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Keywords:

  • androgen deprivation therapy;
  • bicalutamide;
  • bisphosphonate;
  • fracture;
  • gonadotropin-releasing hormone agonist;
  • osteoporosis

Abstract

  1. Top of page
  2. Abstract
  3. DEFINITION OF OSTEOPOROSIS
  4. DIAGNOSIS
  5. CLINICAL MANIFESTATIONS OF OSTEOPOROSIS
  6. CAUSES OF OSTEOPOROSIS IN MEN
  7. ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS
  8. ROLE OF ESTROGENS IN MALE BONE METABOLISM
  9. BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS
  10. PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY
  11. CONCLUSIONS
  12. REFERENCES

Osteoporosis is a complication of androgen deprivation therapy in men with prostate carcinoma. Androgen deprivation therapy, caused by either bilateral orchiectomy or treatment with a gonadotropin-releasing hormone agonist, decreases bone mineral density and increases fracture risk. Other factors including diet and lifestyle may contribute to bone loss. There is limited information regarding the best strategy to prevent osteoporosis in men with prostate carcinoma. Lifestyle modification including smoking cessation, moderation of alcohol consumption, and regular weight-bearing exercise should be encouraged. Supplemental calcium and vitamin D are also recommended. Additional treatment may be warranted for men with osteoporosis, fractures, or high rates of bone loss during androgen deprivation therapy. Intravenous pamidronate, a second-generation bisphosphonate, prevents bone loss during androgen deprivation therapy. Zoledronic acid, a more potent third-generation bisphosphonate, not only prevents bone loss but also increases bone mineral density during androgen deprivation therapy. Other bisphosphonates may be effective although they have not been evaluated in this clinical setting. Treatment with estrogens or selective estrogen receptor modulators may also be effective. Monotherapy with bicalutamide or other antiandrogens may cause less bone loss than androgen deprivation therapy. Cancer 2003;97(3 Suppl):789–95. © 2003 American Cancer Society.

DOI 10.1002/cncr.11149

Osteoporosis is generally considered a disease of older women although it is also common in men. In the U.S., osteoporosis is prevalent in more than 1.5 million men older than 65 years and another 3.5 million men are at risk.1 Men experience approximately 33% of all hip fractures and mortality after hip fractures is higher in men than in women.2 The pathogenesis and treatment of male osteoporosis have not been adequately studied. Management decisions concerning male osteoporosis are often based on extrapolation from studies of postmenopausal women with osteoporosis.

DEFINITION OF OSTEOPOROSIS

  1. Top of page
  2. Abstract
  3. DEFINITION OF OSTEOPOROSIS
  4. DIAGNOSIS
  5. CLINICAL MANIFESTATIONS OF OSTEOPOROSIS
  6. CAUSES OF OSTEOPOROSIS IN MEN
  7. ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS
  8. ROLE OF ESTROGENS IN MALE BONE METABOLISM
  9. BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS
  10. PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY
  11. CONCLUSIONS
  12. REFERENCES

Bone mineral density (BMD) is inversely correlated with fracture risk in men and women.3–6 A Working Group of the World Health Organization (WHO) has defined normal, osteopenia, and osteoporosis in women based on BMD compared with the value in young adults (Table 1).7 The WHO definitions are often applied to men. Whether the same limits should be used in men is controversial, however, because men have larger bones and a higher peak bone mass.8 Each standard deviation decrease in BMD increases the relative risk of fracture by approximately twofold in women.9

Table 1. World Health Organization Classification of Osteoporosis
ClassificationBone mineral densitya
  • SD: Standard deviations.

  • a

    Standard deviations are derived from the mean peak value in young adults.

Normal−1.0 SD and above
OsteopeniaBetween −1.0 SD and −2.5 SD
Osteoporosis−2.5 SD and below
Severe osteoporosis−2.5 SD and below with fragility fractures

DIAGNOSIS

  1. Top of page
  2. Abstract
  3. DEFINITION OF OSTEOPOROSIS
  4. DIAGNOSIS
  5. CLINICAL MANIFESTATIONS OF OSTEOPOROSIS
  6. CAUSES OF OSTEOPOROSIS IN MEN
  7. ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS
  8. ROLE OF ESTROGENS IN MALE BONE METABOLISM
  9. BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS
  10. PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY
  11. CONCLUSIONS
  12. REFERENCES

Bone mineral density can be determined by several noninvasive methods.9 Dual-energy X-ray absorptiometry (DEXA) is the method of choice for BMD measurement in most cases. This technique easily and precisely measures BMD at multiple skeletal sites with minimal radiation exposure. Measurement of the posteroanterior lumbar spine BMD is most useful for evaluating the efficacy of treatment, whereas measurement of hip BMD is most useful for predicting fractures. However, DEXA has limitations. When measured by DEXA, the average BMD of the posteroanterior lumbar spine increases in men after age 55 years due to development of osteoarthritis in the posterior spinous elements.10–14 The DEXA method estimates trabecular bone mass better and detects osteoporosis more readily in the lateral projection of the lumbar spine compared with the posteroanterior projection.13, 14 However, BMD cannot be determined reliably in the lateral projection in many older men because of their large body size.

Quantitative computed tomography scan is a more sensitive but less precise method than DEXA for detecting osteoporosis in men. It measures trabecular BMD in the central region of the vertebral bodies, avoiding the confounding effects of osteoarthritis.15

Ultrasound measurements of the heel, finger, tibia, or patella are inexpensive and portable. However, measurement of BMD by ultrasound is relatively imprecise and the skeletal sites evaluated are unresponsive to treatment.

Secondary causes of bone loss should be considered in men with an established diagnosis of osteoporosis. A focused history, physical examination, and selected laboratory tests are sufficient in most cases. Measurements of serum concentrations of parathyroid hormone and 25-hydroxyvitamin D are recommended to exclude hypothyroidism and vitamin D deficiency. Serum thyroid-stimulating hormone levels can exclude hypothyroidism and routine serum chemistries can exclude renal or liver disease. Serum concentrations of calcium, inorganic phosphate, and alkaline phosphatase (AP) are usually normal. Fractures may result in transient elevation of serum AP levels. Persistent elevation of serum AP levels suggests liver disease, osteomalacia, Paget disease, or bone metastases.

Measurement of biochemical markers of bone resorption and bone formation in the serum and urine complements BMD assessment. Biochemical marker of bone turnover may also provide an early indication of response to treatment. High levels of bone turnover are associated with greater rates of bone loss and may be an independent predictor of fracture risk. The clinical utility of bone turnover markers has not been established and biochemical markers should not be used in place of BMD measurements.

CLINICAL MANIFESTATIONS OF OSTEOPOROSIS

  1. Top of page
  2. Abstract
  3. DEFINITION OF OSTEOPOROSIS
  4. DIAGNOSIS
  5. CLINICAL MANIFESTATIONS OF OSTEOPOROSIS
  6. CAUSES OF OSTEOPOROSIS IN MEN
  7. ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS
  8. ROLE OF ESTROGENS IN MALE BONE METABOLISM
  9. BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS
  10. PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY
  11. CONCLUSIONS
  12. REFERENCES

Osteoporosis causes no symptoms until it results in a fracture. The most common events are vertebral body compression fractures or fractures of the wrist, hip, ribs, pelvis, or humerus. Vertebral body compression fractures may result from minimal stress such as bending or lifting. Pain results from collapse of the vertebra and may be exacerbated by standing or sudden movements. The lumbar and thoracic regions are most frequently involved. Multiple vertebral fractures may result in loss of height and characteristic dorsal kyphosis and cervical lordosis.

Hip fractures are the most damaging complication of osteoporosis. Secondary complications of hip fracture, including thromboembolic events and infection, result in mortality rates of about 20% in the elderly. Approximately 33% of elderly hip fracture victims require long-term nursing home care.

Vertebral body compression fractures are a common manifestation of osteoporosis and may be mistaken for bone metastases in men with prostate carcinoma. Both bone metastases and vertebral body compression fractures from osteoporosis commonly present with back pain and share radiographic findings including tracer accumulation by bone scan.16 Because of the high prevalence of osteoporosis in this population, osteoporotic fractures should be considered when men with prostate carcinoma present with skeletal complaints.

CAUSES OF OSTEOPOROSIS IN MEN

  1. Top of page
  2. Abstract
  3. DEFINITION OF OSTEOPOROSIS
  4. DIAGNOSIS
  5. CLINICAL MANIFESTATIONS OF OSTEOPOROSIS
  6. CAUSES OF OSTEOPOROSIS IN MEN
  7. ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS
  8. ROLE OF ESTROGENS IN MALE BONE METABOLISM
  9. BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS
  10. PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY
  11. CONCLUSIONS
  12. REFERENCES

Adult bone mass is determined by both the peak bone mass achieved during development and the subsequent adult bone loss. Accordingly, osteoporosis can result from poor accumulation of bone during development, accelerated bone loss as an adult, or both. Most cases of osteoporosis result from accelerated adult bone loss. Smoking, excess alcohol intake, deficient dietary calcium intake, vitamin D deficiency, and a sedentary lifestyle contribute to adult bone loss.17

Alcohol abuse, chronic glucocorticoid therapy, and hypogonadism are the major causes of osteoporosis in men.8 These three causes account for approximately 50% of all cases of male osteoporosis. Other less common causes of male osteoporosis are hyperparathyroidism, hyperthyroidism, and multiple myeloma. Idiopathic osteoporosis refers to osteoporosis without any known cause.

ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS

  1. Top of page
  2. Abstract
  3. DEFINITION OF OSTEOPOROSIS
  4. DIAGNOSIS
  5. CLINICAL MANIFESTATIONS OF OSTEOPOROSIS
  6. CAUSES OF OSTEOPOROSIS IN MEN
  7. ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS
  8. ROLE OF ESTROGENS IN MALE BONE METABOLISM
  9. BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS
  10. PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY
  11. CONCLUSIONS
  12. REFERENCES

Androgen deprivation therapy is the mainstay of treatment for metastatic prostate carcinoma. Options for androgen deprivation therapy include bilateral orchiectomy, administration of a gonadotropin-releasing hormone (GnRH) agonist, or combination therapy with a GnRH agonist and an antiandrogen.18, 19 Estrogens are no longer routinely used for androgen deprivation therapy because of excess cardiovascular toxicity.20 Most men prefer treatment with a GnRH agonist because of the psychological implications of orchiectomy.18, 19

Orchiectomy and treatment with GnRH agonists have equivalent response rates and duration of response. Gonadotropin-releasing hormone agonists decrease serum concentrations of testosterone by greater than 95% and estrogen by approximately 80%.21, 22 The effects of GnRH agonists on gonadal steroid production are reversible in most men.

Four retrospective studies reported that androgen deprivation therapy increases fracture risk in men with prostate carcinoma.23–26 One retrospective study evaluated the incidence of clinical fractures in 235 men with prostate carcinoma.23 Approximately 14% of men with a history of bilateral orchiectomies experienced at least 1 osteoporotic fracture compared with only 1% of men with prostate carcinoma without a history of androgen deprivation therapy (P = 0.001). The cumulative rates of clinical fracture 7 years after castration or diagnosis were 28% and 1%, respectively (P = 0.001). Osteoporotic fractures were more common than traumatic or pathologic fractures. Approximately 38% of men surviving for more than 5 years after orchiectomy experienced 1 or more osteoporotic fractures.

Another study determined the incidence of fractures in men with prostate carcinoma during androgen deprivation therapy with a GnRH agonist.24 The median duration of GnRH agonist treatment was 22 months. Approximately 9% of men had at least one fracture. The median interval between initiation of androgen deprivation therapy and fracture was 22.2 months. Approximately 33% of fractures resulted from osteoporosis. The remaining fractures resulted from trauma, bone metastases, or multiple causes.

In a Japanese study, osteoporotic fractures were observed in 14 of 218 men during androgen deprivation therapy for prostate carcinoma.25 The average interval from start of androgen deprivation therapy to fracture was 28 months. Men with fractures had a lower BMD and higher biochemical markers of bone resorption than men without fractures.

In another retrospective review, fractures were evaluated in 181 consecutive men receiving androgen deprivation therapy for prostate carcinoma.26 Eighty-percent of men survived for 10 years on androgen deprivation therapy without a clinical fracture. Duration of androgen deprivation therapy was significantly associated with fracture risk. Increased body mass index and black race were associated with decreased fracture risk.

Several studies have prospectively evaluated BMD changes during initial androgen deprivation therapy for nonmetastatic prostate carcinoma (Table 2).27–29 Most studies reported 4–10% decreases in BMD as measured by DEXA during the first year of androgen deprivation therapy. The reported rates of bone loss during initial androgen deprivation therapy are higher than the rates associated with menopause.9 Other factors including vitamin D deficiency and inadequate dietary intake of calcium may contribute to bone loss in men with prostate carcinoma.30

Table 2. Prospective Studies of BMD during Androgen Deprivation Therapy for Stage M0 Prostate Carcinoma
StudyNo.TreatmentAnnual change in BMD (%)
  1. BMD: bone mineral density; GnRH: gonadotropin-releasing hormone.

Sweden2727Orchiectomy (n = 11)−10
  estrogen (n = 16)−1
France2812GnRH agonist−4
United States2926Orchiectomy or GnRH agonist−4

Some men develop osteoporosis during androgen deprivation therapy. Baseline BMD varies among men due to individual differences in peak bone mass and the amount of adult bone loss before androgen deprivation therapy. Accordingly, men begin androgen deprivation therapy with different relative risks for developing osteoporosis. Average bone loss is accelerated during androgen deprivation therapy although there are also individual differences in rates of bone loss during androgen deprivation therapy. In a study of elderly men with benign prostatic hyperplasia, for example, treatment with a GnRH agonist decreased average the BMD by approximately 10% although one-third of men had little or no bone loss after 1 year.31

Androgen deprivation therapy has other adverse effects on body composition including decrease in lean body mass and muscle size.32 These body composition changes may result in frailty and increase the risk of falls in older men.33 Therefore, androgen deprivation therapy may increase fracture risk by decreasing both BMD and lean body mass.

ROLE OF ESTROGENS IN MALE BONE METABOLISM

  1. Top of page
  2. Abstract
  3. DEFINITION OF OSTEOPOROSIS
  4. DIAGNOSIS
  5. CLINICAL MANIFESTATIONS OF OSTEOPOROSIS
  6. CAUSES OF OSTEOPOROSIS IN MEN
  7. ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS
  8. ROLE OF ESTROGENS IN MALE BONE METABOLISM
  9. BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS
  10. PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY
  11. CONCLUSIONS
  12. REFERENCES

Estrogens play an important role in male bone metabolism. Estrogen receptors are expressed in both osteoblasts and osteoclasts.34 Estrogens regulate bone remodeling by modifying the growth factor microenvironment.35, 36 In older men, serum estradiol levels are significantly correlated with spinal BMD37–39 and are inversely correlated with vertebral fracture risk.40

Rare genetic defects resulting in estrogen deficiency or estrogen resistance also suggest that estrogens are important in male bone metabolism. Skeletal maturation was delayed and BMD was decreased in a man with complete estrogen resistance due to a mutation in the estrogen receptor-alpha gene.41 Severe osteoporosis and delayed skeletal maturation were also observed in a man with severe estrogen deficiency due to an inactivating mutation in the aromatase gene.42, 43 Estrogen therapy markedly increased his BMD.43

In contrast to standard androgen deprivation therapy by orchiectomy or administration of a GnRH agonist, medical castration with estrogens is not associated with bone loss in men with prostate carcinoma. In a Swedish study, changes in BMD were evaluated in men with nonmetastatic prostate carcinoma treated with either bilateral orchiectomies (n = 11) or estrogens (n = 16).27 Orchiectomy decreased BMD of the hip by 10% after 1 year, whereas androgen deprivation therapy with estrogens decreased BMD by only 1%. Larger randomized studies are required to confirm this preliminary observation.

BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS

  1. Top of page
  2. Abstract
  3. DEFINITION OF OSTEOPOROSIS
  4. DIAGNOSIS
  5. CLINICAL MANIFESTATIONS OF OSTEOPOROSIS
  6. CAUSES OF OSTEOPOROSIS IN MEN
  7. ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS
  8. ROLE OF ESTROGENS IN MALE BONE METABOLISM
  9. BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS
  10. PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY
  11. CONCLUSIONS
  12. REFERENCES

Bicalutamide is a nonsteroidal antiandrogen that inhibits the action of androgens by binding to androgen receptors in the target tissue.44 Bicalutamide (50 mg by mouth daily) is indicated for use in combination with a GnRH agonist to treat men with metastatic prostate carcinoma. In addition, 150 mg bicalutamide has been approved in many countries for the treatment of men with early-stage prostate carcinoma. A supplemental new drug application has been filed with the Food and Drug Administration for bicalutamide 150-mg monotherapy for the treatment of men with early-stage prostate carcinoma based on the results from the early prostate carcinoma trial program.45, 46 If this new indication is approved, adjuvant treatment with bicalutamide monotherapy may become part of the routine management of men with early-stage prostate carcinoma in the U.S.

Bicalutamide monotherapy increases serum concentrations of estradiol.47 Because estrogens are important determinants of BMD and fracture risk in men, bicalutamide monotherapy may maintain or increase BMD. Consistent with this hypothesis, preliminary evidence from a small cross-sectional study suggests that bicalutamide monotherapy maintains BMD in men with prostate carcinoma.48 We recently completed accrual to a randomized controlled study to compare the effects of bicalutamide monotherapy and androgen deprivation therapy on BMD. Preliminary results from a multicenter randomized controlled study of similar design were reported at the 2002 annual meeting of the American Urological Association.49

PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY

  1. Top of page
  2. Abstract
  3. DEFINITION OF OSTEOPOROSIS
  4. DIAGNOSIS
  5. CLINICAL MANIFESTATIONS OF OSTEOPOROSIS
  6. CAUSES OF OSTEOPOROSIS IN MEN
  7. ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS
  8. ROLE OF ESTROGENS IN MALE BONE METABOLISM
  9. BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS
  10. PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY
  11. CONCLUSIONS
  12. REFERENCES

Lifestyle modification including smoking cessation, moderate alcohol consumption, and regular weight-bearing exercise should be encouraged. The initial treatment considerations are similar to the approach used to treat postmenopausal women. Consistent with the National Institutes of Health and Food and Nutrition Board recommendations, dietary calcium intake should be maintained at 1200–1500 mg per day and supplemental vitamin D intake should be 400 IU per day.8

High dietary calcium intake (> 2000 mg per day) is associated with increased prostate carcinoma risk.50, 51 This association has been attributed to decreased conversion of 25-hydroxyvitamin D to the more active 1,25 dihydroxyvitamin D.52 These observations have led to concerns about the potential impact of calcium on disease progression in men with prostate carcinoma. There is no established casual relationship between calcium intake and prostate carcinoma risk and there is no evidence to indicate that recommended dietary calcium intake of 1200–1500 mg per day is associated with prostate carcinoma progression. In addition, concurrent treatment with supplemental calcium and vitamin D during androgen deprivation therapy increases serum concentrations of both 25-hydroxyvitamin D and 1,25 dihydroxyvitamin D.53

Diamond et al.54 reported the results of a randomized crossover study of pamidronate in men with prostate carcinoma and bone metastases. Twenty-one men receiving androgen deprivation therapy for at least 6 months were assigned randomly to pamidronate (90 mg) or placebo administered once. Subjects were crossed over to the other treatment after 6 months. Primary study end points were BMD by DEXA and quantitative CT scan. Subject data for the two placebo treatment periods (the first 6 months and the 6 months after crossover) were combined and compared with the combined data for subjects during the two pamidronate treatment periods. Among 18 evaluable men, pamidronate significantly increased BMD of the hip and spine.55

The results of a randomized controlled study to prevent osteoporosis during androgen deprivation therapy for prostate cancer were reported by Smith et al.53 Forty-seven men with locally advanced or recurrent prostate carcinoma and no bone metastases were randomly assigned to receive leuprolide alone or leuprolide and pamidronate (Aredia [Novartis Oncology, East Hanover, NJ], 60 mg intravenously every 12 weeks), a potent bisphosphonate. BMDs of the posteroanterior lumbar spine and proximal femur were measured by DEXA. The trabecular BMD of the lumbar spine was measured by quantitative CT scan. In men treated with leuprolide alone, their mean (± standard error) BMD decreased by 3.3 ± 0.7% in the posteroanterior lumbar spine and by 1.8 ± 0.4% in total hip. The mean trabecular BMD of the lumbar spine decreased by 8.5 ± 1.8% after 12 months (P < 0.001 for each comparison with baseline). In contrast, mean BMD did not change significantly at any skeletal site in men treated with both leuprolide and pamidronate. Mean changes in BMD at 48 weeks differed significantly between groups in the posteroanterior lumbar spine (P < 0.001), trochanter (P = 0.003), and total hip (P = 0.005). Mean changes in trabecular BMD of lumbar spine also differed significantly between groups (P = 0.02). These finding indicate that pamidronate prevents bone loss in the hip and lumbar spine during androgen deprivation therapy.

Zoledronic acid (Zometa [Novartis Oncology]) is a third-generation bisphosphonate indicated for the treatment of bone metastases from multiple myeloma and solid tumors including prostate carcinoma. It is the most potent tested bisphosphonate with 100–850 times the potency of the second-generation bisphosphonate pamidronate (Aredia). Zoledronic acid given at intervals as infrequently as once yearly increases BMD in postmenopausal women with a low baseline BMD.56 In a randomized, placebo-controlled study, zoledronic acid (4 mg intravenously every 3 months) not only prevented bone loss but also increased BMD during androgen deprivation therapy for prostate carcinoma.57

Alendronate (Fosamax [Merck & Co., Whitehouse Station, NJ]) has been approved to treat men with osteoporosis. Oral alendronate increases BMD and helps to decrease vertebral fracture in men with osteoporosis and normal or near normal serum testosterone concentrations.58 The efficacy of alendronate in hypogonadal men is not known. Additional studies are necessary to evaluate the effects of alendronate and other oral bisphosphonates on BMD and fracture risk in men receiving androgen deprivation therapy for prostate carcinoma.

CONCLUSIONS

  1. Top of page
  2. Abstract
  3. DEFINITION OF OSTEOPOROSIS
  4. DIAGNOSIS
  5. CLINICAL MANIFESTATIONS OF OSTEOPOROSIS
  6. CAUSES OF OSTEOPOROSIS IN MEN
  7. ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS
  8. ROLE OF ESTROGENS IN MALE BONE METABOLISM
  9. BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS
  10. PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY
  11. CONCLUSIONS
  12. REFERENCES

Androgen deprivation therapy accelerates bone loss and increases fracture risk. Other factors including diet, lifestyle, and treatment-related loss of lean body mass may contribute to fracture risk. Some men develop osteoporosis during androgen deprivation therapy. There is limited information about the prevention or treatment of osteoporosis in men with prostate carcinoma. Lifestyle modification including smoking cessation, moderation of alcohol consumption, and regular weight-bearing exercise should be encouraged. Supplemental vitamin D (400 IU per day) and supplemental calcium to maintain a calcium intake of 1200–1500 mg per day are also recommended. Pamidronate (60 mg intravenously every 3 months) prevents bone loss during androgen deprivation therapy. Zoledronic acid (4 mg intravenously every 3 months) increases BMD during androgen deprivation therapy. Alendronate and other oral bisphosphonates may be effective but have not been evaluated in hypogonadal men with prostate carcinoma. Bicalutamide monotherapy may cause less bone loss than androgen deprivation therapy.

REFERENCES

  1. Top of page
  2. Abstract
  3. DEFINITION OF OSTEOPOROSIS
  4. DIAGNOSIS
  5. CLINICAL MANIFESTATIONS OF OSTEOPOROSIS
  6. CAUSES OF OSTEOPOROSIS IN MEN
  7. ANDROGEN DEPRIVATION THERAPY AND OSTEOPOROSIS
  8. ROLE OF ESTROGENS IN MALE BONE METABOLISM
  9. BICALUTAMIDE MONOTHERAPY AND OSTEOPOROSIS
  10. PREVENTION AND TREATMENT OF OSTEOPOROSIS FROM ANDROGEN DEPRIVATION THERAPY
  11. CONCLUSIONS
  12. REFERENCES