Effects of body iron stores and haemochromatosis genotypes on coronary heart disease outcomes in the Busselton health study

被引:25
作者
Fox, CJ
Cullen, DJ
Knuiman, MW
Cumpston, GN
Divitini, ML
Rossi, E
Gochee, PA
Powell, LW
Olynyk, JK
机构
[1] Fremantle Hosp, Dept Gastroenterol, Fremantle, WA, Australia
[2] Univ Western Australia, Dept Med, Nedlands, WA 6009, Australia
[3] Univ Western Australia, Dept Publ Hlth, Nedlands, WA 6009, Australia
[4] Perth Cardiovasc Inst, Nedlands, WA, Australia
[5] Busselton Populat Med Res Fdn, Perth, WA, Australia
[6] Queen Elizabeth II Med Ctr, Pathctr, Perth, WA, Australia
[7] Western Australian Inst Med Res, Brisbane, Qld, Australia
[8] Queensland Inst Med Res, Brisbane, Qld 4006, Australia
[9] Univ Queensland, Brisbane, Qld, Australia
来源
JOURNAL OF CARDIOVASCULAR RISK | 2002年 / 9卷 / 05期
关键词
myocardial infarction; angina; genes; iron; HFE gene; coronary heart disease; haemochromatosis;
D O I
10.1097/00043798-200210000-00010
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background Increased iron stores and haemochromatosis gene mutations may be risk factors for coronary heart disease. The aims of this study:were to determine in a stable community population whether increased iron stores or haemochromatosis gene mutations were risk factors for coronary heart disease. Design Cross-sectional and prospective cohort studies. Methods We evaluated 1185 men and 1141 women aged 20-79 years of predominantly Anglo-Celtic descent from the 1994-95 assessment of the Busselton population in Western Australia. Subjects underwent haemochromatosis genotyping, serum iron studies, clinical, biochemical and ECG evaluation for coronary heart disease and associated risk factors. Hospital admissions or death from cardiovascular disease were determined by linkage with the Western Australian morbidity and mortality database. The study design was cross-sectional for the 1994-95 cohort comparing coronary heart disease cases with unaffected subjects and unaffected subjects were followed prospectively until December 1998. Results Cross-sectional and prospective cohort analyses demonstrated that elevated serum iron parameters or possession of either the C282Y or H63D mutations in the HFE gene were not predictive of increased risk for coronary heart disease in men or women. Conclusions Increased iron stores or haemochromatosis gene mutations are not significant risk factors for coronary heart disease. J Cardiovasc Risk 9 : 287-293 (C) 2002 Lippincott Williams Wilkins.
引用
收藏
页码:287 / 293
页数:7
相关论文
共 34 条
  • [1] HFE genotype in patients with hemochromatosis and other liver diseases
    Bacon, BR
    Olynyk, JK
    Brunt, EM
    Britton, RS
    Wolff, RK
    [J]. ANNALS OF INTERNAL MEDICINE, 1999, 130 (12) : 953 - 962
  • [2] Haemochromatosis gene mutations and risk of coronary artery disease
    Battiloro, E
    Ombres, D
    Pascale, E
    D'Ambrosio, E
    Verna, R
    Arca, M
    [J]. EUROPEAN JOURNAL OF HUMAN GENETICS, 2000, 8 (05) : 389 - 392
  • [3] THE ELECTROCARDIOGRAM IN POPULATION STUDIES - A CLASSIFICATION SYSTEM
    BLACKBURN, H
    KEYS, A
    SIMONSON, E
    RAUTAHARJU, P
    PUNSAR, S
    [J]. CIRCULATION, 1960, 21 (06) : 1160 - 1175
  • [4] Bozzini C, 2002, CLIN CHEM, V48, P622
  • [5] Neonatal screening for the hemochromatosis defect
    Cullen, LM
    Summerville, L
    Glassick, TV
    Crawford, DHG
    Powell, LW
    Jazwinska, EC
    [J]. BLOOD, 1997, 90 (10) : 4236 - 4237
  • [6] Coronary heart disease and iron status - Meta-analyses of prospective studies
    Danesh, J
    Appleby, P
    [J]. CIRCULATION, 1999, 99 (07) : 852 - 854
  • [7] A novel MHC class I-like gene is mutated in patients with hereditary haemochromatosis
    Feder, JN
    Gnirke, A
    Thomas, W
    Tsuchihashi, Z
    Ruddy, DA
    Basava, A
    Dormishian, F
    Domingo, R
    Ellis, MC
    Fullan, A
    Hinton, LM
    Jones, NL
    Kimmel, BE
    Kronmal, GS
    Lauer, P
    Lee, VK
    Loeb, DB
    Mapa, FA
    McClelland, E
    Meyer, NC
    Mintier, GA
    Moeller, N
    Moore, T
    Morikang, E
    Prass, CE
    Quintana, L
    Starnes, SM
    Schatzman, RC
    Brunke, KJ
    Drayna, DT
    Risch, NJ
    Bacon, BR
    Wolff, RK
    [J]. NATURE GENETICS, 1996, 13 (04) : 399 - 408
  • [8] Franco RF, 1998, BRIT J HAEMATOL, V102, P1172
  • [9] A population-based study of the biochemical and clinical expression of the H63D hemochromatosis mutation
    Gochee, PA
    Powell, LW
    Cullen, DJ
    Du Sart, D
    Rossi, E
    Olynyk, JK
    [J]. GASTROENTEROLOGY, 2002, 122 (03) : 646 - 651
  • [10] Association studies between haemochromatosis gene mutations and the risk of cardiovascular diseases
    Hetet, G
    Elbaz, A
    Gariepy, J
    Nicaud, V
    Arveiler, D
    Morrison, C
    Kee, F
    Evans, A
    Simon, A
    Amarenco, P
    Cambien, F
    Grandchamp, B
    [J]. EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 2001, 31 (05) : 382 - 388