Estrogen therapy arrests bone loss in elderly women

Quigley, M. E.; Martín, Pedro; Am, Burnier; Brooks, Patricia W.

doi:10.1016/0378-5122(88)90104-1

Cited by 22 publications

(29 citation statements)

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“…This would be in keeping with studies which showed that HRT does not decrease the rate of bone loss at the distal radius in women aged 71 -80 years 17 and possibly does not have as great an impact on reducing the relative risk of non-vertebral fracture in women over 60 years of age as it does in younger women 18 . However, because of the size of our study, the relationship between marker response and age should be regarded with caution.…”

Section: Oestradiol Implants Bone Turnover and Bone Density 817supporting

confidence: 64%

The impact of subcutaneous oestradiol implants on biochemical markers of bone turnover and bone mineral density in postmenopausal women

Pereda¹

2002

BJOG: An International Journal of Obstetrics and Gynaecology

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Objective To evaluate the anabolic effect of oestrogen on bone by comparing the response of markers of bone formation (and resorption) and bone mineral density (BMD) to subcutaneous oestradiol implants. Design One year double-blind placebo controlled randomised study.Setting Clinical research unit within a teaching hospital.Population Twenty-one hysterectomised postmenopausal women were randomised to 25 mg oestradiol implants at baseline and at six months or to have a sham procedure at baseline and six months. Methods BMD and quantitative ultrasound (QUS) were assessed at baseline and one year. Bone alkaline phosphatase (bone ALP), procollagen type I N-terminal propeptide (PINP), osteocalcin (OC), free deoxypyridinoline (iFDPD), N-telopeptide of type I collagen (NTX), serum oestradiol and intact parathyroid hormone (PTH) were measured at baseline, 4, 8, 12 and 24 weeks. Main outcome measures Percentage change markers of bone turnover and PTH and change in oestradiol levels over first six months and percentage of changes in DXA and QUS over one year. Results PINP, bone ALP and OC increased by 28%, 7% and 9%, respectively ( P < 0.01) during the first four weeks of treatment and then decreased significantly. Lumbar spine (LS) and total hip (TH) BMD increased by 5.4% and 6.0% ( P < 0.001), respectively, and femoral neck (FN) BMD by 3.7% ( P < 0.05) during the first year of treatment compared with control subjects. The peak serum oestradiol level was achieved four weeks after implant insertion. Mean PTH levels increased significantly in subjects receiving subcutaneous oestradiol. Conclusion Subcutaneous oestrogen exerted an apparent anabolic effect on bone, which was initially reflected by an increase in bone formation markers and later by a large increase in BMD.

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Section: Oestradiol Implants Bone Turnover and Bone Density 817supporting

confidence: 64%

The impact of subcutaneous oestradiol implants on biochemical markers of bone turnover and bone mineral density in postmenopausal women

Pereda¹

2002

BJOG: An International Journal of Obstetrics and Gynaecology

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“…When estrogen administration ceases, loss of bone mass continues, although whether it is at the same rate as in women of similar age who have never used estrogen (65), or at the accelerated rate that occurs just after menopause (64,66) is uncertain. A dose of 0.625 mg per day of conjugated estrogen is sufficient for protection (67).…”

Section: Hormone Replacement Therapymentioning

confidence: 99%

“…If estrogen use is started several years after menopause, it will protect against loss of bone mass as long as it is administered (66,71). However, bone lost between menopause and commencement of estrogen use will not be recovered.…”

Section: Hormone Replacement Therapymentioning

confidence: 99%

Epidemiology of Hip Fractures

Cumming

Nevitt

Cummings

1997

Epidemiologic Reviews

268

148

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“…1 Although there is strong evidence that estrogen replacement therapy reduces postmenopausal risk of cardiovascular disease 2 and osteoporosis, 3,4 the effect of estrogen replacement therapy on stroke risk and outcome is unproven. [5][6][7][8][9] There is an abundance of evidence for estrogen-derived neuroprotection in animal and in vitro models of experimental stroke.…”

mentioning

confidence: 99%

LY353381.HCl, a Selective Estrogen Receptor Modulator, and Experimental Stroke

Rossberg

Murphy

Traystman

et al. 2000

Stroke

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Background and Purpose-The impact of postmenopausal estrogen replacement therapy on stroke prevention and stroke severity remains controversial. Previously we have shown that cerebral tissue infarction volume sustained after middle cerebral artery (MCA) occlusion is smaller in female than in male animals. This protection is lost after ovariectomy but is restored by 17␤-estradiol replacement. However, the therapeutic range for estradiol is suboptimal, since only doses resulting in a narrow range of plasma levels are protective in brain. The present study tested the hypothesis that a benzothiophene analogue and selective estrogen receptor modulator, LY353381.HCl (LY), reduces tissue infarction after MCA occlusion in estrogen-deficient, ovariectomized female rats. Methods-Ovariectomized female Wistar rats received LY 10 mg/kg (nϭ16) or an equivalent volume of vehicle (nϭ14) by gavage for 5 to 8 days. Subsequently, each animal was anesthetized with halothane (1.2%) and treated with 2 hours of MCA occlusion by the intraluminal filament technique and 22 hours of recovery. Infarction volumes in the cerebral cortex and caudoputamen were determined by 2,3,5-triphenyltetrazolium chloride staining and digital image analysis. End-ischemic regional cerebral blood flow (CBF) was measured in separate animal cohorts by quantitative [ 14 C]iodoantipyrine autoradiography. Results-Caudoputamen infarction was reduced by LY treatment (49Ϯ6% versus 64Ϯ4% of ipsilateral caudoputamen inLY and vehicle groups, respectively; PϽ0.05). Cerebral cortical infarction was not different in the LY compared with vehicle group (7Ϯ3% versus 13Ϯ4% of ipsilateral cerebral cortex, respectively). Intra-ischemic blood pressure, arterial blood gases, and temporalis muscle temperature were controlled and equivalent between treatment groups. Averaged laser-Doppler flow during MCA occlusion was 36Ϯ3% of baseline in the LY group versus 29%Ϯ2% in the vehicle group. However, end-ischemic CBF or blood flow distribution within the MCA territory was not altered by LY treatment. Cortical or caudoputamen tissue volumes with end-ischemic CBF Ͻ20 mL/100 g per minute were similar in both groups. Conclusions-We conclude that LY confers neuroprotection from focal cerebral ischemia in caudoputamen in ovariectomized female rats. The mechanism of protection is not linked to preservation of ischemic cerebral blood flow, as determined by end-occlusion quantitative autoradiography. (Stroke. 2000;31:3041-3046.)Key Words: cerebral infarction Ⅲ cerebral ischemia, focal Ⅲ estrogens Ⅲ hormones Ⅲ stroke Ⅲ women C erebrovascular disease and stroke rates increase significantly in women after menopause. 1 Although there is strong evidence that estrogen replacement therapy reduces postmenopausal risk of cardiovascular disease 2 and osteoporosis, 3,4 the effect of estrogen replacement therapy on stroke risk and outcome is unproven. [5][6][7][8][9] There is an abundance of evidence for estrogen-derived neuroprotection in animal and in vitro models of experimental stroke. 10 -15 The stero...

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Estrogen therapy arrests bone loss in elderly women

Cited by 22 publications

References 0 publications

The impact of subcutaneous oestradiol implants on biochemical markers of bone turnover and bone mineral density in postmenopausal women

The impact of subcutaneous oestradiol implants on biochemical markers of bone turnover and bone mineral density in postmenopausal women

Epidemiology of Hip Fractures

LY353381.HCl, a Selective Estrogen Receptor Modulator, and Experimental Stroke

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