinas, Hematol Hemotherapy Ctr, BR-13081970 Campinas, SP, Brazil
[2] Univ Sao Paulo, Inst Heart, Sao Paulo, Brazil
关键词
myocardial infarction; risk factors; prothrombin; DNA polymorphism;
D O I
10.1016/S0008-6363(97)00211-3
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: The aim of this study was to determine the prevalence of the prothrombin variant allele 20210A among survivors of myocardial infarction Background: The prothrombin gene variant has been identified as a novel genetic risk factor for venous thrombosis. However, the risk of developing arterial thrombosis as a result of the presence of this mutated allele is unknown. Methods: The G --> A transition at position 20210 of the 3'-untranslated region was determined in 220 survivors of myocardial infarction and in 295 individuals from the general population. Results: The prevalence of heterozygotes for the prothrombin mutated allele was 3% among patients with myocardial infarction and 0.7% in the general population (P = 0.03). No age-related difference in the prevalence of the mutated allele was observed. However, for individuals over 45 years old the prevalence among females was higher than among males (5% vs. 0%). Conclusion: These data suggest that being heterozygote for the allele variant 20210A of the prothrombin gene could be a genetic risk factor for developing myocardial infarction. (C) 1998 Elsevier Science B.V.
引用
收藏
页码:42 / 45
页数:4
相关论文
共 26 条
  • [1] [Anonymous], 1994, EPI INFO VERSION 6 W
  • [2] MUTATION IN BLOOD-COAGULATION FACTOR-V ASSOCIATED WITH RESISTANCE TO ACTIVATED PROTEIN-C
    BERTINA, RM
    KOELEMAN, BPC
    KOSTER, T
    ROSENDAAL, FR
    DIRVEN, RJ
    DERONDE, H
    VANDERVELDEN, PA
    REITSMA, PH
    [J]. NATURE, 1994, 369 (6475) : 64 - 67
  • [3] FAMILIAL THROMBOPHILIA DUE TO A PREVIOUSLY UNRECOGNIZED MECHANISM CHARACTERIZED BY POOR ANTICOAGULANT RESPONSE TO ACTIVATED PROTEIN-C - PREDICTION OF A COFACTOR TO ACTIVATED PROTEIN-C
    DAHLBACK, B
    CARLSSON, M
    SVENSSON, PJ
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (03) : 1004 - 1008
  • [4] THE COAGULATION CASCADE - INITIATION, MAINTENANCE, AND REGULATION
    DAVIE, EW
    FUJIKAWA, K
    KISIEL, W
    [J]. BIOCHEMISTRY, 1991, 30 (43) : 10363 - 10370
  • [5] Duncan B B, 1992, Rev Assoc Med Bras (1992), V38, P138
  • [6] THE PROTEIN-C ANTICOAGULANT PATHWAY
    ESMON, CT
    [J]. ARTERIOSCLEROSIS AND THROMBOSIS, 1992, 12 (02): : 135 - 145
  • [7] ANTITHROMBOTIC EFFECTS OF COMBINING ACTIVATED PROTEIN-C AND UROKINASE IN NONHUMAN-PRIMATES
    GRUBER, A
    HARKER, LA
    HANSON, SR
    KELLY, AB
    GRIFFIN, JH
    [J]. CIRCULATION, 1991, 84 (06) : 2454 - 2462
  • [8] GENERATION OF ACTIVATED PROTEIN-C DURING THROMBOLYSIS
    GRUBER, A
    PAL, A
    KISS, RG
    SAS, G
    GRIFFIN, JH
    [J]. LANCET, 1993, 342 (8882) : 1275 - 1276
  • [9] HAMSTEN A, 1986, BRIT HEART J, V55, P58
  • [10] INCREASED PLASMA-LEVELS OF A RAPID INHIBITOR OF TISSUE PLASMINOGEN-ACTIVATOR IN YOUNG SURVIVORS OF MYOCARDIAL-INFARCTION
    HAMSTEN, A
    WIMAN, B
    DEFAIRE, U
    BLOMBACK, M
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1985, 313 (25) : 1557 - 1563