Menopause calcitonin

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... 

Calcitonin is indicated for osteoporosis treatment for women at least 5 years past menopause. Although limited data suggest beneficial effects in men and concomitantly with glucocorticoids, these indications are not FDA approved. 

The Ca -selective hormones calcitriol, parathyroid hormone, and calcitonin influence this interaction in the bone cells. Parathyroid hormone promotes Ca "" release by promoting the release of cytokines by osteoblasts. In turn, the cytokines stimulate the development of mature osteoclasts from precursor cells (bottom). Calcitonin inhibits this process. At the same time, it promotes the development of osteoblasts (top). Osteoporosis, which mainly occurs in women following the menopause, is based (at least in part) on a reduc-... 

Disease-induced, dmg-induced, old age-induced, immobility-induced and menopause-induced osteoporosis is all relatively cheap to prevent but become very expensive and difficult to treat as soon as a fractures occur. Oral calcium, vitamin D, biphos-phonates, hormone replacement and parenteral calcitonin in post-menopausal women, achieved annual BMD increases of 0.5-1.5%. Limited efficacy of less than 0.5% annual BMD increase, adverse effects, and high costs have restricted the large scale use of calcitonin. 

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. 

Options for treatment include hormone replacement therapy (HRT), bisphosphonates, calcitriol, calcitonin, raloxifene, strontium ranelate, and teriparatide. Hormone replacement therapy is generally indicated for women who are under 50 years and are experiencing a premature menopause. Symptomatic menopausal women may opt to use HRT also, as the benefits outweigh the risks for up to 5 years treatment. They may choose an alternative treatment for osteoporosis if preferred. Hormone replacement therapy is not recommended for first line treatment for long-term prevention of osteoporosis in women over 50 years of age. 

Osteoporosis is of two forms- primary i.e. idiopathic and secondary. Primary osteoporosis is classified into type I and type II osteoporosis. Type I is referred to post menopausal osteoporosis which is the main type affecting women, characterized by rapid bone loss and affects women after the menopause, mainly in trabecular bone and is associated with vertebrae and distal radio fractures whereas type II also termed as senile osteoporosis occurs due to chronic deficiency of calcium, increase in parathormone activity and decrease in bone formation and is associated with aging. On the other hand secondary type results from inflammatory processes, endocrine changes, multiple myeloma, sedentariness and the use of drugs such as heparin, corticoid and alcohol [3]. Prevention is the main treatment of osteoporosis, for which bone mass peak and the prevention of postmenopausal reabsorption are critical elements. The common treatment of osteoporosis includes calcium consumption as calcium salts, vitamin D supplements, and hormone reposition [4], the use of calcitonin to modulate serum levels of calcium and phosphorous [5], the use of bisphosphonate, mainly alendronates [6], use of ipriflavone and sodium fluoride [7], besides physical activity to strengthen muscles, stimulate osteoblasts formation and prevent reabsorption. 

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). 

Calcitonin is released from the thyroid gland when serum calcium is elevated. Salmon calcitonin is used clinically because it is more potent and longer lasting than the mammalian form. Pharmacologic doses decrease bone resorption. Calcitonin is indicated for osteoporosis treatment for women at least 5 years past menopause. Although the agent is also used in men, it is not approved for this indication. Because calcitonin reduces fracture risk to a lesser extent than other osteoporosis medications, calcitonin is reserved for second-line treatment. 

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