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New Drug May Strengthen Women's Bones

In study, denosumab outperformed a standard osteoporosis therapy


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MONDAY, Oct. 27 (HealthDay News) -- The drug denosumab can boost bone mass in postmenopausal women, according to a study that followed almost 1,200 women, average age 64, with low bone mass for more than one year.

Denosumab inhibits the activation of bone-resorbing cells called osteoclasts.

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The women were randomly assigned to receive either a 60 milligram injection of denosumab every six months plus a weekly oral placebo, or an injection of placebo every six months and 70 milligrams of alendronate orally each week. Alendronate (brand name Fosamax) is commonly used in the prevention and treatment of osteoporosis in postmenopausal women.

The women also took at least 500 milligrams of calcium and at least 400 milligrams of vitamin D daily.

At the end of the study, more of the women who received denosumab had gained at least 3 percent of bone mass at the hip and lumbar spine than those who took alendronate.

In addition, blood and urine tests showed that denosumab suppressed markers of bone turnover. This suggests the drug achieved effective suppression of bone resorption, the researchers said.

The study is to be presented Oct. 29 at the annual scientific meeting of the American College of Rheumatology (ACR), in San Francisco.

"The fact that bone density changes were greater than the most commonly used antiresorptive agent, alendronate, shows that denosumab is an effective agent," lead investigator Dr. Chad Deal, head of the Center for Osteoporosis and Metabolic Bone Disease at the Cleveland Clinic, said in an ACR news release.

He added that patients should talk to their rheumatologists to determine the best course of treatment.

More information

The U.S. National Institute of Arthritis and Musculoskeletal and Skin Diseases has more about bone health.



-- Robert Preidt

Copyright © 2008 ScoutNews, LLC. All rights reserved.
Last updated 10/27/2008

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SOURCE: American College of Rheumatology, news release, Oct. 25, 2008


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