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Bisphosphonates parathyroid hormone

The combination of a bisphosphonate with anabolic therapy (teriparatide) should not be used because a well-controlled trial showed that women receiving the combination actually had smaller increases in bone mineral density than women receiving teriparatide alone.44 However, sequential therapy with these agents may be more promising. In one study, women who received alendronate for 1 year directly after receiving parathyroid hormone for 1 year had greater... [Pg.863]

Osteoporosis Encourage patients to ingest adequate amounts of calcium and vitamin D, encourage smokers to discontinue tobacco use, and consider initiation of medications for osteoporosis (e.g., bisphosphonates, calcitonin, and parathyroid hormone) if the patient is taking glucocorticoids for an extended period of time or if the patient has evidence of low bone mineral density.15,41... [Pg.877]

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... [Pg.709]

CLINICAL USES OF PARATHYROID HORMONE, CALCITONIN, VITAMIN D, AND BISPHOSPHONATES... [Pg.758]

Typical changes in bone mineral density with time after the onset of menopause, with and without treatment. In the untreated condition, bone is lost during aging in both men and women. Fluoride, strontium (Sr2+), and parathyroid hormone (PTH) promote new bone formation and can increase bone mineral density in subjects who respond to it throughout the period of treatment, although PTH also activates bone resorption. In contrast, estrogen, calcitonin, and bisphosphonates block bone resorption. This leads to a transient increase in bone mineral density because bone formation is not initially decreased. However, with time, both bone formation and bone resorption are decreased with these pure antiresorptive agents, and bone mineral density reaches a new plateau. [Pg.971]

Alendronate significantly reduced the anabolic effect of parathyroid hormone when the two were used in combination, both in postmenopausal women (22) and in men (23). It seems likely that this interaction will also apply to other bisphosphonates, although the mechanism has not been determined. [Pg.501]

Osteoporosis Generalized bone demineralization often associated with effects of aging and hormonal changes in postmenopausal women Calcium supplements, vitamin D, calcitonin, bisphosphonates, intermittent parathyroid hormone, estrogen, or SERMs (raloxifene] (see Chapter 30]... [Pg.467]

NICE (National Institute for Health and Clinical Excellence) (2005) Bisphosphonates (alendronate, etidronate, risedronate), selective oestrogen receptor modulators (raloxifene) and parathyroid hormone (teriparatide) for the secondary prevention of osteoporotic fragility fractures in postmenopausal women. Available at www.nice.org.uk/nicemedia/pdf/TA087guidance.pdf [Accessed 4 July 2008],... [Pg.140]

Vitamin D, calcium, parathyroid hormone, calcitonin, bisphosphonates, bone... [Pg.735]

Bones are constantly dissolved by osteoclasts and remineralized by osteoblasts in response to mechanical forces. Osteoclasts possess an acidic compartment and pass demineralized bone products to the periosteum (Sect. 1). They develop in stress-induced bony microcracks and are activated by differentiation factors secreted by osteoblasts, especially after menopause. Menopausal osteoporosis is controlled by drugs that are a stable form of pyrophosphate (bisphosphonate) or cathepsin K inhibitors (Sect. 2). The calcium ion concentration of blood is raised by parathyroid hormone and a vitamin D derivative called calcitriol. Parathyroid hormone causes kidneys to excrete phosphate, retain calcium, and activate calcitriol production (Sect. 3). Calcitriol induces calcium transporter proteins in osteoclasts and intestinal epithelium, where they move calcium from bone or diet into blood (Sect. 4). The chapter concludes with a discussion of calcitonin which lowers blood calcium concentrations by reversing parathyroid hormone effects on the kidney and inhibiting osteoclast activity (Sect. 5). [Pg.153]

Teriparatide contains the first 34 amino acids in human parathyroid hormone and represents a novel approach to osteoporosis treatment. Although hyperparathyroidism leads to bone loss (see Fig. 88-3), therapeutic doses (for shorter periods of time) conversely improve BMD and rednce fractnre risk. Parathyroid hormone is currently the only approved osteoporosis medication that works by stimulating bone formation. Becanse of adverse effects and cost concerns, teriparatide is reserved for treating those at high risk of osteoporosis-related fracture who cannot or will not take or have failed bisphosphonate therapy. [Pg.1660]

OLT, with roughly 20% of patients experiencing a fracture within 1 year of transplant. Poor diets, lack of physical activity, reduced serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, and abnormal parathyroid hormone concentrations are all thought to contribute pretransplant. Post-OLT corticosteroid therapy will also negatively impact bone metabolism, but may not be the sole reason for continued bone loss post-OLT. Mean bone mineral density (BMD) has taken a mean of 85 months to return to pre-OLT levels. Single-dose bisphosphonate infusion did not alter bone formation or resorption in the early (30 days) post-OLT period. " It is likely that lowering steroid doses, BMD screening, preventive measures, and calciiun and vitamin D supplementation will be the mainstay treatment options for this problem. ... [Pg.2647]

Osteoporosis Antiresorptive medications bisphosphonates, calcitonin, estrogen and estrogen agonists/ antagonists anabolic (bone forming) medications parathyroid hormone surgery or bone replacement [5]... [Pg.142]

A 74-year-old woman, who was referred for evaluation of pain and persistently abnormal exposure of jaw bone after extraction of teeth, had been using weekly oral alendronate for osteoporosis for about 5 years. She had the clinical features of bisphosphonate-associated osteonecrosis of the mandible, which was precipitated by extraction of teeth 14 months before she was referred for assessment. She had multiple susceptibility factors for osteonecrosis of the jaw, including older age, type 2 diabetes mellitus, and a long duration of bisphosphonate therapy. The mandibular lesions did not improve despite repeated operations over 14 months. Bisphosphonate therapy was withdrawn and parathyroid hormone therapy was started after 2 months the oral mucosa had healed, after 4 months the pain had completely subsided, and after 6 months the patient s eating and drinking habits had returned. The serum concentration of osteocalcin, a marker of bone formation, which was initially suppressed, increased by 174% from baseline after 6 months of treatment with parathyroid hormone. [Pg.1013]

The goals of osteoporosis treatment are to control pain from the disease, reduce bone loss, and prevent bone fractures with medicines or hormone therapies. There are several types of treatments for osteoporosis including most famous bisphosphonates, estrogen agonists/antagonists, parathyroid... [Pg.418]


See other pages where Bisphosphonates parathyroid hormone is mentioned: [Pg.280]    [Pg.280]    [Pg.280]    [Pg.280]    [Pg.509]    [Pg.257]    [Pg.742]    [Pg.81]    [Pg.1659]    [Pg.1661]    [Pg.289]    [Pg.369]    [Pg.2047]   
See also in sourсe #XX -- [ Pg.1013 ]




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