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Results for “Osteoporosis, Postmenopausal”

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At least 19 recordsLinked to original sources
PubMed1976

Rehabilitation in postmenopausal osteoporosis.

Rehabilitation and nursing care of patients with postmenopausal osteoporosis require a comprehensive team effort. The primary purpose of rehabilitation is to restore these elderly women to an optimal level of well-being and activity and return them to home and community life as soon as possible. Medical management, rehabilitative nursing and physical therapy are interdependent. Emphasis is placed on estrogen replacement to prevent further fractures and height loss, individualization of care, early ambulation, improving patient confidence, physiotherapy procedures, orthopedic supports, optimal nutrition, safety precautions, work simplification, occupational therapy and the need for appropriate social contacts. The economic, physical and emotional consequences of deforming postmenopausal osteoporosis are enormous. Current research indicates that this disease is preventible. An effective program of prophylaxis is needed now; otherwise many more women will need increasing amounts of costly rehabilitation.

Diet↗
PubMed1976

Role of hormonal factors in the pathogenesis of postmenopausal osteoporosis.

In 47 women with postmenopausal osteoporosis, pretreatment studies by microradiography, radioimmunoassay and other methods showed increased bone resorption, normal bone formation, and decreased serum immunoreactive parathyroid hormone (PTH). In patients treated with a physiologic replacement dose of estrogen, bone resorption decreased to normal and PTH increased after short-term therapy; bone formation decreased to very low levels after long-term therapy. These data indicate that, in most patients, both an intrinsic abnormality of bone cell function and a disruption of the normal regulation of bone turnover by PTH and sex hormones, as a result of the menopause, are important in the pathogenesis of osteoporosis.

Bone Resorption↗
PubMed1977

Postmenopausal osteoporosis: cause, prevention and treatment.

At this point, I think I should point out that it now seems possible that postmenopausal osteoporosis, like smallpox and poliomyelitis, can be eradicated. Although full replacement doses of oestrogen prevents progression of the disease in women who have already lost a great deal of bone, this is like locking the stable door after the horse is gone. Present evidence is that smaller doses will probably suffice to prevent loss of bone at the menopause: mestranol 20 microng (Aitken et al, 1973) or conjugated oestrogens USP 0.625 mg (Meema, Bunker and Meema, 1975). The minimal prophylactic osteotrophic dose has not yet been determined since the two doses indicated were the smallest tested. These two studies provide hope that a dose can be found which will prevent postmenopausal osteoporosis without necessarily producing endometrial hyperplasia. It is very likely that the prevention of bone loss by small, prophylactic doses of oestrogen will reduce the number of fractures of vertebrae, wrists and hips so common in postmenopausal women and will reduce the mortality presently caused by hip fractures.

Age Factors↗
PubMed1978

[Incidence of lactose intolerance in postmenopausal osteoporosis].

The incidence of lactose intolerance was determined in 31 women with idiopathic postmenopausal osteoporosis. Nine subjects exhibited a pathological rise in blood glucose (less than 20 mg/100 ml) after receiving 50 g lactose. The absorption of glucose and galactose, xylose, and fat was normal in the 31 patients. Daily intake of calcium was below the normal range in 3 subjects with and in 6 subjects without lactose intolerance. The association between lactase deficiency and osteoporosis is stressed.

Adult↗
PubMed1975

Postmenopausal osteoporosis: the effect of parathormone and large dose vitamin D3 on the serum calcium level in sex hormone deficient rats.

Rats deprived of adrenal and gonadel sex hormones are more sensitive than normal rats to the hypercalcaemic (osteolytic) effect of parathormone and toxic doses of vitamin D3. It is suggested that sex hormone deficiency and the consecutive decrease of calcitonin sensitivity in postmenopausal osteoporosis makes the patients unprotected against factors inducing increased bone resorption, and this leads over the years of osteoporosis.

Adrenalectomy↗
PubMed2026

Implementing a novel digital health platform for self-management of postmenopausal osteoporosis: A qualitative study of user experiences, perspectives and implementation outcomes.

BACKGROUND: Osteoporosis self-management requires scalable support, and digital health platforms may meet this need. This study aimed to characterise the experiences and perspectives of postmenopausal women who participated in a 12-month randomised controlled trial (RCT) of a digital voice assistant (DVA) delivered osteoporosis self-management intervention, and to assess key implementation outcomes. METHODS: This was a qualitative analysis of interviews with postmenopausal women from the intervention arm (DVA group) of the RCT. The DVA program broadcast education videos, medication reminders, home-based exercise, nutrition advice and monthly quizzes through a DVA device. Semi-structured interviews were recorded, transcribed and managed in NVivo through reflexive thematic analysis, guided by the Practical Planning for Implementation and Scale-Up and Proctor's implementation outcome taxonomy frameworks. Evidence weighting summarised participant coverage and code density. RESULTS: Twenty-two of 25 (88%) DVA group participants completed semi-structured interviews. Thematic analysis identified seven themes mapped to Proctor's implementation outcomes. Evidence weighting indicated strong support for the intervention's appropriateness and acceptability, moderate support for its adoption, fidelity, feasibility and sustainability, and limited support for costs. Participants valued clear audiovisual guidance, conversation-based interactions with natural language, and flexible home-based access to self-management. CONCLUSION: Digital health platforms for osteoporosis self-management appear feasible, acceptable and sustainable among postmenopausal women. Findings indicate that these platforms are approaching readiness for evaluation in implementation-focused settings, contingent on streamlined content, reliable delivery modalities, accessible user support, clear privacy regulations and pragmatic pricing models.

Humans↗
PubMed1976

Anabolic effect of low doses of a fragment of human parathyroid hormone on the skeleton in postmenopausal osteoporosis.

Parathyroid hormone, injected daily in low dosage, exerted anabolic effects on the human skeleton, just as it does in the rat. Four postmenopausal women with primary osteoporosis were treated for six months with a synthetic fragment of human parathyroid hormone (hP.T.H. 1-34), given as a daily injection of 100 mug. This treatment caused a remarkable acceleration of bone turnover, indicated both by isotopic tracer and histological methods. At this normocalcaemic dose level, the increases in bone formation outweighed increases in resorption. Three of the four patients showed more positive calcium balances, and mean increases in calcium and phosphorus balances were statistically significant for the group as a whole, the changes being principally due to increased intestinal absorption of both elements. Many modifications of the present method of hormone administration are possible which could further increase the preponderance of anabolic effects. These results suggest that low doses of hP.T.H. 1-34, alone or in combination with other agents, may prove useful in the treatment of osteoporosis.

Absorption↗
PubMed1979

The role of growth hormone in the pathogenesis of postmenopausal osteoporosis.

The secretory response of somatotropic hormone (STH) to arginine hydrochloride stimulation (0.5 g/kg) was studied in 13 postmenopausal women. Eight showed evidence of osteoporosis, based on clinical and morphoradiological data and on metacarpal cortical thickness measurement, and five had normal bone mass. In addition, the response to levodopa (500 mg) was determined in four of the osteoporotic patients. Baseline STH concentrations in the osteoporotic subjects did not differ from those in the nonosteoporotic group, but the latter showed a significant increase over the former at 45, 60, 90, and 120 minutes after stimulation. Similar findings were obtained with levodopa stimulation. Without necessarily implying a cause-effect relationship, our data appear to support the hypothesis that the poor secretory response of STH may be to some degree responsible for the osteopenia observed during the climateric.

Adult↗
PubMed1976

Senile and postmenopausal osteoporosis.

Obviously, the relentless decrease in bone mass that accompanies aging will continue the long sought "elixir of youth" is discovered. Individuals, because of race, sex, environmental, dietary, genetic or activity differences, will be more or less predisposed to symptomatic osteoporosis with increasing age. The careful and knowledgeable physician should, however, make every attempt to rule out potentially remediable, subtle forms of demineralizing disorders, such as apathetic or T3-thyrotoxicosis, hyperparathyroidism, malabsorption and osteomalacia or multiple myeloma. Not only do these diseases result in an accelerated loss of bone mass and an increased incidence of skeletal fractures but they mimic postmenopausal or senile osteoporosis radiologically. Once the metabolic or malignant disorders of bone metabolism have been effectively considered and ruled out, the senescent or postmenopausal osteoporotic patient should be treated judiciously with short-term estrogen therapy, a diet sufficient in vitamin D and calcium content and continued attempts to insure adequate skeletal mobilization. The addition of sodium fluoride and/or calcitonin to this regimen should not be attempted without extreme caution until the potentially harmful systemic effects of prolonged therapeutic trials have been appropriately assessed.

Aged↗
PubMedDate not supplied

[Current research in therapy of postmenopausal osteoporosis (author's transl)].

The goals of osteoporosis treatment are not only to decrease bone resorption, but also and mainly to increase bone formation. Present research is based on bone histomorphometry and prospective double blind therapeutic studies. Physical exercise, adequate calcium intake oestrogen therapy in postmenopausal or oophorectomized women have been shown to be effective in prevention of the disease. A moderate beneficial effect of the association of synthetic anabolic steroids with oral calcium has been recognized. Better results are expected from combined treatments such as low doses of calcitonin and oral calcium, or vitamin D metabolites and sodium fluoride, and from stimulating bone formation by low doses of parat-hormone.

Anabolic Agents↗
PubMed1976

Etidronate disodium in postmenopausal osteoporosis.

Calcium-balance, calcium-kinetic, and physiologic observations were made in 10 osteoporotic patients treated for 6 to 12 mo with disodium etidronate (EHDP) in oral doses of 20 mg/kg/day. Absorption of EHDP averaged 10%, and effective retained dose was approximately 1.6 mg/kg/day. Patient acceptance was excellent, and there were no detectable clinical or biochemical untoward effects of treatment. Serum phosphorus was elevated on average of 1.1 mg/100 ml, and serum calcium, 0.4 mg/100 ml. EHDP reduced bone resorption by about 50% and depressed bone mineralization by almost as much. Both the total miscible calcium pool and its component compartments were smaller on EHDP, presumably because of a combination of interference with bone mineral reactivity and the decrease in mineralization rate. Urine calcium was increased by a small, but highly significant, amount, and gastrointestinal calcium absorption was also significantly increased. Calcium balance shifted slightly but significantly in the positive direction. The magnitude of these changes correlated with the urinary level of EHDP.

Aged↗
PubMed1976

Long-term prevention of postmenopausal osteoporosis by oestrogen. Evidence for an increased bone mass after delayed onset of oestrogen treatment.

Treatment of 63 oophorectomised women with oestrogen for five years prevented the reduction in bone mineral content observed in 57 women treated with a placebo preparation. When onset of therapy was delayed for three to six years there was a highly significant increase in bone mineral content mainly during the first three years of treatment. During the next two years there was no further increase in bone mineral, while the placebo-treated groups continued to lose bone at about 1% per annum. In association with the changes in bone mass, the expected biochemical effects of oestrogen therapy also persisted for at least three years, and were compatible with a prolonged increase in parathyroid activity but a reduction in bone turnover.

Adult↗
PubMed1979

Treatment of postmenopausal osteoporosis.

Bone loss can be prevented by standard oestrogen replacement therapy and delayed by the administration of calcium supplements. The most suitable patients to treat are those with a raised urinary hydroxyproline or other evidence of rapid bone loss. Patients aged below 65 years with established osteoporosis, and in whom oestrogens are not contraindicated, will derive some benefit from oestrogen therapy. In those with malabsorption of calcium, vitamin D may be added to oestrogen therapy in a dose not exceeding 10,000 units daily or alternatively, small doses of one of the vitamin D metabolites, e.g. 1 alpha OHD3 (alfacalcidol) 1 microgram daily, or 1,25(OH)2D3 (calcitriol) 0.5 microgram daily. In patients aged over 65 years, supplementary calcium (not less than 1000 mg daily) is recommended.

Calcium↗