Blood coagulation in postmenopausal women given estrogen treatment: Comparison of transdermal and oral administration

Alkjaersing, N; Ap, Fletcher; Ziegler, D. De

doi:10.1016/0378-5122(88)90053-9

Cited by 10 publications

(12 citation statements)

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“…The effects of estrogen on coagulation/fibrinolytic factors are complex and dependent on the agent, dose, and route of administration, as well as interaction with individual coagulation factors and common estrogen‐sensitive clotting mutations 56,57. In particular, it has been observed that oral estrogen is more likely than transdermal estrogen to produce a hypercoagulable state 58‐60. These factors could enhance acute arterial occlusion and thus accentuate the increase in CHD events already occurring due to an increase in rupture of preexisting non‐obtructive atherosclerotic plaques, related to the factors previously noted.…”

Section: Factors Possibly Accounting For Discordant Resultsmentioning

confidence: 97%

Is the Estrogen Controversy Over? Deconstructing the Women's Health Initiative Study: A Critical Evaluation of the Evidence

Harman

Naftolin

Brinton

et al. 2005

Annals of the New York Academy of Sciences

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The Women's Health Initiative (WHI) hormone trials have been widely interpreted as demonstrating that combined menopausal hormone therapy (HT) fails to protect against-and may increase-cardiovascular disease (CVD), stroke, and dementia in menopausal women, regardless of whether initiated early in the menopause or later. This conclusion does not agree with results of large epidemiological studies showing protection by HT and by estrogen replacement alone (ET) against CVD and dementia. One possible reason for this inconsistency is that the epidemiologic data are confounded by "healthy user bias." Another possible explanation is that most women in the observational studies initiated ET or HT at or near the menopausal transition, at which point there is little or no arterial injury, whereas, in the WHI studies, older women, averaging approximately 12 years postmenopausal, many of whom would have had significant asymptomatic atherosclerosis, were treated. Substantial data demonstrate atheropreventive effects of estrogen before vascular damage occurs, whereas adverse effects of oral estrogen on thrombosis and inflammation may predominate once complex atheromas are present. Similarly, the excess of dementia observed in older WHI women treated with oral conjugated estrogen could be due to cerebral thromboses (multi-infarct dementia). Given the uncertain relevance of the WHI (and other published randomized clinical trials) to initiation of HT in perimenopausal women, and its subsequent continuation for atheroprevention, new trials will be needed to resolve whether early intervention with estrogen may prevent CVD and/or dementia. The Kronos Early Estrogen Prevention Study (KEEPS), which began in mid-2005, is a randomized, controlled multicenter trial of HT in recently menopausal women. It will examine surrogate end points as well as risk factors for atherosclerosis.

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Section: Factors Possibly Accounting For Discordant Resultsmentioning

confidence: 97%

Is the Estrogen Controversy Over? Deconstructing the Women's Health Initiative Study: A Critical Evaluation of the Evidence

Harman

Naftolin

Brinton

et al. 2005

Annals of the New York Academy of Sciences

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“…Global coagulation tests may not detect hemostatic C Acta Obstet Gynecol Scand 77 (1998) changes that may have clinical implications, and molecular markers of blood coagulation are more appropriate for this purpose. Caine et al reported elevation of fibrinopeptide A and F1π2 after hormonal replacement therapy with oral conjugated estrogen (8), which suggests the presence of a hypercoagulable state, but it has not been observed by others (15,18).…”

Section: Discussionmentioning

confidence: 96%

“…Administration form or type of estrogen may be the causative factor. In fact, it has been observed by Akjaersig et al that the route of estrogen administration may influence the level of some coagulation factors (15). ATIII reduction does not seem to be a result of natural menopausal changes, since it increases in post menopausal women without hormonal replacement therapy, as shown by Meade et al (16).…”

Section: Discussionmentioning

confidence: 96%

Effect of estrogen‐progestin hormonal replacement therapy on plasma antithrombin III of postmenopausal women

Bonduki¹,

Lourenço

Baracat³

et al. 1998

Acta Obstet Gynecol Scand

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“…Oestrogens could act on the coagulation pathway and indirectly influence the risk of coronary heart disease. However, transdermal oestradiol therapy has been reported to have no significant effects on various haemostasis variables, in both short and long term studies (Alkjaersig et al 1988; Boschetti et al 1991; Erkkola et al 1992; Fox et al 1993; Kroon et al 1994).…”

Section: Effects Of Oestrogens On Haemodynamic Parametersmentioning

confidence: 99%

Transdermal oestradiol and cardiovascular risk factors

Cheang

Sitruk-Ware

Samsioe

1994

BJOG

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Blood coagulation in postmenopausal women given estrogen treatment: Comparison of transdermal and oral administration

Cited by 10 publications

References 0 publications

Is the Estrogen Controversy Over? Deconstructing the Women's Health Initiative Study: A Critical Evaluation of the Evidence

Is the Estrogen Controversy Over? Deconstructing the Women's Health Initiative Study: A Critical Evaluation of the Evidence

Effect of estrogen‐progestin hormonal replacement therapy on plasma antithrombin III of postmenopausal women

Transdermal oestradiol and cardiovascular risk factors

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