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The authors did not mention the potential role of progesterone in bone formation. Evidence that progesterone acts as a bone trophic hormone3 has recently been extended by in vitro work documenting the presence of progesterone receptors on osteoblasts. Progesterone may be found to have a particularly important role if one examines the one half to two thirds of bone loss that Riggs and Melton acknowledge is not "attributable to the menopause"1.
Jerilynn C. Prior, M.D., F.R.C.P.C.
University of British Columbia
Vancouver, BC V6T 1W5, Canada
John D. Wark, M.B., B.S., Ph.D., F.R.A.C.P.
University of Melbourne
Parkville, Victoria 3052, Australia
Susan I. Barr, Ph.D.
University of British Columbia
Vancouver, BC V6T 1W5, Canada
References
The authors also do not seem to realize that long-term estrogen therapy is difficult for both doctors and their patients to accept, as has been confirmed by the very high degree of noncompliance with long-term estrogen therapy. For example, in a recent study, 40 percent of women stopped taking the medication eight months after beginning therapy.1
Daniele Coen, M.D.
Emanuela Terzian, M.D.
Istituto di Ricerche Farmacologiche "Mario Negri"
20157 Milan, Italy
Nicola Magrini, M.D.
University of Bologna
40126 Bologna, Italy
References
To the Editor: Prior and colleagues are correct that the scanning electron micrograph of cancellous bone in Figure 2A, reproduced from the paper by Dempster et al., in fact showed bone from a normal 44-year-old man, not bone from a normal premenopausal woman as we stated. We appreciate their calling this error to our attention. The figure was intended to demonstrate the effect of excessive osteoclastic resorption on cancellous bone. This point is made equally well by comparing the micrograph of the woman with osteoporosis with that of the normal man.
Prior et al. have developed the interesting hypothesis that postmenopausal bone loss is caused by a deficiency of both estrogen and progesterone and that some bone loss in premenopausal women may be caused by progesterone deficiency associated with anovulatory menstrual cycles. Because of space constraints, we limited our review largely to studies in which the effectiveness of a drug in the prevention or treatment of osteoporosis had been demonstrated by randomized, controlled clinical trials using changes in bone density or fracture rates as end points. Studies of the effects of progestins on bone that will serve as an important test of this hypothesis should soon be forthcoming.
Coen and colleagues question the value of calcitonin treatment and remind the reader that many postmenopausal women are unwilling to take estrogen. Despite certain disadvantages, we believe that calcitonin is a useful antiresorptive drug. In a two-year controlled study in elderly women with moderate osteoporosis, Overgaard et al.1 found that treatment with intranasal salmon calcitonin significantly reduced the rates of vertebral and peripheral fractures. Acceptance of estrogen-replacement therapy can be improved by careful discussion with the patient of the well-documented, favorable ratio of benefits to risks2. Moreover, Rubin and Cummings3 have shown that the results of bone densitometry substantially influence a woman's decision about beginning such therapy. Our own unpublished data on random samples of women living in Rochester, Minnesota, show that the proportion receiving replacement estrogen within 20 years after menopause increased from 4 percent in 1980 to 33 percent in 1992. Thus, acceptance of estrogen-replacement therapy appears to be increasing.
B. Lawrence Riggs, M.D.
L. Joseph Melton, III, M.D.
Mayo Clinic and Foundation
Rochester, MN 55905
References
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