Estrogen therapy in the prevention and management of osteoporosis

Lindsay, R

doi:10.1016/0378-5122(88)90106-5

Cited by 7 publications

(7 citation statements)

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“…It is now well recognized that the chronic hypoestrogenism in the ®rst postmenopausal years can cause a critical decrease in bone density [1±4]. Hormone replacement therapy prevents the reduction in bone density related to the postmenopausal hypoestrogenism [5,6]. However, in premenopausal oligomenorrheic women, the progressive ovarian failure is associated with a decrease in estradiol production.…”

Section: Introductionmentioning

confidence: 99%

Longitudinal Evaluation of Perimenopausal Femoral Bone Loss: Effects of a Low-Dose Oral Contraceptive Preparation on Bone Mineral Density and Metabolism

Gambacciani

Ciaponi

Cappagli

et al. 2000

Osteoporosis International

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To characterize the pattern of biochemical markers of bone metabolism and femoral bone mineral density in eumenorrheic and oligomenorrheic perimenopausal women, and assess the effects of a low-dose oral contraceptive (OC) on bone metabolism and femoral bone density, bone biochemical markers and femoral bone density (measured at the neck, Ward's triangle and trochanter regions) were evaluated in a longitudinal 2-year follow-up study. The study was conducted in healthy, normally menstruating perimenopausal women (n = 18), perimenopausal oligomenorrheic women (n = 18), and perimenopausal oligomenorrheic women treated with an OC containing 20 microg ethinylestradiol plus 0.15 mg desogestrel (n = 19). The results were analyzed by factorial or repeated measures analysis of variance, as appropriate. During the observation period, in normally menstruating women there were no changes in the menstrual cycle, plasma FSH and estradiol levels, biochemical markers of bone turnover or femoral bone density. In oligomenorrheic untreated women an increase in cycle length with a concomitant decrease in plasma estradiol and an increase in plasma FSH levels were found (p < 0.05). In this group a significant increase in urinary excretion of hydroxyproline and in plasma osteocalcin levels with a concomitant significant decrease in femoral bone density (p < 0.05) occurred. In OC-treated women, osteocalcin plasma levels and urinary excretion of hydroxyproline significantly (p < 0.05) decreased, leading to a significant (p < 0.05) increase in femoral bone density. It is concluded that perimenopausal OC administration can avoid the increase in bone turnover and the decrease in femoral bone density due to the perimenopausal impairment of ovarian function.

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Section: Introductionmentioning

confidence: 99%

Longitudinal Evaluation of Perimenopausal Femoral Bone Loss: Effects of a Low-Dose Oral Contraceptive Preparation on Bone Mineral Density and Metabolism

Gambacciani

Ciaponi

Cappagli

et al. 2000

Osteoporosis International

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“…In fact, HRT has been commonly thought to determine an increase in body weight. This concern represents one of the greatest obstacles for the acceptance and diffusion of long term HRT, which not only can alleviate subjective symptoms, but also can prevent osteoporosis and reduce the risk of cardiovascular disease (5)(6)(7)(8)(9)(10)(11)(12). The aim of the present study was to evaluate the pattern of body weight and body fat distribution in early postmenopausal women and the effects of HRT with an oral estrogenprogestin combination.…”

mentioning

confidence: 99%

Body Weight, Body Fat Distribution, and Hormonal Replacement Therapy in Early Postmenopausal Women

Gambacciani

Ciaponi

Cappagli

et al. 1997

The Journal of Clinical Endocrinology & Metabolism

250

108

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Body weight was measured, and body fat distribution was determined by dual energy x-ray in early postmenopausal women given either oral calcium (500 mg/day; control group; n ϭ 12) or hormonal replacement therapy (HRT), a combination of estradiol valerate (2 mg/day for 21 days) with cyproterone acetate (1 mg/day in the last 10 days of the treatment cycle; n ϭ 15). There were no differences in basal body weight or body fat distribution in the two groups before the study. In the control group, a significant (P Ͻ 0.05) increase in body weight (from 61.8 Ϯ 2.1 to 63.3 Ϯ 1.9 kg after 12 months) paralleled a slight, but significant (P Ͻ 0.05), increase in total body fat mass (from 23.8 Ϯ 2.2 to 24.7 Ϯ 2.2 kg), with an increase in fat in the trunk (from 10.2 Ϯ 0.4 to 11.3 Ϯ 0.4 kg; P Ͻ 0.01) and arms (from 2.4 Ϯ 0.5 to 2.7 Ϯ 0.2 kg; P Ͻ 0.05). These findings demonstrate a shift to a prevalent central android fat distribution after 12 months of observation in untreated postmenopausal women. Conversely, in the HRT group, total body bone mineral showed a significant (from 1089 Ϯ 28 to 1106 Ϯ 29 mg/cm 2 ; P Ͻ 0.05) increase after 12 months, with no significant increase in body weight (from 62.2 Ϯ 1.6 to 62.7 Ϯ 1.6 kg), and no modifications in trunk (from 10.0 Ϯ 0.2 to 9.8 Ϯ 0.3 kg) and arm (from 2.43 Ϯ 0.2 to 2.5 Ϯ 0.1 kg) fat, but a significant increase in leg fat (from 7.1 Ϯ 0.3 to 8.3 Ϯ 0.4 kg; P Ͻ 0.05). The present results suggest that HRT can counteract at least in part the postmenopausal increase in body weight and body fat and prevent central body fat distribution after menopause. (J Clin Endocrinol Metab 82: 414 -417, 1997)

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“…ERT also reduces rates of bone resorption, thereby reversing rates of osteoporosis and osteoporotic fractures, by as much as 60% [29,38,39]. Unfortunately, ERT exerts a dose-and duration-of-usedependent proliferative effect on the uterine lining and several studies have demonstrated an increased rate of endometrial cancer associated with ERT [29,37,[40][41][42].…”

Section: General Populationmentioning

confidence: 95%