Osteoporosis calcium therapy

Adequate calcium and vitamin D intake is essential in the prevention and treatment of osteoporosis. Calcium and vitamin D supplements to meet requirements should be added to all drug therapy regimens for osteoporosis. 

Once bone loss is sufficient to result in a compression fracture, pharmacological therapy is much less effective. However, even after fractures have occurred, the use of the bisphosphonates and rPTH has been shown to increase bone densities and reduce the rate of subsequent fractures. Nasal calcitonin (200 units daily) is effective in promoting fracture healing and also exhibits an analgesic effect by reducing pain in persons with acute lumbar compression fractures. Whatever compound is used for prophylaxis or treatment of osteoporosis, calcium and Ds supplementation are required for maximum benefit. 

Sunyecz JA, Weisman SM. The role of calcium in osteoporosis drug therapy. J Womens Health. 2005 14 180-192. 

Calcitonin therapy results in decreased bone resorption. Osteoclasts have calcitonin receptors and calcitonin inhibits their activity. Sodium fluoride stimulates bone formation by unknown mechanisms. In women with osteoporosis, fluoride therapy produced an increased bone mineral density but no reduction in the rate of vertebral fractures. Other drugs known as selective estrogen receptor modulators (raloxifene, droloxifene, idoxifene, and levormeloxifene) may provide an alternative to estrogen replacement therapy (Chapter 34). Administration of low doses of PTH [or recombinant PTH( 1 -34)] does not affect serum calcium concentration, promotes bone formation, and increases mineral density. This anabolic action of PTH is probably mediated by decreasing osteoblast apoptosis. 

Patients with IBD, particularly those with CD, are also at risk for bone loss. This may be a function of malabsorption or an effect of repeated courses of corticosteroids. Patients with IBD should receive a baseline bone density measurement prior to receiving corticosteroids. Vitamin D and calcium supplementation should be used in all patients receiving long-term corticosteroids. Oral bisphosphonate therapy may also be considered in patients receiving prolonged courses of corticosteroids or in those with osteopenia or osteoporosis. 

Hormone-replacement therapy is also indicated for the prevention of osteoporosis but is not recommended for longterm use. Alternatives such as bisphosphonates or raloxifene should be considered as first-line therapy for the prevention of osteoporosis, in addition to appropriate doses of calcium and vitamin D. 

BMD will increase and the risk of fractures will decrease in women taking HRT. However, when therapy is discontinued, a decline in BMD will resume at the same rate as in women not on HRT. Therefore, therapy for osteoporosis prevention should be considered long term. Since HRT should be maintained only for the short term, alternative therapies such as bisphosphonates or raloxifene should be considered as first-line therapy for the prevention of postmenopausal osteoporosis, in addition to appropriate doses of calcium and vitamin D. Because of the risks associated with HRT, it should not be prescribed solely for the prevention of osteoporosis. 

Osteoporosis Oral calcium supplementation (1000-5000 mg/day) Oral vitamin D Calcifediol (1000 lU/day) Calcitriol (0.5 mcg/day) Hormone-replacement therapy Calcitonin or oral bisphosphonates If daily intake less than 1000 mg elemental calcium Documented deficiency If kidney functioning If kidney not functioning Post-menopausal women without contraindications Documented loss in bone mineral density greater than 3% Data lacking for bisphosphonates in patients with Rl... 

Age, calcium intake, hormonal status, exercise and vitamin status have all been implicated in the development of osteoporosis. Estrogen levels represent an important factor in skeletal calcium retention and homeostasis. In therapeutic trials in which post-menopausal women were given daily doses of estrogens, such therapy has been demonstrated to be partially effective in reducing the rate of bone resorption. However, this therapy has the concomitant hazard of endometrial cancer (10). Vitamin D and its hormones have been given considerable attention in the more recent studies. Without adequate dietary and tissue levels of such vitamins, calcium absorption and bone status will be impaired. 

Non-compliance is a serious problem in the prevention of osteoporosis and osteoporotic fractures. This is due to adverse effects, lack of noticeable benefit and ignorance. It is difficult to convince regular intake of oral calcium, biphosphonates, vitamin D and in post-menopausal women hormone replacement. Long-term compliance to hormone replacement is worse in developing countries. The most cost-effective therapy for osteoporosis is primary prevention. 

Alternatives to steroid hormone therapy for osteoporosis include raloxifene, bisphosphonates, sodium fluoride, vitamin D and calcium supplementation, calcitonin, and parathyroid hormone. Tamoxifen has estrogenic effects on bone and delays bone loss in postmenopausal women. However as a result of estrogenic activity in the uterus, long-term tamoxifen administration has been associated with an increased risk of... 

J.D. Ringe, A. Dorst, C. Kipshoeven, L.C. Rovati, I. Setnikar, Avoidance of vertebral fractures in men with idiopathic osteoporosis by a three year therapy with calcium and low-dose intermittent monofluorophosphate, Osteoporos. Int. 8 (1998) 47-52. 

Gastrointestinal complaints (eg, nausea, diarrhea, vomiting, flatulence) are the most common adverse effects but rarely require discontinuation of therapy. Other potential adverse effects include headache and asthenia. Tenofbvir-associated proximal renal tubulopathy causes excessive renal phosphate and calcium losses and 1-hydroxylation defects of vitamin D, and preclinical studies in several animal species have demonstrated bone toxicity (eg, osteomalacia). Monitoring of bone mineral density should be considered with long-term use in those with risk factors for or with known osteoporosis, as well as in children. Reduction of renal function over time, as well as cases of acute renal failure and Fanconi s syndrome, have been reported in patients receiving tenofovir alone or in combination with emtricitabine. For this reason, tenofovir should be used with caution in patients at risk for renal dysfunction. Tenofovir may compete with other drugs that are actively secreted by the kidneys, such as cidofovir, acyclovir, and ganciclovir. 

Glucocorticoids can even cause osteoporosis when they are used for long-term replacement therapy in the Addison s disease, as has been shown by a study of 91 patients who had taken glucocorticoids for a mean of 10.6 years, in whom bone mineral density was reduced by 32% compared with age-matched controls (SEDA-19, 377 198). However, these results contrasted with the results of a Spanish study in patients with Addison s disease, in which no direct relation was found between replacement therapy and either bone density or biochemical markers of bone turnover of calcium metabolism (alkaline phosphatase, osteocalcin, procollagen I type, parathormone, and 1,25-dihydroxycolecalciferol) (SEDA-19, 377 199). 

Ten patients who had taken lithium for less than 1 year and 13 who had taken it for more than 3 years were assessed for alterations in bone metabolism and parathyroid function (654). There were no differences in bone mineral density, serum calcium concentration, or PTH concentration, but both groups had increased bone turnover and the longterm group had nonsignificantly higher calcium and PTH concentrations (including one hyperparathyroid patient who had an adenoma excised). The authors conclusion that lithium therapy is not a risk factor for osteoporosis needs to be tempered by the small sample size, the case of adenoma, and the blood concentration trends. 

The polypeptide parathormone is released from the parathyroid glands when the plasma Ca2+ level falls. It stimulates osteoclasts to increase bone resorption in the kidneys it promotes calcium reabsorption, while phosphate excretion is enhanced. As blood phosphate concentration diminishes, the tendency of Ca2+ to precipitate as bone mineral decreases. By stimulating the formation of vitamin D hormone, parathormone has an indirect effect on the enteral uptake of Ca2+ and phosphate. In parathormone deficiency, vitamin D can be used as a substitute that, unlike parathormone, is effective orally. Teriparatide is a recombinant shortened parathormone derivative containing the portion required for binding to the receptor. It can be used in the therapy of postmenopausal osteoporosis and promotes bone formation. While this effect seems paradoxical in comparison with hyperparathyroidism, it obviously arises from the special mode of administration the once daily s.c. injection generates a quasi-pulsatile stimulation. Additionally, adequate intake of calcium and vitamin D must be ensured. 

Idiopathic osteoporosis cannot be prevented by prophylactic therapy, but its development can be delayed. This requires a healthy lifestyle with plenty of physical exercise (sports, hiking), daily intake of calcium (lOOOmg/day Ca2+) and of vitamin D (1000 IU/day). The same principle holds for postmenopausal osteoporosis. Hormone Luellmann, Color Atlas of Pharmacology All rights reserved. Usage subject to terms... 

Glucocorticoid treatment for arthritis or other ailments can very quickly produce a form of osteoporosis caused by the inhibition of bone formation [334]. In such cases, the decrease in bone mass may be as much as 10-20%, but examination of trabecular bone reveals a much greater (30-40%) decrease in this component of bone [335]. Combination therapies with vitamin D and bisphosphonates, calcitonin or fluoride can be effective [336]. Therapy employing vitamin D or 1,25-(OH)2D3, the latter being highly calcaemic, should also include serum calcium monitoring and the use of thiazide diuretics as appropriate. 

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