The Physician and Sportsmedicine
Menubar Home Journal Personal Health Resource Center CME Advertiser Services About Us

Osteoporosis in Active Women: Prevention, Diagnosis, and Treatment

Steven M. Erickson, MD; Thomas L. Sevier, MD

Internal Medicine Series Editor: Donald M. Christie, Jr, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 25 - NO. 11 - NOVEMBER 97


In Brief: Insufficient estrogen can cause osteoporosis in young female athletes, like the 17-year-old runner described here, as well as in postmenopausal women, whose management is also detailed. The most common technique for diagnosis is dual-energy x-ray absorptiometry. Prevention and treatment depend on a woman's age but may include increased calcium intake, weight gain, weight-bearing and resistance exercise, and estrogen replacement therapy. Alendronate and/or calcitonin may be used as alternatives to estrogen therapy.

Osteoporosis has been defined as "a disease characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk (1)." Although anyone can develop osteoporosis, postmenopausal women and young females with menstrual irregularities are most commonly affected. An estimated 20% of women more than 50 years old have osteoporosis (2,3). Although most studies have focused on women of this age-group, osteoporosis is potentially more deleterious in younger women because they haven't yet attained peak bone mass, and early bone loss therefore can affect the rest of their lives.

Whether patients are younger or older, the social costs of osteoporosis are enormous. The yearly estimated healthcare bill for osteoporotic fractures is between $2 billion and $6 billion (4,5). About 200,000 osteoporosis-related hip fractures occur each year in the United States, and the mortality rate 1 year after fracture is estimated to be as high as 20% (6).

Causes of Osteoporosis

Understanding the pathophysiology of osteoporosis begins with a knowledge of normal bone development. Bone health partially depends on physical stress and on adequate levels of calcium, parathyroid hormone, and estrogen. In normal individuals, bone density increases throughout childhood and adolescence and until about 30 years of age. A longitudinal study (7) in 1992 showed that cortical and trabecular bone mass continues to increase slightly in healthy young women until approximately 28 years of age. Other studies (8-10) show that trabecular bone loss may begin in the third decade, but cortical bone may increase or remain constant until the fifth decade (11).

Following achievement of peak bone mass, some bone loss occurs in both men and women. The average bone loss for women at age 50 is estimated at 7% in the lumbar spine and 16% in the femoral neck (12).

Excessive bone loss most commonly occurs in females who have insufficient levels of estrogen. Rencken et al (13), in a case-control study involving 49 athletes, 17 to 39 years old, showed that the age of menarche predicts lumbar bone mineral density (BMD) in both amenorrheic and eumenorrheic athletes and that delayed menarche predicts lower BMD in amenorrheic athletes. The study also demonstrated that extended periods of amenorrhea can result in decreased bone density at multiple skeletal sites, including weight-bearing sites such as the femoral shaft and tibia. This means that osteoporosis in young athletes (see "Osteoporosis and Stress Fractures in a Young Runner," below) can be more devastating than in older women because it interferes with attainment of peak bone mass.

Besides delayed menarche and amenorrhea, other risk factors for the development of osteoporosis include a family history of osteoporosis, low calcium intake, malnutrition, eating disorders, premature menopause, oligomenorrhea, and prolonged exposure to certain medications, such as corticosteriods, excess thyroid replacement, and phenytoin.

Screening and Diagnosis

The Scientific Advisory Committee of the National Osteoporosis Foundation (14) recommends screening for osteoporosis in estrogen-deficient women who are considering hormone replacement or other therapy, patients with osteopenia or vertebral abnormalities revealed on radiographs, those who will receive long-term glucocorticoid therapy, and those with asymptomatic primary hyperparathyroidism who would benefit from surgical intervention. We would add to this list patients with multiple risk factors for osteoporosis and those who have fractures with suspected osteoporotic causes.

Patients who may have osteoporosis should receive a screening evaluation to identify reversible causes. This evaluation should include a complete blood count, chemistry panel, sedimentation rate, and thyroid-stimulating hormone assay. In adolescent patients with menstrual irregularities, an evaluation for secondary amenorrhea should also be considered and should include a laboratory examination of estrogen, luteinizing and follicle-stimulating hormones, prolactin, and a urine pregnancy test.

The gold standard for diagnosing osteoporosis is a bone biopsy, an invasive procedure that is usually not necessary because accurate information can be obtained using noninvasive measures. The current diagnostic techniques include quantitative computed tomography, dual-photon absorptiometry, and dual-energy x-ray absorptiometry (DEXA). DEXA scanning is the most widely used technique in the United States today. It has a margin of error of 1% to 2% and exposes the patient to less radiation than a typical chest x-ray. DEXA results are usually reported as a T-score (table 1), the number of standard deviations (SD) below the average BMD for the sex-matched young adult population. Studies have shown that a 1-SD reduction in bone density results in a twofold to threefold increased risk of fracture (15).


Table 1. Bone Health Diagnostic Categories Based on Bone Density Values Relative to the Young Adult Mean, Reported as T-scores*

Normal <1 standard deviation (SD) below the mean
Osteopenia 1 to 2.5 SD below the mean
Osteoporosis >2.5 SD below the mean
Severe Osteoporosis >2.5 SD below the mean, plus one or more fragility fractures

*World Health Organization: Assessment of Fracture Risk and Its Application to Screening for Postmenopausal Osteoporosis. WHO Technical Report Series No. 843. Geneva, World Health Organization, 1994


PREVENTION AND TREATMENT

Many advances have been made recently in the prevention and treatment of osteoporosis in young athletes as well as postmenopausal women. We now have a better understanding of the role of exercise, calcium intake, estrogen, alendronate, and calcitonin in the management of this condition.

Exercise

The role of exercise in preventing and treating osteoporosis is best summarized by the American College of Sports Medicine position statement (16), which makes five points: (1) Weight-bearing physical activity is essential for developing and maintaining a healthy skeleton; (2) strength exercises may also be beneficial, particularly for non-weight-bearing bones; (3) if sedentary women increase their activity, they may avoid the further loss of bone that inactivity can cause and may even slightly increase bone mass; (4) exercise is not a substitute for postmenopausal hormone replacement therapy; and (5) an optimal exercise program for older women includes activities for improving strength, flexibility, and coordination, since improvement in these areas lessens the likelihood of falls and fractures.

Physical stress is a major stimulus for the remodeling and strengthening of bone. In fact, two studies (17,18) have shown that weight-bearing exercise can increase BMD; women who were 50 or more years old and ran regularly had lumbar spine BMDs between 9.2% and 35% higher than women who did not run.

Though exercise can increase premenopausal women's BMD, this benefit reaches only to a point: Excessive exercise interferes with the hypothalamic-pituitary axis and can lead to a hypoestrogenic state, resulting in a reduction in BMD. In addition, weight-bearing exercise should not be used as a single treatment for osteoporosis in either young or older women. Exercise cannot offset the negative effect of decreased estrogen production on the skeleton of young amenorrheic athletes (13). Likewise, exercise alone has not been shown to prevent the bone loss that occurs after menopause, so it should be used only as an adjuvant treatment for osteoporosis in this age-group.

We recommend that older women get 30 minutes of weight-bearing exercise most days of the week. The vast majority of young women need to exercise more, not less. However, younger women whose high level of exercise may be interfering with their menstrual cycle should seek medical advice regarding the relationship of their physical activities with abnormal menses.

Dietary Calcium

Adequate calcium intake is recommended for both the prevention and treatment of osteoporosis. Recently, the National Institutes of Health released a consensus statement(19) recommending that individuals from 11 to 24 years of age consume 1,200 to 1,500 mg of calcium per day. It also recommended that 25- to 50-year-old women and 50- to 65-year-old women who take estrogen should consume 1,000 mg of calcium per day, and that postmenopausal women who are not taking estrogen and women older than 65 years get 1,500 mg per day. In addition, the statement says that young athletes who have menstrual dysfunction and/or eating disorders should consume 1,200 to 1,500 mg of calcium and 400 to 800 IU of vitamin D per day. Consuming adequate amounts of dairy products can help individuals reach these levels of calcium intake, (for example, 3 cups of milk contain about 900 mg of calcium), but taking supplemental calcium is often necessary as well. Eating other calcium-rich foods (table 2: not shown) can also help.

Estrogen

The importance of estrogen for the development and maintenance of bone health is well-documented. Estrogen replacement therapy in the prevention and treatment of osteoporosis in postmenopausal women is widely accepted, but its effectiveness in treating osteoporosis in adolescent athletes is debatable.

Premenopausal estrogen therapy. Keen and Drinkwater (20) recently reported that previously amenorrheic, younger athletes with osteoporosis who had either regained menses or had been taking hormone replacement for up to 9 years did not significantly improve bone density, suggesting that bone loss is irreversible.

Several other studies, however, suggest the opposite. In a recent retrospective study (21), Cumming demonstrated that eight amenorrheic women, 24 to 34 years old, who took hormone replacement (conjugated equine estrogen 0.625 mg/day, or estradiol transdermal patch, 50 micrograms/day, with medroxyprogesterone acetate 10 mg/day for 14 days per month) had BMD increases of 8% in the lumbar spine and 4% in the femoral neck after 24 to 30 months of hormone replacement therapy, while the control group, who took no hormones, had nonsignificant decreases at each site. In a randomized trial by Hergenroeder et al (22), 14- to 28-year-old amenorrheic females who took oral contraceptive pills (OCPs) for 6 months increased their spinal bone density by 2%, while an amenorrheic control group had a 3% decrease. Gulekli et al (23) found that 17- to 40-year-old amenorrheic women with associated osteopenia treated with either hormone replacement or OCPs for an average of 19 months increased BMD by 3.5%, while controls had a nonsignificant loss of bone mass.

Though the weight of evidence indicates that estrogen increases BMD in young, amenorrheic women, there is no consensus on the amount of estrogen necessary to achieve maximal gains. Furthermore, experts agree that premature adolescent osteoporosis is best prevented by maintaining eumenorrhea. (Of particular note for younger athletes: OCPs, conjugated equine estrogen, and medroxyprogesterone acetate are not banned by the US Olympic Committee or the National Collegiate Athletic Association.)

Postmenopausal estrogen therapy. Estrogen is the only drug with US Food and Drug Administration (FDA) approval for the prevention of postmenopausal osteoporosis. Further, two recent double-blind, placebo-controlled clinical trials document the effectiveness of estrogen replacement therapy for the treatment of postmenopausal osteoporosis.

The Postmenopausal Estrogen/Progestin Interventions Trial (24) followed postmenopausal women assigned to receive either estrogen replacement therapy or a placebo for 36 months. Comparisons of the subjects' baseline and final BMDs showed that the placebo group lost an average of 1.8% in the spine and 1.7% in the hip, while the women who received estrogen replacement therapy increased their BMD by 3.5% to 5% in the spine and 1.7% in the hip. In addition, this study showed that women who followed a regimen of conjugated equine estrogen plus continuous medroxyprogesterone acetate had greater increases in spinal BMD (5% average) than those who took other estrogen regimens (3.8% average).

Another study (25) showed that women who were treated with unopposed ethinyl estradiol—the estrogen widely used for contraception—for 2 years had no increase in bone mass. However, when ethinyl estradiol was given in continuous combination with norethindrone acetate, dose-dependent increases in spinal bone mass occurred, suggesting that norethindrone acetate may have a positive effect on bone density. This trial also found that ethinyl estradiol and norethindrone decreased serum lipids. However, the combination of conjugated equine estrogen and medroxyprogesterone acetate has even more favorable effects on lipid profiles.

These trials suggest that conjugated equine estrogen (0.625 mg/day) with medroxyprogesterone (2.5 mg/day) is the treatment of choice for postmenopausal osteoporosis patients who have a uterus. Most experts still recommend conjugated equine estrogen alone (0.625 mg/day) for patients without a uterus (25).

Reduced fracture risk. Estrogen not only increases BMD, but also reduces the risk of osteoporotic fractures. In a recent study (26), patients who began estrogen replacement therapy soon after menopause and continued taking estrogen for 5 years had a lower risk of hip and wrist fractures than women who did not have replacement therapy (relative risk, 0.29). Patients who had previously been taking estrogen replacement—some for as long as 10 years—but were not currently using estrogen had no significant decrease in their risk of fracture. A second study (27) showed that the duration of exposure to estrogen (years of menstruation plus postmenopausal estrogen use) was associated with higher BMD and a reduced incidence of atraumatic fractures. Estrogen therapy that is initiated at the time of menopause and is continued into later life results in the greatest increases in bone density. However, even when it is started after age 60, estrogen replacement also results in some increased BMD and reduced fracture risk (28).

Encouraging estrogen use. Despite estrogen therapy's positive effects on bones, only 15% to 20% of eligible women currently receive this preventive care, partly because of fear that estrogen replacement increases the risk of breast cancer. Recent studies (29,30) have yielded conflicting results; but experts conclude (31) that the estrogen regimens that have been shown to protect against osteoporosis and cardiovascular disease are not currently associated with any clear increase in the risk of breast cancer. In addition, estrogen therapy for women who have a uterus does not appear to increase their risk of endometrial cancer if they also take progestins (25).

Estrogen therapy also benefits patients' heart health. A 1991 report from the Nurses' Health Study (32) showed that women taking estrogen replacement decreased their risk of myocardial infarction and cardiac death by 44% and of overall mortality by 11% relative to women who had never been treated with estrogen.

Risk/benefit counseling. Women who are considering hormone replacement should receive information about the risks and benefits of this therapy. A 50-year-old woman, for example, may expect the following risks with and without estrogen replacement therapy (33):

  • Breast cancer, about 3% without and 4% with therapy,
  • Death from hip fracture, about 3% without and 1.5% to 2% with therapy; and
  • Lifetime risk of cardiac death, about 30% without and 15% with therapy.

Thus, the cardiovascular benefits of estrogen replacement should encourage women to begin this therapy.

Two studies may also be useful in counseling patients. Grady et al (34) concluded that most postmenopausal women who use estrogen could increase their life expectancy by 1 or 2 years; exceptions are those with a history of breast cancer or with a first-degree relative who has had premenopausal breast cancer. More recently, Col et al (35) concluded that hormone therapy should extend the life of women who have at least one risk factor for cornonary heart disease, even if they also have first-degree relatives with breast cancer. However, these authors do not recommend hormone replacement for women who have no risk factors for coronary heart disease or hip fracture, but have two first-degree relatives with breast cancer.

Alendronate

Postmenopausal patients who have a contraindication to estrogen replacement therapy should be treated with alendronate. Alendronate is a bisphosphonate that inhibits osteoclastic activity and is approved for the treatment of postmenopausal osteoporosis. It has been shown to increase BMD and reduce fracture risk. A recent trial (36) showed that alendronate, 10 mg/day for 2 years, increased BMD in the hip by 5% and in the spine by 7%. A second trial (37) found that 10 mg/day for 3 years reduced the risk of vertebral fractures by 48%. In addition, this study demonstrated that alendronate also reduced the loss of height and the progression of vertebral deformities often associated with osteoporosis in postmenopausal women. Results from the Fracture Intervention Trial (38) showed that the same dose of alendronate reduced the number of fractures in the hip and wrist by 50% and also decreased new vertebral fractures. Though alendronate is highly effective in increasing BMD and decreasing risk of fracture, its gastrointestinal side effects include nausea, abdominal pain, and dyspepsia.

Alendronate can be used to treat younger women who have severe osteoporosis and who do not respond to estrogen. However, few physicians are willing to prescribe alendronate to women of childbearing age because of the potential teratogenicity to a fetus; those who do, do so with great caution and only along with adequate birth control.

Calcitonin

In the authors' estimation, only patients with a contraindication to estrogen and alendronate should be treated initially with nasal calcitonin. Calcitonin-salmon is an antiresorptive agent that targets osteoclasts directly and has recently been approved by the FDA in the form of a nasal spray (200 IU/day) for the treatment of postmenopausal osteoporosis. However, the efficacy of calcitonin in reducing the risk of osteoporotic fractures is uncertain. A recent study(39) suggests that moderately osteoporotic women who take calcitonin increase their lumbar spine BMD in a dose-dependent fashion and reduce the incidence of new fractures by two-thirds relative to moderately osteoporotic women who take calcium alone. However, this and other studies(40,41) do not demonstrate that calcitonin unequivocally reduces vertebral and nonvertebral fractures among patients with premature or postmenopausal osteoporosis. Hence, in spite of nasal calcitonin's favorable side-effect profile, the authors suggest that alendronate and estrogen are more effective treatments for postmenopausal osteoporosis.

Summing Up Treatment

New therapies for osteoporosis are currently being developed. Raloxifene, a tamoxifen derivative, is one of the most promising drugs on the horizon. Preliminary research indicates that this drug may yield the same benefits as estrogen for osteoporosis and cardiovascular diseases without increasing the risk of breast cancer.

Meanwhile, the state-of-the-art treatment of postmenopausal osteoporosis is still estrogen replacement therapy during menopause and beyond. Patients for whom estrogen therapy is condraindicated should be treated with alendronate. Those with a contraindication to estrogen and alendronate should be prescribed nasal calcitonin. Additionally, all patients should receive adequate amounts of calcium, vitamin D, and weight-bearing exercise.

Adolescent athletes and premenopausal women can avoid osteoporosis if they maintain eumenorrhea, adequate calcium intake, and appropriate weight-bearing exercise. Premature osteoporosis is usually related to low estrogen and menstrual dysfunction; these conditions can often be alleviated if the patients decrease their energy expenditure, gain weight, and/or replace estrogen with oral contraceptives or through standard estrogen replacement therapy. Estrogen therapy in adolescents is complicated by the fact that current research has not answered the question of how much estrogen is sufficient to reverse premature osteoporosis. In addition, it may not be easy to convince young athletes to take oral contraceptives or to follow estrogen replacement therapy regimens for their bone health.

References

  1. Consensus development conference: prophylaxis and treatment of osteoporosis. Am J Med 1991;90(1):107-110
  2. Looker AC, Johnston CC Jr, Wahner HW, et al: Prevalence of low femoral bone density in older U.S. women from NHANES III. J Bone Miner Res 1995;10(5):796-802
  3. Melton LJ III: How many women have osteoporosis now? J Bone Miner Res 1995;10(2):175-177
  4. Owen RA, Melton LT III, Gallagher JC, et al: The national cost of acute care of hip fractures associated with osteoporosis. Clin Orthop 1980;150(Jul-Aug):172-176
  5. Holbrook TL: The Frequency of Occurrence, Impact and Cost of Musculoskeletal Conditions in the United States. Chicago, American Academy of Orthopedic Surgeons, 1984
  6. Ray WA, Griffin MR, Baugh DK: Mortality following hip fracture before and after implementation of the prospective payment system. Arch Intern Med 1990;150(10):2109-2114
  7. Recker RR, Davies KM, Hinders SM, et al: Bone gain in young adult women. JAMA 1992;268(17):2403-2408
  8. Birkenhager-Frenkel DH, Courpron P, Hupscher A, et al: Age-related changes in cancellous bone structure: a two-dimensional study in the transiliac and iliac crest biopsy sites. Bone Miner 1988;4(2):197-216
  9. Marcus R, Kosek J, Pfefferbaum A, et al: Age-related loss of trabecular bone in premenopausal women: a biopsy study. Calcif Tissue Int 1983;35(4-5):406-409
  10. Riggs BL, Wahner HW, Dann WL, et al: Differential changes in bone mineral density of the appendicular and axial skeleton with aging: relationship to spinal osteoporosis. J Clin Invest 1981;67(2):328-335
  11. Mazess RB: On aging bone loss. Clin Orthop 1982;165(May):239-252
  12. Drinkwater BL: Exercise in the prevention of osteoporosis, in Christiansen C, Riis B (eds): Osteoporosis Proceedings, Rodovre, Denmark, Osteopress Aps 1993, pp 105-108
  13. Rencken ML, Chesnut CH III, Drinkwater BL: Bone density at multiple skeletal sites in amenorrheic athletes. JAMA 1996;276(3):238-240
  14. The Scientific Advisory Board of the National Osteoporosis Foundation: Clinical indications for bone mass measurement. J Bone Miner Res 1989;4(suppl 2):1-28
  15. Kanis JA, Melton LJ III, Christiansen C, et al: The diagnosis of osteoporosis. J Bone Miner Res 1994;9(8):1137-1141
  16. American College of Sports Medicine: ACSM Position Stand on Osteoporosis and Exercise. Med Sci Sports Exerc 1995;27(4):i-vii
  17. Lane NE, Block DA, Jones HH, et al: Long distance running, bone density, and osteoarthritis. JAMA 1986;255(9):1147-1151
  18. Michel BA, Bloch DA, Fries JF: Weight-bearing exercise, overexercise, and lumbar bone density over age 50 years. Arch Intern Med 1989;149(10):2325-2329
  19. NIH consensus conference: Optimal calcium intake. JAMA 1994;272(24):1942-1948
  20. Keen AD, Drinkwater BL: No gain in vertebral bone density over 10 years in previously amenorrheic athletes, abstracted. J Bone Miner Res 1995;10(suppl 1):S243
  21. Cumming DC: Exercise-associated amenorrhea, low bone density, and estrogen replacement therapy. Arch Intern Med 1996;156(19):2193-2195
  22. Hergenroeder AC, Klish WJ, Smith EO, et al: A randomized clinical trial of bone mineral density changes in young women with hypothalamic amenorrhea treated with oral contraceptive pills. Med Sci Sports Exerc 1995;27(5):S94
  23. Gulekli B, Davies MC, Jacobs HS: Effect of treatment on established osteoporosis in young women with amenorrhea. Clin Endocrinol 1994;41(3):275-281
  24. The Writing Group for the PEPI Trial: Effects of hormone therapy on bone mineral density: results from the Postmenopausal Estrogen/Progestin Interventions (PEPI) trial. JAMA 1996;276(17):1389-1396
  25. Speroff L, Rowan J, Symons J, et al: The comparative effect on bone density, endometrium, and lipids of continuous hormones as replacement therapy (CHART Study): a randomized controlled trial. JAMA 1996;276(17):1397-1403
  26. Cauley JA, Seeley DG, Ensrud K, et al: Estrogen replacement therapy and fractures in older women. Ann Intern Med 1995;122(1):9-16
  27. Nguyen TV, Jones G, Sambrook PN, et al: Effects of estrogen exposure and reproductive factors on bone mineral density and osteoporotic fractures. J Clin Endocrinol Metab 1995;80(9):2709-2714
  28. Schneider DL, Barrett-Connor EL, Morton DJ: Timing of postmenopausal estrogen for optimal bone mineral density. JAMA 1997;277(7):543-547
  29. Colditz GA, Hankinson SE, Hunter DJ, et al: The use of estrogens and progestins and the risk of breast cancer in postmenopausal women. N Engl J Med 1995;332(24):1589-1593
  30. Stanford JL, Weiss NS, Voigt LF, et al: Combined estrogen and progestin hormone replacement therapy in relation to risk of breast cancer in middle-aged women. JAMA 1995;274(2):137-142
  31. Speroff L: Postmenopausal hormone therapy and breast cancer. Obstet Gynecol 1996;87(2 suppl):44S-54S
  32. Stampfer MJ, Colditz GA, Willett WC, et al: Postmenopausal estrogen therapy and cardiovascular disease: ten-year follow-up from the Nurses' Health Study. N Engl J Med 1991;325(11):756-762
  33. Isenbarger DW, Chapin BL: Osteoporosis: current pharmacologic options for prevention and treatment. Postgrad Med 1997;101(1):129-143
  34. Grady D, Rubin SM, Petitti DB, et al: Hormone therapy to prevent disease and prolong life in postmenopausal women. Ann Intern Med 1992;117(12):1016-1037
  35. Col NF, Eckman MH, Karas RH, et al: Patient specific decisions about hormone replacement therapy in postmenopausal women. JAMA 1997;277(14):1140-1147
  36. Chesnut CH III, McClung MR, Ensrud KE, et al: Alendronate treatment of the postmenopausal osteoporotic woman: effect of multiple dosages on bone mass and bone remodeling. Am J Med 1995;99(2):144-152
  37. Liberman UA, Weiss SR, Broll J, et al: Effect of oral alendronate on bone mineral density and the incidence of fractures in postmenopausal osteoporosis. N Engl J Med 1995;333(22):1437-1443
  38. Black DM, Cummings SR, Karpf DB, et al: Randomized trial of effect of alendronate on risk of fracture in women with existing vertebral fractures. Lancet 1996;348(9041):1535-1541
  39. Overgaard K, Hansen MA, Jensen SB, et al: Effect of calcitonin given intranasally on bone mass and fracture rates in established osteoporosis: a dose-response study. BMJ 1992;305(6853):556-561
  40. Kanis JA, Johnell O, Gullberg B, et al: Evidence for efficacy of drugs affecting bone metabolism in preventing hip fracture. BMJ 1992;305(6862):1124-1128
  41. Reginster JY, Deroisy R, Lecart MP, et al: A double-blind, placebo-controlled, dose-finding trial of intermittent nasal salmon calcitonin for prevention of postmenopausal lumbar spine bone loss. Am J Med 1995;98(5):452-458


Osteoporosis and Stress Fractures in a Young Runner

A 17-year-old cross-country runner presented with right foot pain that had begun 3 weeks earlier at the start of the season. Her pain came on after running less than 1 mile and at times when walking barefoot. She had been running about 35 miles per week for the past 8 to 10 weeks. She denied any acute right foot or ankle injury but reported a stress fracture of the left tibia the previous year.

She was 5'2'', weighed 100 lb, and had oligomenorrhea. She had pain on palpation over the shaft of the first metatarsal but none over the second through fifth metatarsals and no soft-tissue swelling of the foot. Her gait showed mild hyperpronation. Right foot radiographs revealed no bony abnormalities, but a bone scan showed increased uptake in the first metatarsal and cuboid. Given her past stress fracture and the unusual location of the present fracture, an evaluation for osteoporosis was undertaken.

Results of tests, including a complete blood count, chemistry panel, and thyroid-stimulating hormone assay, were all within normal limits. Dual-energy x-ray absorptiometry revealed a T-score (table 1) of -2.59 for the spine and -1.69 for the hip, both diagnostic of osteoporosis. A sports psychologist and a nutritionist were consulted and agreed that the patient had an eating disorder.

She was treated with oral contraceptives, supplemental calcium, vitamin D, avoidance of weight bearing, and counseling. Her stress fracture healed over the next 6 weeks, but she did not return to competition until the next cross-country season. She has continued to be treated with oral contraceptives and calcium supplements and is being followed by an eating disorder specialist.

This case demonstrates that a seemingly healthy young woman can have significant osteoporosis. Physicians and trainers must recognize that multiple or unusual stress fractures can be "red flags" for osteoporosis.


Dr Erickson completed a residency in internal medicine at St Joseph's Hospital in Phoenix and is a primary care sports medicine fellow at Ball Memorial Hospital/Central Indiana Sports Medicine in Muncie, Indiana. He is a member of the American Medical Society for Sports Medicine (AMSSM). Dr Sevier is the program director of the Sports Medicine Fellowship in Muncie. Dr Christie practices internal medicine and sports medicine at the Community Health Plan in Poughkeepsie, New York. He is a fellow of the American College of Physicians, and a member of the editorial board of The Physician and Sportsmedicine. Drs Sevier and Christie are board certified in internal medicine, charter members of the AMSSM, and fellows of the American College of Sports Medicine. All three hold certificates of added qualification in sports medicine. Address correspondence to Steven Erickson, MD, Ball Memorial Hospital, Central Indiana Sports Medicine, 100 N Tillotson, Muncie, IN 47304; e-mail correspondence to [email protected].


RETURN TO NOVEMBER 1997 TABLE OF CONTENTS

HOME  |   JOURNAL  |   PERSONAL HEALTH  |   RESOURCE CENTER  |   CME  |   ADVERTISER SERVICES  |   ABOUT US  |   SEARCH


The McGraw-Hill Companies Gradient

Copyright (C) 1997. The McGraw-Hill Companies. All Rights Reserved
Privacy Policy.   Privacy Notice.