Randomized Trial of Estrogen Plus Progestin for Secondary Prevention of Coronary Heart Disease in Postmenopausal Women

Hulley, Stephen B.; Grady, Deborah; Bush, Trudy L.; Furberg, Curt D.; Herrington, David M.; Riggs, Betty S.; Vittinghoff, Eric

doi:10.1097/00006254-199901000-00022

Cited by 651 publications

(891 citation statements)

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“…[115][116][117][118] A range of retrospective "explanations" were proposed for this apparent discrepancy with the results in the observational studies (e.g. that the wrong type of adjustment had been used or the timing of initiating treatment mattered), 119,120 but these were eventually refuted.…”

Section: Biases Due To Differences In Underlying Risks Of Health Outcmentioning

confidence: 99%

Interpretation of the evidence for the efficacy and safety of statin therapy

et al. 2016

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General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/pure/about/ebr-terms SummaryThis review is intended to help clinicians, patients and the public make informed decisions about statin therapy for the prevention of heart attacks and strokes. It explains how the evidence that is available from randomized controlled trials yields reliable information about both the efficacy and safety of statin therapy. In addition, it discusses how claims that statins commonly cause adverse effects reflect a failure to recognise the limitations of other sources of evidence about the effects of treatment.Large-scale randomized trial evidence shows that statin therapy reduces the risk of heart attacks, ischaemic strokes and coronary revascularization procedures ("major vascular events") by about one quarter for each mmol/L reduction in low density lipoprotein (LDL) cholesterol during each year (after the first) that it continues to be taken. The absolute benefits of statin therapy depend on an individual's absolute risk of occlusive vascular events and the absolute reduction in LDL cholesterol that is achieved. For example, lowering LDL cholesterol by 2 mmol/L (77 mg/dL) with an effective low-cost statin regimen (e.g. atorvastatin 40 mg daily, costing about £2 per

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Section: Biases Due To Differences In Underlying Risks Of Health Outcmentioning

confidence: 99%

Interpretation of the evidence for the efficacy and safety of statin therapy

et al. 2016

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“…Although the risk-benefit profile of menopause hormonal therapy has been established by the results of the HERS and the WHI trials (3,4), the population included in those studies does not exactly correspond with that included in this study. Our population was composed of younger women, half of whom were in the menopausal transition or in early postmenopause (28), when menopause symptoms are most severe and bone loss is accelerated.…”

Section: Discussionmentioning

confidence: 98%

“…Although menopause hormonal therapy is the most effective treatment for vasomotor and urogenital symptoms, the results of the Heart and Estrogen/Progestin Replacement Study (HERS) and the Women's Health Initiative (WHI) trials, which showed that the risks outweigh the benefits (3,4), dramatically altered the medical practices of such therapy (5). Despite a striking decrease in the use of menopause hormonal therapy, many women remain eligible for it.…”

Section: Systemic Lupus Erythematosus (Sle) Is An Autoimmune Disease mentioning

confidence: 99%

Menopause hormonal therapy in women with systemic lupus erythematosus

Sánchez‐Guerrero

González-Pérez

Durand-Carbajal

et al. 2007

Arthritis & Rheumatism

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Objective. To evaluate the effects of menopause hormonal therapy on disease activity in women with systemic lupus erythematosus (SLE).Methods. We conducted a double-blind, randomized clinical trial involving 106 women with SLE who were in the menopausal transition or in early or late postmenopause. Patients received a continuoussequential estrogen-progestogen regimen (n ‫؍‬ 52) or placebo (n ‫؍‬ 54). Disease activity was assessed at baseline and at 1, 2, 3, 6, 9, 12, 15, 18, 21, and 24 months, according to the SLE Disease Activity Index (SLEDAI). The primary outcome measure was global disease activity, estimated by measuring the area under the SLEDAI curve. Secondary outcome measures included maximum SLEDAI score, change in SLEDAI score, incidence of lupus flares, median time to flare, medication use, and adverse events. Results were studied using intent-totreat analysis.Results. At baseline, demographic and disease characteristics were similar in both groups. Mean ؎ SD SLEDAI scores were 3.5 ؎ 3.3 and 3.1 ؎ 3.4 in the menopause hormonal therapy and placebo groups, respectively (P ‫؍‬ 0.57). Disease activity remained mild and stable in both groups throughout the trial. There were no significant differences between the groups in global or maximum disease activity, incidence or probability of flares, or medication use. Median time to flare was 3 months in both groups. Thromboses occurred in 3 patients who received menopause hormonal therapy and in 1 patient who received placebo. One patient in each group died during the trial due to sepsis.Conclusion. Menopause hormonal therapy did not alter disease activity during 2 years of treatment. However, an apparently increased risk of thrombosis seems to be a real threat in women with SLE who receive menopausal hormone therapy.

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“…4,5 It is estimated that beneficial alterations in lipoproteins account for one-third of decline in coronary heart disease (CHD) incidence. 3 However, these estimations do not consider the possible genetic variation in genes in pathways of female steroid hormones that could determine a subgroup of women that would benefit more from estrogens.…”

Section: Esr2 and Pgr Variants And Lipid Levels In Women S Almeida Et Almentioning

confidence: 99%

“…2 The beneficial changes in these lipoproteins should be associated with at least 30-35% decline in coronary heart disease (CHD) incidence. 3 However, the results from the Heart and Estrogen/Progestin Replacement Study (HERS) 4 and the Women's Health Initiative (WHI) trial 5 demonstrated that oral HRT does not provide cardiovascular benefit or even some evidence of cardiovascular harm.…”

Section: Introductionmentioning

confidence: 99%

Estrogen receptor 2 and progesterone receptor gene polymorphisms and lipid levels in women with different hormonal status

et al. 2004

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Sex steroid hormones have multiple effects on lipid metabolism. We investigated the association between two common single nucleotide polymorphisms of the estrogen receptor 2 gene (ESR2), 1082G4A and 1730A4G, and PROGINS polymorphism of the progesterone receptor gene (PGR) with lipoprotein levels in a cross-sectional study with 472 women of European descent. The women were classified into three subgroups according to hormonal status, premenopausal women (n ¼ 187; mean age ¼ 3479.7 years), postmenopausal women exposed to hormone replacement therapy (HRT) (n ¼ 118; 5676.7 years) and postmenopausal women unexposed to HRT (n ¼ 167; 5879.8 years). The premenopausal and postmenopausal women exposed to HRT, both carriers of G/A genotype, exhibited LDL-C (P ¼ 0.027 and 0.001, respectively) and T-chol levels (P ¼ 0.035 and 0.001, respectively) lower than carriers of G/G genotype. This association was not observed in postmenopausal women unexposed to HRT. These results suggest that ESR2 1082G4A genotype may influence LDL-C levels in women with abundant estrogen levels, due to either endogenous or exogenous sources. INTRODUCTIONEndogenous and exogenous sex steroid hormones have multiple effects on lipid and lipoprotein metabolism. The oral estrogen replacement therapy (ERT) in postmenopausal women decreases serum total cholesterol (T-chol) and lowdensity lipoprotein cholesterol (LDL-C) concentrations, as well as increases serum high-density lipoprotein cholesterol (HDL-C) and triglyceride (TG) levels. 1 The effects of combined (estrogen plus progestin) hormone replacement therapy (HRT) are uncertain; the addition of a progestogen to estrogens tends to attenuate the increase in serum HDL-C and the decrease in LDL-C, obtained with ERT, although this effect seems to be related to the dose and to androgenic potency of the progestogen. 2 The beneficial changes in these lipoproteins should be associated with at least 30-35% decline in coronary heart disease (CHD) incidence. 3 However, the results from the Heart and Estrogen/Progestin Replacement Study (HERS) 4 and the Women's Health Initiative (WHI) trial 5 demonstrated that oral HRT does not provide cardiovascular benefit or even some evidence of cardiovascular harm.

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Randomized Trial of Estrogen Plus Progestin for Secondary Prevention of Coronary Heart Disease in Postmenopausal Women

Cited by 651 publications

References 0 publications

Interpretation of the evidence for the efficacy and safety of statin therapy

Interpretation of the evidence for the efficacy and safety of statin therapy

Menopause hormonal therapy in women with systemic lupus erythematosus

Estrogen receptor 2 and progesterone receptor gene polymorphisms and lipid levels in women with different hormonal status

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