12 Haemostatic activation in post-menopausal women taking low dose hormone therapy: less effect with transdermal administration?

Brosnan, Jeanette F.; Sheppard, B. L.; Norris, L.A.

doi:10.1016/s0049-3848(07)70057-9

Cited by 5 publications

(8 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In fact, estrogens seem to reduce fibrinogen levels, a fact which is reverted by progestagen, as observed here and in other studies. 41,[43][44][45] As in our previous study, 26 we did not detect changes in fibrinolytic activity, as evaluated by the euglobulin lysis time. Reduced PAI-1 levels and higher t-PA levels after HRT have been reported, which can increase the fibrinolytic potential in these patients.…”

Section: Group C At-iii (%)mentioning

confidence: 82%

See 1 more Smart Citation

Effect of Estrogen-Progestin Hormonal Replacement Therapy on Blood Coagulation and Fibrinolysis in Postmenopausal Women

Bonduki

Lourenço

Motta

et al. 2007

Clinics

View full text Add to dashboard Cite

Tests were performed before (T0) and after 3 (T3), 6 (T6) and 12 (T12) months of treatment. AT was determined by an amidolytic method, whereas F1+2 and TAT complex were measured by ELISA. RESULTS: There was a significant reduction in the AT level of patients who received oral CEE plus MP at T3. There was no AT reduction in patients taking either oral CEE alone or transdermal 17beta-estradiol plus MP. F1+2 increased in all patients, but it reached statistical significance only in patients receiving transdermal 17beta-estradiol MP at T3. CONCLUSIONS: The CEE associated with MP treatment may reduce AT levels, whereas unopposed CEE or transdermal 17beta-estradiol plus MP does not change AT. These changes might not be clinically relevant in the general population; however, hormonal replacement therapy may increase the risk of thrombosis in women with congenital or acquired thrombophilia.

show abstract

Section: Group C At-iii (%)mentioning

confidence: 82%

“…Other authors did not observe an increase of F1+2 or TAT in users of oral CEE or transdermal 17beta-estradiol. [40][41] The shortening of PT observed in all groups could be related to the increase in factor VII. Meade 42 observed a PT reduction, and Lindberg 33 found higher factor VII levels in women on HRT.…”

Section: Group C At-iii (%)mentioning

confidence: 89%

Effect of Estrogen-Progestin Hormonal Replacement Therapy on Blood Coagulation and Fibrinolysis in Postmenopausal Women

Bonduki

Lourenço

Motta

et al. 2007

Clinics

View full text Add to dashboard Cite

show abstract

“…In this regard, transdermal HRT avoids the first-pass effect of estrogen in the liver and decreases PAI-1 and t-PA antigen to a lesser extent than oral HRT. 18 Estrogen has been reported to have no effect or to increase 31 peripheral t-PA activity. The present study is unique in measuring the effect of 17␤-estradiol on basal vascular release of active t-PA and confirms that 17␤-estradiol has a profibrinolytic effect.…”

Section: Discussionmentioning

confidence: 99%

“…17,18,25,31,32 The route of administration also determines the effect of HRT on the fibrinolytic system. In this regard, transdermal HRT avoids the first-pass effect of estrogen in the liver and decreases PAI-1 and t-PA antigen to a lesser extent than oral HRT.…”

Section: Discussionmentioning

confidence: 99%

“…On the one hand, oral HRT increases circulating fibrin split products (FSP), concentrations of inflammatory cytokines, and C-reactive protein. [13][14][15] On the other, estradiol exerts many salutary effects on the vasculature, including improving endothelial-dependent vasodilation, 16 decreasing fibrinogen and plasminogen activator inhibitor (PAI)-1 (PAI-1), [17][18][19] increasing the secretion of nitric oxide from intact platelets, 20 and attenuating platelet-derived growth factor (PDGF) receptor-activated smooth muscle cell migration and proliferation. 21 HRT decreases circulating t-PA antigen in parallel with PAI-1 antigen, to which it is complexed.…”

mentioning

confidence: 99%

See 1 more Smart Citation

17β-Estradiol Increases Basal but Not Bradykinin-Stimulated Release of Active t-PA in Young Postmenopausal Women

et al. 2008

View full text Add to dashboard Cite

Abstract-Angiotensin-converting enzyme inhibition potentiates basal and bradykinin-stimulated tissue-type plasminogen activator (t-PA) release to a greater extent in women than in men. This study tested the hypothesis that 17␤-estradiol enhances the effect of angiotensin-converting enzyme inhibition on t-PA release in young postmenopausal women. We conducted a double-blind, prospective, crossover study in 14 young postmenopausal women (mean age 48.2Ϯ2.3 years) who were randomized to receive 17␤-estradiol (1 mg/d) or matching placebo for 4 weeks. At the end of each treatment period, we measured the effect of intraarterial infusion of bradykinin, methacholine, and nitroprusside on forearm blood flow and net t-PA release, before and during intraarterial enalaprilat (0.33 g/min/100 mL forearm volume Key Words: estradiol Ⅲ angiotensin-converting enzyme inhibition Ⅲ postmenopausal women Ⅲ plasminogen activator Ⅲ bradykinin E strogen deficiency of menopause causes vascular and metabolic changes that increase the risk for cardiovascular disease. 1,2 In contrast to observational studies that suggest that hormone replacement therapy (HRT) reduces the risk of coronary heart disease (CHD), 3-5 recent randomized controlled trials indicate that treatment with conjugated estrogen plus progestin increases the risk of pulmonary emboli, CHD, and stroke, whereas treatment with conjugated estrogen alone increases risk of stroke without affecting embolic events or risk of CHD. 6 -8 This discrepancy in results has been attributed to the type of HRT used, the timing of intervention of HRT after menopause, 9,10 or the route of administration. 11 For example, the Heart and Estrogen/progestin Replacement Study (HERS) 8 and the Women's Health Initiative (WHI) 6,7 study assessed the effect of treatment with conjugated equine estrogens, a mixture of estrogens extracted from horse urine that also contains progestins and androgens, whereas estradiol is the major endogenous estrogen. 12 Differences in the outcomes of epidemiological studies and clinical trials are best interpreted in the context of an understanding of the biological effects of estrogen. On the one hand, oral HRT increases circulating fibrin split products (FSP), concentrations of inflammatory cytokines, and C-reactive protein. [13][14][15] On the other, estradiol exerts many salutary effects on the vasculature, including improving endothelial-dependent vasodilation, 16 decreasing fibrinogen and plasminogen activator inhibitor (PAI)-1 (PAI-1), [17][18][19] increasing the secretion of nitric oxide from intact platelets, 20 and attenuating platelet-derived growth factor (PDGF) receptor-activated smooth muscle cell migration and proliferation. 21 HRT decreases circulating t-PA antigen in parallel with PAI-1 antigen, to which it is complexed. Circulating t-PA antigen does not reflect the capacity of the vasculature to release t-PA, however, and the effect of HRT or estrogen on endothelial fibrinolytic function has not been studied exten-

show abstract

Vascular Actions of Estrogens: Functional Implications

2008

View full text Add to dashboard Cite

12 Haemostatic activation in post-menopausal women taking low dose hormone therapy: less effect with transdermal administration?

Cited by 5 publications

References 0 publications

Effect of Estrogen-Progestin Hormonal Replacement Therapy on Blood Coagulation and Fibrinolysis in Postmenopausal Women

Effect of Estrogen-Progestin Hormonal Replacement Therapy on Blood Coagulation and Fibrinolysis in Postmenopausal Women

17β-Estradiol Increases Basal but Not Bradykinin-Stimulated Release of Active t-PA in Young Postmenopausal Women

Vascular Actions of Estrogens: Functional Implications

Contact Info

Product

Resources

About