Estrogen replacement therapy, thrombophilia, and atherothrombosis

In a consecutive case series, cross-sectional study of 401 women referred for hyperlipidemia therapy, (110 [27%] on estrogen replacement therapy [ERT]), we assessed whether ERT-mediated thrombophilia and heritable thrombophilia (20210 G[rarr ]A prothrombin gene [PTG], Factor V Leiden gene mutation [...

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Published in:Metabolism, clinical and experimental clinical and experimental, 2002-06, Vol.51 (6), p.724-732
Main Authors: Glueck, Charles J., Wang, Ping, Fontaine, Robert N., Sieve-Smith, Luann, Lang, James E.
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cardiovascular Diseases - epidemiology
Cohort Studies
Comorbidity
Cross-Sectional Studies
Estrogen Replacement Therapy - adverse effects
Factor V - genetics
Female
Genetic Testing
Genital system. Reproduction
Heterozygote
Humans
Hyperlipidemias - epidemiology
Logistic Models
Medical sciences
Mutation
Odds Ratio
Pharmacology. Drug treatments
Prothrombin - genetics
Risk Assessment
Risk Factors
Thrombophilia - chemically induced
Thrombophilia - epidemiology
Thrombophilia - genetics
Thrombosis - epidemiology
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Summary:In a consecutive case series, cross-sectional study of 401 women referred for hyperlipidemia therapy, (110 [27%] on estrogen replacement therapy [ERT]), we assessed whether ERT-mediated thrombophilia and heritable thrombophilia (20210 G[rarr ]A prothrombin gene [PTG], Factor V Leiden gene mutation [FV]) interacted as risk factors for atherothrombotic cardiovascular disease (ATCVD). Thirty-eight percent of women (152/401) had [ge ] 1 ATCVD event, 57 (14%) had [ge ] 2 ATCVD events. Fifteen women (3.7%) were PTG heterozygotes, 24 (6.0%) were FV heterozygotes, (there was 1 double heterozygote [0.25%]); 363 (91%) were wild-type normal for both genes. Of the 152 women with [ge ] 1 ATCVD event, 21 (14%) had [ge ] 1 thrombophilic gene mutation, versus 17/249 (7%) without events (X 2 = 5.4, P = .02). In women on ERT and with both genes wild-type normal, 23 of 96 (24%) had [ge ] 1 ATCVD event versus 8 of 14 (57%) on ERT and with [ge ] 1 thrombophilic mutation, X 2 = 6.6, P = .01. By stepwise logistic regression, in 401 women (152 with [ge ] 1 ATCVD event, 249 no events), positive explanatory variables for ATCVD included FV and/or PTG (risk odds ratio, 2.59, 95% confidence interval [CI] 1.26 to 5.36, P = .01) and a PTG*ERT interaction term (risk odds ratio, 2.27, 95% CI 1.36 to 3.79, P = .0017). After deleting 23 FV heterozygotes and 14 PTG heterozygotes and 1 double heterozygote from the 401 women, ERT was protective against ATCVD events, with a risk odds ratio of 0.50 and 95% CI of 0.29 to 0.87 P = .014. PTG and FV may increase risk for ATCVD, particularly in the presence of ERT, whereas ERT may be protective against ATCVD when PTG and FV are absent.
ISSN:0026-0495
1532-8600
DOI:10.1053/meta.2002.32729