

Author: Koval Peter Seaton Terry
Publisher: Humana Press, Inc
ISSN: 1534-8644
Source: Clinical Review in Bone and Mineral Metabolism, Vol.3, Iss.1, 2005-03, pp. : 31-38
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Abstract
Parathyroid hormone (PTH) is the most recently approved agent for osteoposis treatment. It differs from other therapies that act by inhibiting bone resorption, because it stimulates bone formation. The resultant increases in bone mineral density are therefore greater than those associated with therapy with bisphosphonates (BPs), selective estrogen receptor modulators, or calcitonin. Despite being available for at least 2 yr. PTH has not been exten sively studied. Although some existing data support its use for reducing the risk of vertebral fractures in women. data are still limited with regard to nonvertebral fracture prevention in women and fracture prevention in men. Preliminary studies have demonstrated a potential role in the management of patients with glucocorticoid-induced osteoporosis, but more data are needed. PTH is administered daily by subcutaneous injection for a maximum of 24 mo. Common adverse effects include pain with injection, arthralgia, and nausea. PTH caused an increase in osteosarcoma in rats and therefore, its use should be avoided in patients at increased risk of osteosarcoma, such as those with Paget's disease, unexplained baseline elevations of alkaline phosphatase, open epiphyses, or previous skeletal radiation exposure. At this time. PTH should not be combined with other agents, but a 2-yr treatment period may be sequentially followed by a BP. Because of high cost, the need for parenteral administration and potential for adverse effects, PTH use should be reserved for patients with severe osteoporosis who fail BP therapy.
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