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October 31, 2002 — Osteoporosis, a "silent" disease characterized by low bone mass and deterioration, which can lead to bone fragility and an increased risk of fracture, is a public health threat for more than 28 million Americans — 80 percent of which are women. New Research published this month in two Endocrine Society journals demonstrates the effectiveness of diagnostic testing for postmenopausal women with osteoporosis and also evaluates two treatments for the disease — alendronate and parathyroid hormone (PTH). The findings could lead to more effective treatments and quicker diagnosis for women who suffer from the disease.
Although estrogen deficiency at menopause and aging are the most common causes of osteoporosis in women, many other disorders and diseases also may lead to bone loss. Unless identified by specific laboratory testing, these disorders can continue to affect bone health and cause sub-optimal or ineffective treatment of osteoporosis. It is important to detect these disorders, because in many cases they can be treated medically or surgically, with the potential for blocking or removing the cause for the osteoporosis. In the past, the prevalence of these underlying, yet undiagnosed, causes of osteoporosis among postmenopausal women was unknown. A study published in the October issue of The Journal of Clinical Endocrinology and Metabolism (JCEM) evaluated the incidence of undetected disorders that can cause loss of bone in otherwise healthy women who have osteoporosis. The study also sought to determine the most useful and cost efficient screening tests to detect these disorders.
The researchers who worked on the study discovered that 32 percent of the postmenopausal women who were evaluated suffered from a previously undiagnosed bone and mineral metabolism disorder, which can cause bone loss or affect response to osteoporosis treatment.
"Nearly a third of the postmenopausal women who we evaluated were suffering from another disorder, which could be contributing to their osteoporosis," said Marjorie Luckey, M.D., Medical Director of the Saint Barnabas Osteoporosis and Metabolic Bone Disease Center and the lead investigator on the study. "Examples of the disorders found were overactivity of the parathyroid glands, vitamin D deficiency, excessive urinary calcium excretion, calcium malabsorption and excessive thyroid hormone supplementation. Unless these disorders are identified and treated, standard therapy for osteoporosis could be ineffective. However, a simple, cost effective testing strategy can identify 85 percent of the women who have an underlying disorder affecting their skeleton which requires specific treatment to optimize the management of their osteoporosis."
In the JCEM study, Dr. Luckey and her colleagues suggested a series of tests for all postmenopausal women with osteoporosis, including measurements of urine calcium, serum calcium and serum PTH, as well as serum thyroid stimulating hormone (TSH) for women taking thyroid hormone. The series of tests would cost about 75 dollars per patient. An editorial that accompanies the study, written by Rachel Wagman, M.D., and Robert Marcus, M.D., concurs with the need for routine diagnostic testing for osteoporosis patients and points out that an additional measurement of vitamin D also may also be prudent in view of widespread vitamin D insufficiency at northern latitudes.
Another study published in this month's JCEM compared the effects of teriparatide — an investigational form of recombinant human parathyroid hormone (PTH), which regulates calcium and phosphorus in the blood, and alendronate sodium — a bisphosphonate. In the study, teriparatide increased BMD and decreased nonvertebral fractures more than alendronate.
Previous research, including the study above, has shown that PTH is a promising, novel investigational therapy for the treatment of osteoporosis. However, scientists are still trying to understand exactly how PTH works to stimulate new bone formation. A study published this month in Endocrinology helps to shed some light on that important question. Researchers at the University of Michigan, lead by Laurie McCauley, M.D., used mice with an altered genetic background to show that a specific factor that affects the molecular machinery of the cell (the transcription factor, c-fos) was necessary for PTH to stimulate bone formation during growth. In the study, normal mice responded to daily injections of PTH with an increase in bone mass, while mice without the c-fos gene did not experience an increase in bone formation and actually lost bone volume following PTH treatments.
"Our findings suggest that c-fos may be a key factor for targeting therapies for osteoporosis in the future and also suggest that PTH therapy may be even more effective at increasing bone formation during growth," said Dr. McCauley. "As a next step, it will be necessary to confirm these data in a model that recapitulates the post-menopausal condition of osteoporosis in order to better translate these findings to the treatment of osteoporosis in humans."