Expert Commentary
STOP enforcing a 5-year rule for menopausal hormone therapy
START individualizing therapy to optimize health and quality of life
Steven R. Goldstein, MD, is Professor of Obstetrics and Gynecology at New York University School of Medicine in New York City. He is Director of Gynecologic Ultrasound and Co-Director of Bone Densitometry at New York University Medical Center in New York City. He serves on the OBG Management Board of Editors.
The author reports that he is a speaker for Warner Chilcott and Shionogi.
When serial BMD assessment is appropriate
Diagnosis of osteoporosis
A move away from use of the term “osteopenia”
WHAT THIS EVIDENCE MEANS FOR PRACTICE
DXA testing remains the cornerstone of diagnosis for patients at risk for fragility fracture. It also is the optimal method to determine the need for pharmacotherapy. In some instances, however, overutilization of DXA imaging has led to overtreatment, especially in younger women with low bone mass, when treatment is based on variables other than diminished bone quality (including, “small-boned” women, genetics, and failure to achieve peak bone mass as high as one’s peer group prior to menopause).
These recommendations help to clarify the rationale for follow-up DXA imaging for patients on therapy, an area in which scientific unanimity is lacking.
Related Article: What is the optimal interval for osteoporosis screening in postmenopausal women before fracture occurrence and osteoporosis treatment initiation? Steven R. Goldstein, MD (Examining the Evidence, August 2012)
IN ADOLESCENTS AND YOUNG WOMEN, CONSIDER THE BONE EFFECTS OF ORAL CONTRACEPTIVES
Ziglar S, Hunter TS. The effect of hormonal oral contraception on acquisition of peak bone mineral density of adolescents and young women. J Pharm Pract. 2012;25(3):331–340.
The bone loss observed in adolescents and young women who use depot medroxyprogesterone acetate (Depo-Provera) for contraception led to an FDA-mandated boxed warning on the medication’s package insert. The effect of oral contraceptives (OCs) on bone growth has received little publicity, however.
The best strategy to offset the natural loss of bone associated with aging and the menopausal transition is to ensure the development of maximal bone mass in youth. When maximal BMD is not achieved, the risk of osteoporosis is increased.
Adolescence is a critical period of bone mineralization, which is mediated by endogenous estradiol. The highest rate of bone mass accrual occurs 1 year before and 3 years after menarche. Young women who consume a diet low in calcium or who have an eating disorder, who fail to exercise, who smoke, or who have low estrogen status are most likely to have low peak bone mass.
OCs suppress endogenous estradiol production by interrupting the hypothalamic-pituitary-ovarian axis. By replacing endogenous estradiol with ethinyl estradiol (EE), OCs establish and maintain new hormone levels. Early initiation and use of very-low-dose EE increases the likelihood that the accrual of bone mass will be jeopardized at a critical time of bone mineralization.
Details of this meta-analysis
Ziglar and Hunter reviewed 11 prospective trials that showed a decrease in bone mass in adolescents and young women who used low-dose OCs, six trials that showed a neutral effect, and one trial that found an increase in bone mass. This last study involved only members of the US military whose level of daily exercise may not be representative of the general population of women the same age. Investigators also theorized that the use of norethindrone acetate as an androgenic progestin in this study may have exerted a positive effect on bone accrual.
START individualizing therapy to optimize health and quality of life
For postmenopausal women with newly diagnosed osteoporosis, assessing the risk of breast cancer prior to prescribing a bone medicine could...
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Our understanding deepens of the benefits and risks of hormone therapy in different formulations and populations