The effect of various menopausal hormone therapies on markers of inflammation, coagulation, fibrinolysis, lipids, and lipoproteins in healthy postmenopausal women

Žegura, Branka; Guzic-Salobir, B; Šebeštjen, Miran; Keber, Irena

doi:10.1097/01.gme.0000198485.70703.7a

Cited by 79 publications

(58 citation statements)

References 39 publications

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“…37 An increase in plasma fibrinolytic activity primarily related to a significant increase in tissue-type plasminogen activator and a decrease in plasminogen activator inhibitor Type 1 has been observed in women receiving HRT. 9,32,36 Cerebral vasodilation 4 and transient elevation in systemic blood pressure 31 associated with HRT may additionally contribute to risk of SAH in postmenopausal women.…”

Section: Discussionmentioning

confidence: 99%

Hormone replacement therapy and the risk of subarachnoid hemorrhage in postmenopausal women

Qureshi¹,

Malik²,

Saeed³

et al. 2016

JNS

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T he risk of intracranial aneurysm formation and subarachnoid hemorrhage (SAH) is higher in postmenopausal women compared with premenopausal women. 8,13,18,19,28 Reduced levels of estrogen in postmenopausal women may increase the risk of aneurysm formation and rupture by reduction in collagen and elastin content and reduced elasticity of arterial walls. 3 In an experimental intracranial aneurysm mouse model, estrogen prevented aneurysmal rupture in ovariectomized mice. 30The protective effect of estrogen seemed to occur through activation of estrogen receptor-b, a predominant subtype of estrogen receptor in human intracranial aneurysms and cerebral arteries. Hormone replacement therapy (HRT) was associated with reduced risk of spontaneous SAH in postmenopausal women in most 19,22 but not all case control studies. 25 The Women's Health Initiative (WHI) randomized trial 33 assessed the effect of estrogen plus progestin on ischemic and hemorrhagic stroke in 608 women 50-79 years of age with an average follow-up of 5.6 years. There was a nonsignificant protective effect on hemorrhagic stroke (HR 0.82, 95% CI 0.43-1.56). However, the study was underpowered because there were only 10 SAH events among the randomized patients. A meta-analysis 24 found a small nonsignificant protective effect of HRT on risk of SAH (HR 0.8, 95% CI 0.57-1.04).We performed this study to determine the effect of abbreviatioNs HRT = hormone replacement therapy; RR = relative risk; SAH = subarachnoid hemorrhage; SE = standard error; WHI = Women's Health Initiative. obJective The incidence of subarachnoid hemorrhage (SAH) increases after menopause. Anecdotal data suggest that hormone replacement therapy (HRT) may reduce the rate of SAH and aneurysm formation in women. The goal of this study was to determine the effect of HRT on occurrence of SAH in a large prospective cohort of postmenopausal women. methods The data were analyzed for 93,676 women 50-79 years of age who were enrolled in the observational arm of the Women's Health Initiative Study. The effect of HRT on risk of SAH was determined over a period of 12 ± 1 years (mean ± SD) using Cox proportional hazards analysis after adjusting for potential confounders. Additional analysis was performed to identify the risk associated with "estrogen only" and "estrogen and progesterone" HRT among women. results Of the 93,676 participants, 114 (0.1%) developed SAH during the follow-up period. The rate of SAH was higher among women on active HRT compared with those without HRT used (0.14% vs 0.11%, absolute difference 0.03%, p < 0.0001). In unadjusted analysis, participants who reported active use of HRT were 60% more likely to suffer an SAH (RR 1.6, 95% CI 1.1-2.3). Compared with women without HRT use, the risk of SAH continued to be higher among women reporting active use of HRT (RR 1.5, 95% CI 1.0-2.2) after adjusting for age, systolic blood pressure, cigarette smoking, alcohol consumption, body mass index, race/ethnicity, diabetes, and cardiovascular disease. The risk of SAH was nonsignificantly h...

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Section: Discussionmentioning

confidence: 99%

Hormone replacement therapy and the risk of subarachnoid hemorrhage in postmenopausal women

Qureshi¹,

Malik²,

Saeed³

et al. 2016

JNS

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“…Insulin levels were also significantly lower in hormone therapy users in our data set, and a wide range of other factors may also be altered by the use of oral estrogen. For example, oral estrogen significantly increases C-reactive protein levels (50), decreases low-density lipoprotein, reduces lipoprotein(a) (50), and has a significant effect on coagulation-related proteins (51). The first-pass effect undoubtedly also causes a number of as yet undiscovered changes, and it remains unclear which factor(s) altered by the first-pass effect might be the most likely to explain the protective effects of oral estrogen + progesterone against colorectal cancer.…”

Section: Discussionmentioning

confidence: 99%

Insulin, Insulin-like Growth Factor-I, Endogenous Estradiol, and Risk of Colorectal Cancer in Postmenopausal Women

et al. 2008

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Obesity is a risk factor for colorectal cancer, and hyperinsulinemia, a common condition in obese patients, may underlie this relationship. Insulin, in addition to its metabolic effects, has promitotic and antiapoptotic activity that may be tumorigenic. Insulin-like growth factor (IGF)-I, a related hormone, shares sequence homology with insulin, and has even stronger mitogenic effects. However, few prospective colorectal cancer studies directly measured fasting insulin, and none evaluated free IGF-I, or endogenous estradiol, a potential cofactor in postmenopausal women. Therefore, we conducted a casecohort investigation of colorectal cancer among nondiabetic subjects enrolled in the Women's Health Initiative Observational Study, a prospective cohort of 93,676 postmenopausal women. Fasting baseline serum specimens from all incident colorectal cancer cases (n = 438) and a random subcohort (n = 816) of Women's Health Initiative Observational Study subjects were tested for insulin, glucose, total IGF-I, free IGF-I, IGF binding protein-3, and estradiol. Comparing extreme quartiles, insulin [hazard ratio (HR) q4-q1 , 1.73; 95% confidence interval (CI), 1.16-2.57; P trend = 0.005], waist circumference (HR q4-q1 , 1.82; 95% CI, 1.22-2.70; P trend = 0.001), and free IGF-I (HR q4-q1 , 1.35; 95% CI, 0.92-1.98; P trend = 0.05) were each associated with colorectal cancer incidence in multivariate models. However, these associations each became nonsignificant when adjusted for one another. Endogenous estradiol levels, in contrast, were positively associated with risk of colorectal cancer (HR comparing high versus low levels, 1.53; 95% CI, 1.05-2.22), even after control for insulin, free IGF-I, and waist circumference. These data suggest the existence of at least two independent biological pathways that are related to colorectal cancer: one that involves endogenous estradiol, and a second pathway broadly associated with obesity, hyperinsulinemia, and free IGF-I. [Cancer Res 2008;68(1):329-37]

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“…They detected no change in ATIII levels in their 4 groups after treatment which is supported by results of our study. Zegura et al, (2006) studied 112 postmenopausal women. They compared the influence of oral E2 with and without NETA and transdermal E2 on markers of coagulation, fibrinolysis, lipids and lipoproteins.…”

Section: Discussionmentioning

confidence: 99%

Effect of Postmenopausal Hormone Treatment on Serum Lipid Profile and Coagulation Factors

BEDEN¹

2010

jecm

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To assess the effects of different hormone treatment regimes on blood lipids, lipoproteins, ATIII, fibrinogen in postmenopausal patients. We studied retrospectively 115 patients who recieved one of four different estrogen treatment protocols. Of the 115 patiens; 25 had received transdermal estradiol patch 3.9 mg/week(TD) (Group-1), 22 patients had received TD + MPA 2.5 (Group-2), 19 patients had received oral CEE 0.625 mg/day (Group-3), 23 patients had received CEE 0.625 mg/day + MPA 2.5 mg/day (Group-4), 26 postmenopausal patients who had no hormonal treatment composed control group. Plasma cholesterol, lipids, lipoproteins, ATIII, and fibrinogen levels before and 6 months after treatment were checked from their recordings retrospectively. Serum cholesterol level increased in control group, decreased in MPA taking Group-2, and Group-4. Serum LDL level decreased significantly in Group 2, 3, and 4 while it increased insignificantly in control group. Serum HDL level increased significantly only in oral CEE taking Group-3 (24% increase). Trigliseride level significantly decreased in Group-2 (10.1% decrease). Fibrinogen decreased in all treatment groups, ATIII did not change in treatment groups but increased in control group by 22.9%. Estrogen alone or in combination with progestin effects plasma lipid levels in a positive way. It also decreases fibrinogen level that might be protective for CVD.

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The effect of various menopausal hormone therapies on markers of inflammation, coagulation, fibrinolysis, lipids, and lipoproteins in healthy postmenopausal women

Cited by 79 publications

References 39 publications

Hormone replacement therapy and the risk of subarachnoid hemorrhage in postmenopausal women

Hormone replacement therapy and the risk of subarachnoid hemorrhage in postmenopausal women

Insulin, Insulin-like Growth Factor-I, Endogenous Estradiol, and Risk of Colorectal Cancer in Postmenopausal Women

Effect of Postmenopausal Hormone Treatment on Serum Lipid Profile and Coagulation Factors

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