Researchers Note Link between Depression & Lowered Bone Mass
National Osteoporosis Foundation Newsletter Spring 2007, Volume 22
Studies have long associated depression with low bone mass and an increased risk of fracture, and have reported more symptoms of depression in women with osteoporosis. According to a study published in the October 17, 1996 issue of The New England Journal of Medicine, the bone density of people with depression is up to 15 percent lower than that of people without depression. Researchers have not been able to determine whether major depression causes low bone mass density and increased risk of fracture, or whether the depression is a result of the diminished quality of life and disability that occurs in many patients with osteoporosis. New research findings offer more evidence about the relationship of depression to osteoporosis. A team led by researchers from Hebrew University of Jerusalem is providing clues to how depression reduces bone mineral density and discovering ways to prevent bone loss. After inducing depression in mice by exposing them to chronic stress, the study team gave the mice the antidepressant imipramine (Tofranil®). The drug improved both the behavior and the bones of the mice; some mice responded by a reversal in bone loss and also became less depressed. An earlier study conducted by researchers at the Forsyth Institute in Boston, Mass. found that the antidepressant drug, Prozac®, increased bone mass in adult mice. Both studies suggest that depression most likely affects the bone-forming cells, the osteoblasts, rather than the bonedegrading cells, the osteoclasts. Major depression is also associated with increased production of steroids in the body, which may affect function of those osteoblast cells. The Forsyth Institute study was funded by the U.S. National Institute of Dental and Craniofacial Research, and is expected to be published in an upcoming issue of the Journal of Cellular Biochemistry. The Hebrew University of Jerusalem study, “Depression induces bone loss through stimulation of the sympathetic nervous system,” is published in the November 7, 2006 issue of the Proceedings of the National Academies of Science, volume 103, #45.
Most Postmenopausal Women Can Discontinue Use of Osteoporosis Drug with No Risk
National Osteoporosis Foundation Newsletter Spring 2007, Volume 22
A recent study published in the Journal of the American Medical Association (“Effects of Continuing or Stopping Alendronate After Five Years of Treatment,” JAMA, December 27, 2006) suggests that women who discontinue taking alendronate after five years of treatment do not significantly increase their fracture risk for up to an additional five years. Women who discontinued the alendronate treatment had the same rate of non-spine fractures as women who continued using the drug. However, the study also finds that women at very high risk of spine fractures may benefit by continuing to take alendronate beyond the initial five years. Prior to this study, it had not been known whether treatment of osteoporosis should be continued indefinitely. These findings are especially welcome for older post-menopausal women taking multiple drugs for a variety of conditions. Alendronate — the most widely used osteoporosis drug — reduces bone loss, increases bone density, and reduces the risk of spine, wrist and hip fractures, and is approved by the FDA for both prevention and treatment of osteoporosis in postmenopausal women and for the treatment of osteoporosis in men. Alendronate belongs to a class of drugs called bisphosphonates, all of which are antiresorptive medications. Antiresorptives slow the part of the bone remodeling cycle in which old bone is removed (bone resorption). The long-term study on the use of alendronate among postmenopausal women in 10 clinical centers around the U.S. was led by researchers from the University of California, San Francisco. The new findings are from a follow-up study to the initial trial that examined the effect of a daily dose of alendronate on bone mineral density and fracture risk in postmenopausal women with low bone mineral density for up to 3.8 years.
First IV Osteoporosis Medication Approved by the FDA National Osteoporosis Foundation
Newsletter Fall 2006, Volume 21
Earlier this year, the Food and Drug Administration (FDA) approved intravenous ibandronate sodium (brand name Boniva®) for the treatment of postmenopausal osteoporosis. Ibandronate is in a class of drugs called bisphosphonates, and it is the first intravenous (IV) medication approved to treat osteoporosis. Ibandronate was approved in a once-monthly oral dose in 2005. IV ibandronate is administered in a dose of 3 mg once every three months by a healthcare professional in either a doctor’s office or other outpatient setting; the infusion takes less than one minute. Healthcare professionals can order ibandronate from their medical suppliers, but not all have the capability to administer an IV medication in their offices. The IV dose bypasses the stomach and intestine, making it is less likely to cause heartburn or stomach upset than are oral bisphosphonates. Patients need to have a serum creatinine lab test prior to each dose. This drug should not be given to patients with severe renal impairment. Insurance benefits for the new drug vary from plan to plan. Patients need to check with their health insurance carrier to determine whether this drug is a covered benefit and whether there are any special requirements, such as obtaining preauthorization. Unlike other osteoporosis medications, IV ibandronate is covered as a medical benefit rather than a drug benefit by most insurance companies because it must be given in a doctor’s office. For people with Medicare, this means it is reimbursed under Medicare Part B while the oral dose is reimbursed under Medicare Part D.
IV ibandronate is a product of Roche. The toll free customer service number is (800) 526-6367.
