Disease relevance of Hormone Replacement Therapy

• 5. The type of estrogen used and the addition of progestins to hormone-replacement therapy may alter the risk of breast cancer [1].
• CONTEXT: Estrogens are known to be prothrombotic, and findings from the Heart and Estrogen/progestin Replacement Study suggest that in women with clinically recognized heart disease, hormone replacement therapy (HRT) may be associated with early harm and late benefit in terms of coronary events [2].
• Effects of hormone replacement therapy and antioxidant vitamin supplements on coronary atherosclerosis in postmenopausal women: a randomized controlled trial [3].
• However, combined hormone replacement therapy is more frequently used owing to the risk of uterine cancer with estrogen-only therapy [4].
• P4 is used therapeutically to oppose the effect of E2 during hormone replacement therapy and in the treatment of uterine adenocarcinoma [5].

Psychiatry related information on Hormone Replacement Therapy

• Effect of short-term hormone replacement therapy on breast cancer risk reduction after bilateral prophylactic oophorectomy in BRCA1 and BRCA2 mutation carriers: the PROSE Study Group [6].
• The current data from humans suggest that the use of estrogen hormone-replacement therapy (HRT) in healthy, postmenopausal women might reduce the risk of developing Alzheimer's disease (AD) and preserve certain aspects of cognitive function [7].
• Additional adjustment for body mass index, physical activity, hormone replacement therapy, multivitamin intake and intake of saturated fat, vitamin C, vitamin E and folate did not change the results [8].
• Carcinoma developed in one patient in the estrogen replacement therapy group in the contralateral breast after 4 years of hormone replacement therapy; she is living and well 2.5 years later with no evidence of disease [9].
• Sociodemographic characteristics, smoking and alcohol drinking habits, marital status, education level, urine thiocyanate concentrations, and specifically in women, parity and previous or current use of oral contraceptives and hormone replacement therapy, were considered as candidate risk factors for multivariable statistical tests [10].

High impact information on Hormone Replacement Therapy

• We studied the effects of hormone-replacement therapy on PAI-1 levels [11].
• To examine the associations of hormone-replacement therapy with concentrations of plasma lipids and hemostatic factors, fasting serum concentrations of glucose and insulin, and blood pressure, we studied 4958 postmenopausal women participating in a population-based investigation [12].
• These findings emphasize the importance of hormone-independent activation of the estrogen receptor, and have implications for the therapeutic use of estrogens, such as hormone replacement therapy [13].
• This section summarizes the results of the seven systematic reviews of osteoporosis therapies published in this series [calcium, vitamin D, hormone replacement therapy (HRT), alendronate, risedronate, raloxifene, and calcitonin] and systematic reviews of etidronate and fluoride we have published elsewhere [14].
• Mean (SD) increases in bone mass at the hip in women treated with alendronate alone were significantly greater than in those treated with hormone replacement therapy alone (4.2% [3.8] vs 3.0% [4.9]; P<.05, respectively), and alendronate resulted in more responders to therapy [15].

Chemical compound and disease context of Hormone Replacement Therapy

• BACKGROUND: Recent studies suggest that the use of combined estrogen and progestin hormone replacement therapy is associated with an increased risk of invasive lobular carcinoma (ILC), but that it has little association with risk of invasive ductal carcinoma (IDC) [16].
• Prevention of postmenopausal bone loss using tibolone or conventional peroral or transdermal hormone replacement therapy with 17beta-estradiol and dydrogesterone [17].
• RESULTS: Hormone replacement therapy, alendronate therapy, and raloxifene therapy have similar predicted efficacies in preventing hip fractures (estimated relative risk, 0.57, 0.54, and 0.58, respectively) [18].
• Calcitriol and hormone-replacement therapy (HRT) have been shown to maintain bone mineral density (BMD) in certain patients with end-stage renal disease (ESRD) [19].
• Factors associated with a reduced risk of ICH were a history of cardiovascular disease, arthritis, or high cholesterol level; being moderately overweight or using hormone replacement therapy; and drinking coffee [20].

Biological context of Hormone Replacement Therapy

• FINDINGS: Patients taking hormone-replacement therapy and PTH (1-34) had continuous increase in vertebral bone-mineral density during the 3 years, whereas there was no significant change in the control group [21].
• As a model for the menopause, these results also suggest that the long-term administration of hormone replacement therapy would result in endothelium-dependent arterial relaxation, an observation previously attributed only to the acute administration of estrogen [22].
• Effect of long-term hormone replacement therapy on atherosclerosis progression in postmenopausal women relates to functional apolipoprotein e genotype [23].
• Our data suggest that continuously applied dydrogesterone in combined hormone replacement therapy does not annihilate the beneficial effects on bone remodeling and lipid metabolism induced by estrogens [24].
• We have investigated the effects of testosterone implant therapy on arterial reactivity encompassing endothelial-dependent and -independent vasodilation in women using hormone replacement therapy (HRT) [25].

Anatomical context of Hormone Replacement Therapy

• OBJECTIVES: The study objective was to clarify in a randomized, controlled, observer-blind trial whether hormone replacement therapy (HRT) improves elastic properties of the common carotid artery in women with signs of subclinical atherosclerosis, especially in subgroups with increased risk, and whether less progestin enhances the effect [26].
• Cell adhesion molecules in relation to simvastatin and hormone replacement therapy in coronary artery disease [27].
• Combination therapy compared with hormone replacement therapy/estrogen replacement therapy alone produced a significantly greater response in trochanter (P = 0.007) and total hip bone mineral density (P = 0.0017) [28].
• No patient with a microprolactinoma required hormone replacement therapy, in contrast to patients with macroprolactinomas, who required thyroid, testosterone, and/or glucocorticoid replacement therapy [29].
• We have thus investigated the possibility of replacing the progestin in hormone replacement therapy by a novel selective estrogen receptor (ER) modulator having potent and pure antiestrogenic activity in the mammary gland and uterus [30].

Associations of Hormone Replacement Therapy with chemical compounds

• Using cross-sectional data, we classified the women into four groups according to their use of hormone-replacement therapy: current users of estrogen alone, current users of estrogen with progestin, nonusers who had formerly used these hormones, nonusers who had never used them [12].
• OBJECTIVE: To identify the effects of raloxifene on markers of cardiovascular risk in postmenopausal women, and to compare them with those induced by hormone replacement therapy (HRT) [31].
• This effect was seen as early as 12 weeks (median reduction in CRP with pravastatin, 14.7%; P<.001) and was present among all prespecified subgroups according to sex, age, smoking status, body mass index, baseline lipid levels, presence of diabetes, and use of aspirin or hormone replacement therapy [32].
• Susceptibility to the breast cancer-enhancing effect of alcohol may also be affected by other dietary factors (such as low folate intake), lifestyle habits (such as use of hormone replacement therapy), or biological characteristics (such as tumor hormone receptor status) [33].
• Monkeys were ovariectomized and divided randomly into two groups, one receiving 17 beta-estradiol and cyclic progesterone treatment (n = 9) and ovariectomized controls receiving no hormone replacement therapy (n = 8) [34].

Gene context of Hormone Replacement Therapy

• They also underline the key role of ERalpha in brain macrophage reactivity and hint toward the usefulness of ERalpha-specific drugs in hormone replacement therapy of inflammatory diseases [35].
• Fifty-one postmenopausal women with glucocorticoid-induced osteoporosis were randomized to receive 12 months of 400 U hPTH (1-34) ( approximately 40 microg) daily and standard hormone replacement therapy, or hormone replacement therapy alone [36].
• The purpose of this study was to evaluate the relationships among hepatic lipase (HL) polymorphism, serum lipids, lipoproteins, and remnant-like particle cholesterol (RLP-C) and to determine the effects of hormone replacement therapy (HRT) [37].
• In postmenopausal women not treated with hormones, a significant reduction in endometrial and myometrial expression of eNOS occurred, which was reversed by continuous hormone replacement therapy [38].
• We have previously shown that natural and synthetic progestins, including those used in hormone replacement therapy and oral contraception, induce the synthesis and secretion of VEGF in a subset of human breast cancer cells in a progesterone receptor-dependent manner [39].

Analytical, diagnostic and therapeutic context of Hormone Replacement Therapy

• RECENT FINDINGS: Studies have unveiled new aspects of estrogen action in the cardiovascular system; however, clinical trials have not demonstrated a protective effect of the most widely used modalities of hormone replacement therapy against cardiovascular disease [40].
• Crucially, oral but not transdermal hormone-replacement therapy increases activated protein C resistance independently of the presence of factor V Leiden. This effect increases the risk of venous thromboembolic events, which is reflected in the results of a hospital case control study of thromboembolism [41].
• Recent epidemiological studies have suggested that estrogen, as hormone replacement therapy in postmenopausal women, may be protective against Alzheimer's disease; the biological basis for a potential neuroprotective effect of estrogen in humans is an area of intense current research [42].
• Sixty postmenopausal women (age range, 44-77 years) were grouped according to HRT received: estrogen replacement therapy (ERT) (n = 13), combined (estrogen and progesterone) replacement therapy (CRT) (n = 16), selective estrogen receptor modulator (SERM) therapy (n = 8), and no (hormone replacement) therapy (NT) (n = 23) [43].
• The Serum CrossLaps One Step ELISA was capable of detecting a highly significant (P <0.001) effect of hormone replacement therapy in a retrospective study involving 22 postmenopausal women [44].

References