Effectiveness of Estrogens for Therapy of Myocardial Infarction in Middle-Age Men

Stamler, Jeremiah; Pick, Ruth; Katz, Louis N.; Pick, Alfred; Kaplan, Benjamin M.; Berkson, David M.; Century, Dolores

doi:10.1001/jama.1963.03700080040013

Cited by 136 publications

(24 citation statements)

References 11 publications

(1 reference statement)

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“…[14][15][16] Two of the trials were small and showed no clinical benefit from the reduced serum cholesterol levels obtained. The largest trial included 275 men with previous myocardial infarction randomly allocated to either placebo or mixed conjugated equine estrogens.…”

Section: Early Drug Trialsmentioning

confidence: 99%

The Success Story of LDL Cholesterol Lowering

Pedersen

2016

Circulation Research

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Abstract:We can look back at >100 years of cholesterol research that has brought medicine to a stage where people at risk of severe or fatal coronary heart disease have a much better prognosis than before. This progress has not come about without resistance. Perhaps one of the most debated topics in medicine, the cholesterol controversy, could only be brought to rest through the development of new clinical research methods that were capable of taking advantage of the amazing achievements in basic and pharmacological science after the second World War. It was only after understanding the biochemistry and physiology of cholesterol synthesis, transport and clearance from the blood that medicine could take advantage of drugs and diets to reduce the risk of atherosclerotic diseases. This review points to the highlights of the history of low-density lipoprotein-cholesterol lowering, with the discovery of the low-density lipoprotein receptor and its physiology and not only the development of statins as the stellar moments but also the development of clinical trial methodology as an effective tool to provide scientifically convincing evidence. (Circ Res. 2016;118:721-731.

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Section: Early Drug Trialsmentioning

confidence: 99%

The Success Story of LDL Cholesterol Lowering

Pedersen

2016

Circulation Research

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“…However, Premarin doses of 30 mg/day have been prescribed for certain indications and uses described therein for ''breast cancer, for palliation only, in appropriately selected women and men with metastatic disease'' [see PDR, 2006], making potential daily exposure to the sodium salt of 17a-estradiol 3-sulfate as high as 2.85 mg. As a component of Premarin, the sulfate conjugate of 17a-estradiol has been administered to both women and men for 3 months or longer. In one long-term study, the effectiveness of estrogens for therapy of myocardial infarction at doses up to 10 mg/day was studied in 275 middle-aged men during the 1950s and 1960s [see, e.g., Stamler et al, 1963].…”

Section: Marketing Experiencementioning

confidence: 99%

Review of the effects of 17α‐estradiol in humans: a less feminizing estrogen with neuroprotective potential

Moos

Dykens

Nohynek

et al. 2009

Drug Development Research

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ABSTRACT17a-Estradiol is a less feminizing isomer of the potent hormonal estrogen, 17b-estradiol. 17a-Estradiol is an orally active small molecule with conflicting reports of efficacy in preclinical models of degenerative diseases. A number of studies suggest neuroprotective potential in human neurodegenerative disorders, including Alzheimer's disease (AD) and Parkinson's disease. Several studies have established an antioxidant effect of 17a-estradiol in humans. The sodium salt of 17a-estradiol 3-sulfate is a minor component (2.5-9.5%) of several widely marketed estrogen hormone replacement products, such as Premarin s , that are approved by the U.S. Food and Drug Administration and have been prescribed and studied in women and men for more than 65 years. Most of the more than 100 published reports on the neurological effects of feminizing estrogens found positive responses in at least one measure relating to cognition or prevention and treatment of AD, notwithstanding the negative results in the Women's Health Initiative studies. Whether these limited, and often not statistically significant, findings are clinically meaningful remains unknown. In many in vitro and in vivo preclinical neuroprotection and related studies, 17a-estradiol and 17b-estradiol are active at similar concentrations and doses. However, 17a-estradiol is less pleiotropic than 17b-estradiol, and thus its potential toxicity might be lower. Given decades of mixed reports regarding the potential efficacy and safety of strongly feminizing hormones in neurodegenerative diseases, the weakly feminizing 17a-estradiol might be a suitable candidate for clinical testing of the neuroprotective potential of this chemical class because it avoids, or significantly reduces, the adverse effects of potent hormonal compounds. Drug Dev Res 70: 1-21, 2009. r

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“…33 The levels do, however, resemble those seen in humans given high dose estrogen for treatment of prostatic carcinoma 4 and myocardial infarction. 5 The latter high dose studies had to be discontinued because of an increased incidence of thromboembolic events. It may be that our data from the two month old mice is relevant to the increased thromboembolic incidence seen in humans given high dose estrogen.…”

Section: In Vitromentioning

confidence: 99%

Effects of estradiol on platelet aggregation in cerebral microvessels of mice.

Rosenblum¹,

El‐Sabban²,

Allen³

et al. 1985

Stroke

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SUMMARY Mice were implanted subcutaneously with a pellet containing 0.5 mg estradiol or with a placebo. Eight to 12 days later platelet aggregation was produced in pial arterioles by injuring their endothelium in vivo with a noxious light/dye stimulus. The time between the onset of the noxious stimulus and the appearance of platelet aggregates was significantly shortened (p < .02) by estradiol treatment in young (2 month old) mice. The same treatment had the opposite effect in 4-6 month old mice and significantly delayed the onset of aggregation (p = .01). When platelet rich plasma (PRP) was prepared, aggregation by sodium arachidonate was always inhibited in PRP from estradiol treated mice, irrespective of age. Estradiol treatment had no effect on aggregation induced ex vivo by ADP. Thus the enhanced aggregation observed in pial arterioles of young estradiol treated mice may not reflect direct effects of estradiol on the platelet itself. The data are discussed in light of the literature suggesting enhancement of ischemic vascular disease, including strokes, in patients receiving estrogens, and especially high doses of estrogens.

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Effectiveness of Estrogens for Therapy of Myocardial Infarction in Middle-Age Men

Cited by 136 publications

References 11 publications

The Success Story of LDL Cholesterol Lowering

The Success Story of LDL Cholesterol Lowering

Review of the effects of 17α‐estradiol in humans: a less feminizing estrogen with neuroprotective potential

Effects of estradiol on platelet aggregation in cerebral microvessels of mice.

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