Effect of hormone replacement therapy on tissue factor activity, C-reactive protein, and the tissue factor pathway inhibitor

Koh, Kwang Kon; Ahn, Jeong Yeal; Kim, Dae Sung; Han, Seung Hwan; Shin, Mi-Seung; Ryu, Won Seok; Park, G.i Soo; Ahn, Tae Hoon; Choi, I.n Suck; Shin, Eak Kyun

doi:10.1016/s0002-9149(02)03176-4

Cited by 22 publications

(24 citation statements)

References 20 publications

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“…In this regard, we recently reported that C-HRT significantly increased CRP and tissue factor activity and increased thrombosis in postmenopausal women. 9 These observations have led many investigators to suggest that the disappointing results of the recent clinical trials may be caused in part by C-HRT-induced increases in hsCRP. 3,39,40 Of interest, we observed that the highest pretreatment CRP levels increased to the least extent after C-HRT.…”

Section: Discussionmentioning

confidence: 99%

“…Assays for lipids, fibrinogen, antithrombin III, F1ϩ2, and plasminogen activator inhibitor type 1 (PAI-1) antigens were measured as previously described. 8,9,[22][23][24] In all patients, plasma was collected for the measurement of high-sensitivity C-reactive protein (hsCRP) levels by commercially available kits (Immundiagnostik CRP ELISA test). The lower limit of detection was 0.0001 mg/dL.…”

Section: Laboratory Assaysmentioning

confidence: 99%

“…The reasons may result from the effects of HRT on C-reactive protein (CRP) levels and thromboembolism risk through activating coagulation pathways evidenced by decreased antithrombin III and increased prothrombin fragment 1ϩ2 (F1ϩ2). 5,6 Activation of coagulation pathways has been detected dose-dependently in postmenopausal women treated with conjugated equine estrogen (CEE) 0.625 and 1.25 mg. 7 In this regard, we reported that conventional dosages of CEE 0.625 mg increased tissue factor activity and F1ϩ2, indicator of coagulation activation, 8,9 and observational studies demonstrated that the risk for thromboembolism increases dosedependently in postmenopausal women. 2,10,11 The apparent protective effect of CEE in the Nurses' Health Study was noted only at the 0.3 mg and 0.625 mg doses; 1.25 mg and higher doses were not cardioprotective.…”

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confidence: 95%

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Effects of Conventional or Lower Doses of Hormone Replacement Therapy in Postmenopausal Women

Koh

Shin²,

Sakuma³

et al. 2004

ATVB

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Objective-The effects of hormone replacement therapy (HRT) can affect many aspects relevant to cardiovascular disease, including vasomotor function, inflammation, and hemostasis. Recent studies have demonstrated that current doses of HRT exert a mixture of both protective and adverse effects. In the current study, we compared the effects of lower doses of HRT (L-HRT) and conventional doses of HRT (C-HRT) on a variety of relevant cardiovascular parameters. Methods and Results-This randomized, double-blind, crossover study included 57 women who received micronized progesterone 100 mg with either conjugated equine estrogen 0.625 mg (C-HRT) or 0.3 mg (L-HRT) daily for 2 months. L-HRT showed comparable effects to C-HRT on high-density lipoprotein cholesterol and triglyceride levels, but not on low-density lipoprotein cholesterol levels. C-HRT and L-HRT significantly improved the percent flow-mediated dilator response to hyperemia from baseline values (both PϽ0.001) by a similar degree (Pϭ0.719). C-HRT significantly increased high-sensitivity C-reactive protein ( Key Words: hormone replacement therapy Ⅲ lower doses Ⅲ endothelial function Ⅲ inflammation Ⅲ hemostasis Ⅲ menopause P rospective cohort surveys suggest that hormone replacement therapy (HRT) decreases the risk of coronary artery disease in relatively young and healthy postmenopausal women. 1,2 In contrast, 2 recent randomized studies, the Heart and Estrogen/progestin Replacement Study (HERS) 3 and the Women's Health Initiative (WHI), 4 reported that HRT did not reduce the risk of cardiovascular events and further demonstrated some trends toward an increased risk of cardiovascular events. The increased risk of coronary heart disease was surprising given that low-density lipoprotein (LDL) cholesterol levels decreased and that high-density lipoprotein (HDL) cholesterol levels increased. The reasons may result from the effects of HRT on C-reactive protein (CRP) levels and thromboembolism risk through activating coagulation pathways evidenced by decreased antithrombin III and increased prothrombin fragment 1ϩ2 (F1ϩ2). 5,6 Activation of coagulation pathways has been detected dose-dependently in postmenopausal women treated with conjugated equine estrogen (CEE) 0.625 and 1.25 mg. 7 In this regard, we reported that conventional dosages of CEE 0.625 mg increased tissue factor activity and F1ϩ2, indicator of coagulation activation, 8,9 and observational studies demonstrated that the risk for thromboembolism increases dosedependently in postmenopausal women. 2,10,11 The apparent protective effect of CEE in the Nurses' Health Study was noted only at the 0.3 mg and 0.625 mg doses; 1.25 mg and higher doses were not cardioprotective. 11 It has been reported that Ϸ59% of women discontinue HRT within 2 years, and the use of lower doses of HRT has been proposed to improve long-term compliance with HRT. 12 Recently, lower doses (CEE 0.3 mg) of HRT (L-HRT) demonstrated comparable effects to conventional doses (CEE 0.625 mg) of HRT (C-HRT) on menopausal symptoms, 13,14 endometria...

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Section: Discussionmentioning

confidence: 99%

Section: Laboratory Assaysmentioning

confidence: 99%

mentioning

confidence: 95%

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Effects of Conventional or Lower Doses of Hormone Replacement Therapy in Postmenopausal Women

Koh

Shin²,

Sakuma³

et al. 2004

ATVB

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“…4,7,21,22 C-reactive protein (CRP) levels were determined with an immunonephelometry system according to methods described by the manufacturer (rate nephelometry; Immage, Beckman Coulter) as previously described. 23,24 …”

Section: Laboratory Assaysmentioning

confidence: 99%

Simvastatin Combined With Ramipril Treatment in Hypercholesterolemic Patients

et al. 2004

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Abstract-Mechanisms underlying biological effects of statin and angiotensin-converting enzyme inhibitor therapies differ. Thus, we studied vascular responses to combination therapy in hypercholesterolemic patients. A randomized, double-blind, placebo-controlled, crossover trial was conducted with 50 hypercholesterolemic patients with simvastatin and either placebo or ramipril (study I) and in 45 hypercholesterolemic diabetic patients with simvastatin or ramipril with placebo or simvastatin combined with ramipril (study II) for 2 months with 2 months washout. In study I simvastatin combined with ramipril significantly reduced blood pressure after 2 months. Simvastatin alone or combined with ramipril significantly changed lipoproteins, improved percent flow-mediated dilator response to hyperemia by 30Ϯ5% and 53Ϯ6%, respectively (PϽ0.001), and reduced plasma levels of malondialdehyde by 4Ϯ7% (Pϭ0.026) and 25Ϯ4% (PϽ0.001), respectively. Monocyte chemoattractant protein-1 levels decreased by 3Ϯ3% and 12Ϯ2%, respectively (Pϭ0.049 and Pϭ0.001, respectively), C-reactive protein levels changed by 0% and 18%, respectively (Pϭ0.036 and PϽ0.001, respectively), and plasminogen activator inhibitor-1 antigen levels changed by Ϫ7Ϯ7% and 17Ϯ5%, respectively (Pϭ0.828 and PϽ0.001, respectively). In study II ramipril alone did not significantly change lipoproteins and C-reactive protein levels, however, simvastatin combined with ramipril significantly changed lipoproteins and C-reactive protein levels more than ramipril alone (PϽ0.001 and Pϭ0.048 by ANOVA, respectively). Ramipril alone or simvastatin combined with ramipril significantly improved the percent flow-mediated dilator response to hyperemia (both PϽ0.001), however, simvastatin combined with ramipril showed significantly more improvement than ramipril alone (PϽ0.001 by ANOVA). Simvastatin combined with ramipril significantly improved endotheliumdependent vasodilation and fibrinolysis potential and reduced plasma levels of oxidant stress and inflammation markers in hypercholesterolemic patients. Key Words: angiotensin-converting enzyme Ⅲ atherosclerosis Ⅲ endothelial growth factors Ⅲ hypercholesterolemia Ⅲ blood pressure L arge-scale clinical studies demonstrate that statins and angiotensin-converting enzyme (ACE) inhibitor prevent or retard the progression of coronary heart disease. 1,2 The mechanisms of this apparent benefit of these therapies may include vascular effects. Statins reduce LDL cholesterol and improve endothelial function, consistent with enhanced NO bioactivity. 3-5 ACE inhibition also improves endothelial function. 6,7 A potential mechanism of this effect is augmented NO bioactivity via diminished bradykinin degradation by ACE with activation of endothelial B 2 kinin receptors and stimulation of NO synthase activity. 8 Alternatively, ACE inhibition may diminish intracellular production of superoxide anions via reduced activity of angiotensin II-dependent oxidases in the endothelium and vascular smooth muscle, 9,10 thus protecting NO from oxidant degradatio...

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“…Assays for lipids, fibrinogen, antithrombin III, F1ϩ2, and plasminogen activator inhibitor type 1 (PAI-1) antigens were measured as previously described. [13][14][15][16][17] In all patients, plasma was collected for the measurement of highsensitivity CRP (hsCRP) levels by commercially available kits (Immundiagnostik CRP ELISA test …”

Section: Laboratory Assaysmentioning

confidence: 99%

Significant Differential Effects of Hormone Therapy or Tibolone on Markers of Cardiovascular Disease in Postmenopausal Women

Koh

Ahn

Jin

et al. 2003

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Objective-The objective was to compare the effects of tibolone and hormone therapy (HT) on lipid profile, vasodilation, and factors associated with inflammation and hemostasis. Methods and Results-Fifty-three women received micronized progesterone (MP, 100 mg) with conjugated equine estrogen (CEE, 0.625 mg) or tibolone (2.5 mg) daily for 2 months, with a 2-month washout period. Key Words: hormone therapy Ⅲ tibolone Ⅲ endothelial function Ⅲ inflammation Ⅲ hemostasis P rospective cohort surveys suggest that hormone therapy (HT) decreases the risk of coronary artery disease in relatively young and healthy postmenopausal women. 1,2 In contrast, 2 recent randomized studies, the Heart and Estrogen/ Progestin Replacement Study (HERS) 3 and the Women's Health Initiative (WHI), 4 reported that HT did not reduce the risk of cardiovascular events and, furthermore, demonstrated some trends toward an increased risk of cardiovascular events. The increased risk of coronary heart disease (CHD) was surprising, given that LDL cholesterol levels decreased and that HDL cholesterol levels increased. The reasons may result from the effects of HT on an increase in triglyceride and C-reactive protein (CRP) levels and thromboembolism risk through activating coagulation pathways, evidenced by decreased antithrombin III and increased prothrombin fragment 1ϩ2 (F1ϩ2). 5,6 Tibolone, a synthetic steroid with estrogenic, androgenic, and progestogenic properties, relieves climacteric symptoms and prevents postmenopausal bone loss. Furthermore, compared with HT, tibolone has no effect on breast cancer incidence and does not promote endometrial hyperplasia or rare vaginal bleeding. 7 Tibolone has some beneficial effects, such as reduction of triglyceride, total cholesterol, LDL cholesterol, and lipoprotein(a) levels, reducing the risk of CHD. 7 Nonetheless, its antiatherosclerotic effects have been questioned because of consistent reductions in the levels of HDL cholesterol, which has antiatherosclerotic properties. However, recent animal studies have demonstrated that the use of tibolone results in significantly less atherosclerosis than does use of placebo 8 or, at least, that use of tibolone compared with control results in no increase in coronary atherosclerosis, 9 despite a marked reduction of HDL choles-

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Effect of hormone replacement therapy on tissue factor activity, C-reactive protein, and the tissue factor pathway inhibitor

Cited by 22 publications

References 20 publications

Effects of Conventional or Lower Doses of Hormone Replacement Therapy in Postmenopausal Women

Effects of Conventional or Lower Doses of Hormone Replacement Therapy in Postmenopausal Women

Simvastatin Combined With Ramipril Treatment in Hypercholesterolemic Patients

Significant Differential Effects of Hormone Therapy or Tibolone on Markers of Cardiovascular Disease in Postmenopausal Women

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