Plasma homocysteine and the risk of venous thromboembolism: insights from the FIELD study
Field | Value | Language |
dc.contributor.author | Herrman, Marcus | |
dc.contributor.author | Whiting, Malcom J | |
dc.contributor.author | Veillard, Anne-Sophie | |
dc.contributor.author | Ehnholm, Christian | |
dc.contributor.author | Sullivan, David R | |
dc.contributor.author | Keech, Anthony C | |
dc.date.accessioned | 2016-02-09 | |
dc.date.available | 2016-02-09 | |
dc.date.issued | 2012-07-15 | |
dc.identifier.citation | Herrmann M, Whiting MJ, Veillard AS, Ehnholm C, Sullivan DR, Keech AC, investigators Fs. Plasma homocysteine and the risk of venous thromboembolism: insights from the FIELD study. Clinical Chemistry and Laboratory Medicine 2012; 50(12): 2213–2219. 10.1515/cclm-2012-0078 | en_AU |
dc.identifier.uri | http://hdl.handle.net/2123/14342 | |
dc.description.abstract | Background The lipid-lowering effect of fenofibrate is accompanied by a rise in plasma homocysteine, a potential risk factor for venous thromboembolism (VTE). This study investigated the relationship between homocysteine and the risk of VTE in patients treated with fenofibrate. Methods and results The relationship between homocysteine and deep-vein thrombosis or pulmonary embolism was investigated in 9522 participants of the 5-year Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial. All subjects received fenofibrate during a 6-week active run-in phase before randomization. A Cox proportional-hazards model was used to assess the effect of homocysteine on risk of venous thromboembolic events. During active-drug run-in, homocysteine rose on average by 6.5 μmol/L, accompanied by a substantial rise in plasma creatinine (+12%). Fenofibrate-induced changes in homocysteine and creatinine were fully reversible in the placebo group but persisted in the treatment group until reversing at the end of therapy. During follow-up, 1.8% had at least one episode of deep-vein thrombosis or pulmonary embolism: 103 on fenofibrate and 68 on placebo (log-rank P=0.006). In multivariate analysis, every 5 µmol/L higher baseline homocysteine was associated with 19% higher risk of VTE. Fenofibrate treatment was associated with 52% higher risk, but the change in homocysteine with fenofibrate was not significantly associated with VTE after adjustment for baseline homocysteine. Conclusions Hyperhomocysteinemia is prospectively associated with VTE. Fenofibrate may predispose individuals with high pretreatment homocysteine towards VTE. The fenofibrate-induced increase in homocysteine did not, however, explain the risk associated with fenofibrate therapy. | en_AU |
dc.language.iso | en | en_AU |
dc.publisher | Walter de Gruyter | en_AU |
dc.relation | NHMRC Program Grant 1037786 | en_AU |
dc.subject | thrombosis | en_AU |
dc.subject | homocysteine | en_AU |
dc.subject | fenofibrate | en_AU |
dc.subject | diabetes mellitus | en_AU |
dc.subject | pulmonary embolism | en_AU |
dc.subject | fibrate | en_AU |
dc.title | Plasma homocysteine and the risk of venous thromboembolism: insights from the FIELD study | en_AU |
dc.type | Article | en_AU |
dc.type.pubtype | Post-print | en_AU |
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