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National Medical Policy Subject: Bone Mineral Density Measurement Policy Number: NMP141 Effective Date*: May 2004 Updated: June 2016 This National Medical Policy is subject to the terms in the IMPORTANT NOTICE at the end of this document For Medicaid Plans: Please refer to the appropriate State's Medicaid manual(s), publication(s), citations(s) and documented guidance for coverage criteria and benefit guidelines prior to applying Health Net Medical Policies The Centers for Medicare & Medicaid Services (CMS) For Medicare Advantage members please refer to the following for coverage guidelines first: Use X X Source National Coverage Determination (NCD) National Coverage Manual Citation Local Coverage Determination (LCD)* Article (Local)* Other Reference/Website Link Bone (Mineral) Density Studies: http://www.cms.gov/medicare-coveragedatabase/search/advanced-search.aspx CMS Manual - Pub 100-04. Bone Mass Measurements (BMMs): http://www.cms.gov/Regulations-andGuidance/Guidance/Transmittals/downloads/R123 6CP.pdf MLN Matters Number: MM5521. Bone Mass Measurements (BMMs): http://www.cms.gov/Outreach-andEducation/Medicare-Learning-NetworkMLN/MLNMattersArticles/downloads/MM5521.pdf Bone Mineral Density Studies Jun 16 1 None Use Health Net Policy Instructions Medicare NCDs and National Coverage Manuals apply to ALL Medicare members in ALL regions • Medicare LCDs and Articles apply to members in specific regions. To access your specific region, select the link provided under “Reference/Website” and follow the search instructions. Enter the topic and your specific state to find the coverage determinations for your region. *Note: Health Net must follow local coverage determinations (LCDs) of Medicare Administration Contractors (MACs) located outside their service area when those MACs have exclusive coverage of an item or service. (CMS Manual Chapter 4 Section 90.2) If more than one source is checked, you need to access all sources as, on occasion, an LCD or article contains additional coverage information than contained in the NCD or National Coverage Manual. If there is no NCD, National Coverage Manual or region specific LCD/Article, follow the Health Net Hierarchy of Medical Resources for guidance. Current Policy Statement Health Net, Inc. considers bone mineral density (BMD) or Bone Mass Measurement (BMM) studies medically necessary for any of the following: Initial Bone Mineral Density Studies 1. Perimenopusal and postmenopausal women who have risk factors for osteoporosis (e.g. low body weight, prior low-trauma fracture or high risk medication) and are willing to consider available interventions. 2. Women age 65 and older and men age 70 and older, regardless of clinical risk factors; or 3. Men age 50 to 69 with specific risk factors for osteoporosis (i.e., low body weight, weight loss, physical inactivity, use of oral corticosteroids, androgen deprivation therapy, and previous fragility fracture) 4. Individuals who are considering therapy for osteoporosis, if BMD testing would facilitate their decision; or 5. An individual with vertebral abnormalities as demonstrated by an x-ray to be indicative of osteoporosis, osteopenia, or vertebral fracture; or 6. An individual receiving (or expecting to receive) glucocorticoid (steroid) therapy equivalent to 5 mg of prednisone, or greater, per day for more than three months; or 7. An individual with a history of long term treatment with any medication that may reduce bone mineral density or cause osteoporosis (e.g., anti-convulsants, heparin, gonadotropin releasing hormone therapy, cytotoxic drugs, immunosuppressants or aromatase inhibitors or thyroid replacement therapy where the TSH level is chronically below the normal range); or 8. An individual with primary hyperparathyroidism; or Bone Mineral Density Studies Jun 16 2 9. Individuals who are known or suspected to have a condition that may relate to osteoporosis, including but not limited to any of the following: a. b. c. d. e. f. g. h. i. Chronic liver disease; or Cushing Syndrome; or Hypercalciuria; or Hyperthyroidism; or Hypogonadism; or Malabsorption syndromes Rheumatoid arthritis Lupus Ankylosing spondylitis 10. In individual being monitored to assess the response to or efficacy of an FDA approved osteoporosis drug therapy (only dual-energy x-ray absorptiometry is considered medically necessary for this indication); or 11. An individual who has completed drug therapy for osteoporosis and is being monitored for response to therapy; or 12. An individual with impaired renal function including chronic renal failure, renal osteodystrophy, and other specified disorders resulting from impaired renal function and cystic kidney disease; or 13. An individual with a history of low trauma fracture(s); or 14. Postmenopausal women discontinuing estrogen should be considered for bone density testing 15. Anyone not receiving therapy in whom evidence of bone loss would lead to treatment Repeat Bone Mineral Density Studies Health Net, Inc follows Medicare policy for repeat bone mineral density measurement for members once every 2 years (if at least 23 months have passed since the month the last bone mass measurement was performed). A member may have a BMD measurement more frequently than every two years if medically necessary Note: DEXAs should not be done more often than yearly, as to do so leads to errors of reliability, i.e., the potential technical error is more than the expected change in bone mass. If someone needs to be monitored for bone loss over a period of less than a year, it should be done with bone turnover markers, such as a resorption marker (urinary Ntelopeptide) or a formation marker (bone alkaline phosphatase). Examples of situations where more frequent BMD studies may be performed are: 1. Monitoring patients on long-term glucocorticoid (steroid) therapy equivalent to 5.0 mgs of glucocorticosteriod (steroid) or greater per day for more than 3 months; and 2. Allowing for a baseline central bone mineral density to permit monitoring of patients in the future if the initial test was performed with a technique that is different from the monitoring method. More specifically, women who have low Bone Mineral Density Studies Jun 16 3 bone density scores found on screening ultrasound densitometry or peripheral DEXA scan should receive a central DEXA scan (including both spine and hip density measurements) both to confirm the findings of the screening test and to serve as a baseline study against which future DEXA scan results can be compared. 3. Monitoring individuals on FDA-approved osteoporosis drug therapy, to assess response and efficacy of therapy, until a response to such therapy has been documented over time and condition is stabilized. 4. Follow up bone mineral density testing after discontinuation of therapy, until a response to such therapy has been documented. 5. Men with prostate cancer undergoing hormonal manipulation Note: In rare instances, both axial and peripheral bone mineral density (BMD) studies may be medically necessary on the same date of service, or within thirty days of each other. These instances include any of the following: 1. Hip or spine cannot be measured (Reason must be documented in the medical record). 2. Hyperparathyroidism 3. Obese patient over the weight limit of the DEXA exam table. 4. Extreme arthritic changes that precludes accurate measurement. Codes Related To This Policy NOTE: The codes listed in this policy are for reference purposes only. Listing of a code in this policy does not imply that the service described by this code is a covered or non-covered health service. Coverage is determined by the benefit documents and medical necessity criteria. This list of codes may not be all inclusive. On October 1, 2015, the ICD-9 code sets used to report medical diagnoses and inpatient procedures have been replaced by ICD-10 code sets. ICD-9 Codes 193 242-242.91 246.0 252.00-252.08 255.0 255.3 256.2 256.31 256.39 257.2 259.3 259.5 259.9 Malignant neoplasm of thyroid gland Thyrotoxicosis with or without goiter Disorders of thyrocalcitonis secretion Hyperparathyroidism Cushing’s syndrome Other corticoadrenal overactivity Postablative ovarian failure Premature menopause Other ovarian failure Other testicular hypofunction Ectopic hormone secretion, not elsewhere classified Androgen insensitivity syndrome Unspecified endocrine disorder Bone Mineral Density Studies Jun 16 4 262 263-263.9 268.2 268.9 275.4-275.49 555-555.9 556-556.9 579-579.9 585-585.9 588.0-588.89 626.0 627.2 627.4 731.0 733.00-733.09 733.10- 733.19 733.7 733.90 733.93 733.94 733.95 753.12 753.13 753.14 753.15 753.16 753.17 753.19 756.50 756.51 758.6 781.91 793.7 793.91 793.99 805-805.9 806-806.9 808-808.9 813.4-813.47 813.5-813.54 820-820.9 995.20 E932.0 V45.77 V49.81 V50.42 V58.61 V58.63 V58.65 V58.69 Other severe, protein-calorie malnutrition Other and unspecified protein-calorie malnutrition Osteomalacia, unspecified Unspecified vitamin D deficiency Disorders of Calcium metabolism Regional enteritis Ulcerative Colitis Intestinal malabsorption Chronic kidney disease Disorders resulting from impaired renal function Absence of menstruation Symptomatic menopausal or female climacteric states Symptomatic states associated with artificial menopause Osteitis deformans without mention of bone tumor Osteoporosis Pathologic fracture Algoneurodystrophy Disorder of bone and cartilage, unspecified Stress fracture of tibia or fibula Stress fracture of the metatarsals Stress fracture of other bone Polycystic kidney, unspecified type Polycystic kidney, autosomal dominant Polycystic kidney, autosomal recessive Renal dysplagia Medullary cystic kidney Medullary sponge kidney Other specified cystic kidney disease Osteodystrophy, unspecified Osteogenesis imperfecta Gonadal dysgenesis Loss of height Nonspecific abnormal findings on radiological and other examinations of body structure Other image test inconclusive due to excess body fat Nonspecific abnormal findings on radiological and other examinations of body structure Fracture of vertebral column without mention of spinal cord injury Fracture of vertebral column with spinal cord injury Fracture of pelvis Lower end, closed Lower end, open Fracture of neck of femur Unspecified adverse effect of unspecified drug, medicinal and biological substance Adrenal cortical steroids (causing adverse effects) Acquired absence of genital organs Asymptomatic postmenopausal status (age-related) (natural) Prophylactic organ removal, ovary Long-term (current) use of anticoagulants Long-term (current) use of antiplatelets/antithrombotics Long-term (current) use of steroids Long-term (current) use of other medications Bone Mineral Density Studies Jun 16 5 V67.51 V67.59 V82.81 Note: Following completed treatment with high-risk medication, NEC Following other treatment, other Screening for osteoporosis Central DXA of the hip and/or spine is the preferred measurement for definitive diagnosis. Bone density measured at the femoral neck by DXA is the best predictor of hip fracture. DXA is the gold standard method for the noninvasive diagnosis of osteoporosis. ICD-10 Codes C73 E05.00-E05.91 E07.0 E21.0-E21.5 E24.0-E24.9 E27.0 E28.310-E28.319 E28.39 E29.1 E34.2 E34.50-E34.52 E34.9 E43 E44.0-E44.1 E55.9 E83.50-E83.59 E89.40-E89.6 K50.00-K50.919 K51.00-K51.919 K90.0-K90.9 M83.9 M80.00-M80.88 M81.0-M81.8 M94.361-M84.369 M84.371-M94.379 M84.38 M84.40-M84.68 M88.9 M89.00-M89.09 M89.9 M94.9 N18.1–N18.9 N25.0-N25.9 N91.2 N95.1 N95.8 Q61.02 Q61.19 Q61.2 Q61.3 Q61.4 Q61.5 Q61.8 Malignant neoplasm of thyroid gland Thyrotoxicosis (hyperthyroidism) Hypersecretion of calcitonin Hyperparathyroidism and other disorders of parathyroid gland Cushing’s syndrome Other adrenocortical overactivity Premature menopause Other primary ovarian failure Testicular hypofunction Ectopic hormone secretion, not elsewhere classified Androgen insensitivity syndrome Endocrine disorder, unspecified Unspecified severe protein-calorie malnutrition Protein-calorie malnutrition of moderate and mild degree Vitamin D deficiency, unspecified Disorders of calcium metabolism Postprocedural ovarian failure Crohn’s disease (regional enteritis) Ulcerative colitis Intestinal malabsorption Adult osteomalacia, unspecified Age-related osteoporisis with current pathological fracture Osteoporosiswithout current pathological fracture Stress fracture, tibia and fibula Stress fracture, ankle, foot and toes Stress fracture, other sites Pathological fracture, not elsewhere classified Osteitis deformans of unspecified bone Algoneurodystrophy Disorder of bone, unspecified Disorder of cartilage, unspecified Chronic kidney disease (CKD) Disorders resulting from impaired renal function Amenorrhea, unspecified Menopausal and female climacteric states Other specified menopausal and perimenopausal disorders Congenital multiple renal cysts Other polycystic kidney, infantile type Polycystic kidney, adult type Polycystic kidney, unspecified Renal dysplasia Medullary cystic kidney Other cystic kidney diseases Bone Mineral Density Studies Jun 16 6 Q78.0 Q78.9 Q96.0-Q96.9 R29.890 R93.6 R93.7 R93.8 R93.9 S20.000-S22.089 S12.00-S12.691 S32.000-S32.399 S52.501-S52.516 S72.001-S72.099 T50.905 Z13.820 Z40.02 Z78.0 Z79.01 Z79.02 Z79.51 Z79.52 Z79.89-Z79.899 Z90.71-Z90.79 Osteogenesis imperfecta Osteochondrodysplasia, unspecified Turner’s syndrome Loss of height Abnormal findings on diagnostic imaging of limbs Abnormal findings on diagnostic imaging of other parts of musculoskeletal system Abnormal findings on diagnostic imaging of other specified body structures Diagnostic imaging inconclusive due to excess body fat of patient Fracture of thoracic vertebra Fracture of cervical vertebra and other parts of the neck Fracture of lumbar sine and pelvis Fracture of lower end of radius Fracture of head and neck of femur Adverse effect of unspecified drugs, medicaments and biological Substances Encounter for screening for osteoporosis Encounter for prophylactic removal of ovary Asymptomatic menopausal state Long term (current) use of anticoagulants Long term (current) use of antithrombotics/antiplatelets Long term (current) use of inhaled steroids Long term (current) use of systemic steroids Other long term (current) therapy Acquired absence of genital organ(s) CPT Codes 76977 77078 77080 77081 77082 77086 Ultrasound bone density measurement and interpretation, peripheral site(s), any method Computed tomography, bone mineral density study, one or more sites; axial skeleton (eg, hips, pelvis, spine) Dual energy x-ray absorptiometry (DEXA), bone density study, one or more sites; axial (central) skeleton (e.g., hips, pelvis, spine) Dual energy absorptiometry (DEXA), bone density study, one or more sites; appendicular (peripheral) skeleton (e.g., radius, wrist, heel) Dual energy x-ray absorptiometry (DXA) bone density study, one or more sites, vertebral fracture assessment (code deleted 12/2014) Vertebral fracture assessment via dual-energy X-ray absorption (DXA) HCPCS Codes G0130 Single energy x-ray absorptiometry (SEXA) bone density study, one or more sites; appendicular skeleton (peripheral) (e.g., radius, wrist, heel) Codes not Covered by Medicare (February 2008) 78350 78351 Bone density (bone mineral content) study, one or more sites, single photon absorptiometry Bone density (bone mineral content) study, dual photon absorptionmetry, one or more sites Scientific Rationale – Update June 2016 Bone Mineral Density Studies Jun 16 7 Wu et al (2016) investigated the osteoporosis risk in patients with peptic ulcer disease (PUD) using a nationwide population-based dataset. This Taiwan National Health Insurance Research Database (NHIRD) analysis included 27,132 patients aged 18 years and older who had been diagnosed with PUD (International Classification of Diseases, Ninth Revision, Clinical Modification [ICD-9-CM] codes 531-534) during 1996 to 2010. The control group consisted of 27,132 randomly selected (age- and gender)-matched patients without PUD. The association between PUD and the risk of developing osteoporosis was estimated using a Cox proportional hazard regression model.During the follow-up period, osteoporosis was diagnosed in 2538 (9.35 %) patients in the PUD group and in 2259 (8.33 %) participants in the non-PUD group. After adjusting for covariates, osteoporosis risk was 1.85 times greater in the PUD group compared to the non-PUD group (13.99 vs 5.80 per 1000 person-years, respectively). Osteoporosis developed 1 year after PUD diagnosis. The 1-year follow-up period exhibited the highest significance between the 2 groups (hazard ratio [HR]=63.44, 95% confidence interval [CI]=28.19-142.74, P<0.001). Osteoporosis risk was significantly higher in PUD patients with proton-pump-inhibitors (PPIs) use (HR=1.17, 95% CI=1.03-1.34) compared to PUD patients without PPIs use. The authors concluded this study revealed a significant association between PUD and subsequent risk of osteoporosis. Therefore, PUD patients, especially those treated with PPIs, should be evaluated for subsequent risk of osteoporosis to minimize the occurrence of adverse events. Scientific Rationale – Update June 2015 Monadi et al (2015) reported the results of studies which addressed the impact of inhaled corticosteroid (ICS) therapy on BMD of patients with asthma are conflicting. A case-control study aimed to compare BMD status in ICS user with asthma with healthy controls according to age. BMD at the lumbar spine (LS), femoral neck (FN) was measured by dual energy X-ray absorptiometry (DEXA). Patients and controls were compared according to BMD gr/cm2, BMD T-score, BMD Z-score, frequency of osteoporosis (defined as BMD T-score ≤-2.5), and frequency of patients with BMD Zscore <-1 at LS and FN with regard to age <50 and ≥50 years old. Forty-four ICS user patients (females 63.6 %) with median treatment duration of 6.5 years and 50 controls (females, 69.4 %) with respective mean age of 49.2±9.5 and 47.4±10.5 years (p=0.38 and p=0.35) entered the study. Overall LS-BMD and FN-BMD gr/cm2 in total patients were lower than in controls by 6 % (p=0.065) and 5.9 % (p=0.09), respectively. In patients <50 years, mean LS-BMD gr/cm2 was lower than controls by 11.3 % (p=0.013) and FN-BMD by 8.8 % (p=0.044). Mean BMD T-score and BMD Zscore in both measurement sites were also lower than controls (p=0.013 and 0.01, respectively. Frequency of osteoporosis did not differ but frequency of patients with BMD Z-score <-1 was significantly higher in patients (odds ratio (OR)=6.57 95 % CI, 1.823.9, p=0.004). In age group ≥50 years old, reduction of BMD in both measurement sites did not reach to a significant level. The authors concluded the study indicates that BMD reduction in ICS user with asthma is dependent on age and appears that younger patients are at greater risk of BMD loss. These findings suggest preventive measures particularly in patients <50 years. Benetti-Pinto et al (2015) sought to analyze long-term variation in bone mineral density among young women with primary ovarian insufficiency. A cohort study evaluated bone mineral density in 72 women with primary ovarian insufficiency who were receiving estrogen + progesterone therapy. Bone mineral density was evaluated every 2 years for 8 years. The women were young, with a mean (SD) age of 34.1 (6.7) years and had a bone density measurement at baseline. The mean (SD) time between the last menstruation and the beginning of hormone treatment was 2.9 (4.2) years. The initial mean (SD) bone mineral density was 1.03 (0.17) and 0.91 (0.16) g/cm for the lumbar Bone Mineral Density Studies Jun 16 8 spine and femoral neck, respectively. The mean (SD) T score was -1.03 (1.39) and – 0.29 (1.09) for the lumbar spine and femoral neck, respectively. Bone mineral density measurements after a follow-up period of 2, 4, 6, and 8 years did not differ from bone mineral density at baseline. Osteopenia and osteoporosis were observed at the lumbar spine and femoral neck in 46% and 25% of women at the time of diagnosis, with no difference in the percentage of affected women across time. The authors concluded although women with primary ovarian insufficiency who are receiving estrogen + progesterone therapy maintain stable bone mass throughout an 8-year follow-up period, this treatment is not sufficient to decrease the number of women who experience some level of low bone density. Therapeutic regimens should be reviewed, probably with resumption of discussions about the need for other therapeutic strategies. Scientific Rationale – Update June 2013 Tuchendler and Bolanowski (2013) evaluated the effects of hyperthyroidism and hypothyroidism on osseous tissue metabolism in premenopausal women. 38 women with hyperthyroidism, 40 with hypothyroidism and 41 healthy women participated in this study. Initially after 6 and 12 months, each patient underwent selected hormonal, immunological and biochemical tests, measurement of concentrations of bone turnover markers and densitometry were also performed. On initial evaluation, lower cortical bone density was found in patients with hyperthyroidism (femoral neck). After 12 months, an increase in BMD was seen, but it was still lower than in the control group. Statistically significantly higher concentrations of bone turnover markers, decreasing from the sixth month of treatment, were noted only in the group with hyperthyroidism. Statistically significant differences were not noted in the femoral neck nor in the lumbar spine BMD in patients with hypothyroidism. Authors concluded hyperthyroidism poses a negative effect on bone metabolism. Hypothyroidism in premenopausal females does not have any influence on bone density. Ulu et al (2012) sought to evaluate bone loss in the early- and late-stage ankylosing spondylitis (AS) patients using posteroanterior (PA) and lateral lumbar and femoral bone mineral density (BMD) measurement methods. Eighty-six AS patients and 50 control subjects were enrolled. PA spine, lateral spine, and femur BMD values of patients and controls were measured. The presence of any syndesmophytes or compression fractures was determined. Patients were divided as early (<10 years) and late stage (≥10 years) according to the onset of the inflammatory pain. Mean PA spinal BMD was similar in patients and controls (p = 0.460). Femoral and lateral spine BMD values were significantly lower in patients (p = 0.012 and p = 0.001). When comparing early- and late-stage AS groups, mean PA spinal BMD was found to be lower in the early group (p = 0.005), while femoral and lateral spinal values were lower (although statistically not significant) in the late group. At least one compression fracture was present in 28 % of patients. Although not statistically significant, mean PA spinal BMD was higher in those with fractures. Femoral and lateral spinal BMD values were significantly lower in the fracture group (p = 0.034 and p = 0.004). Lateral spinal BMD values were significantly lower in patients with syndesmophytes (p = 0.004). Bone loss is increased in AS compared with control subjects. The BMD measurement at the lateral lumbar spine reflects bone loss and fracture risk better than PA spine and femoral measurements. Scientific Rationale – Update October 2010 van der Weijden et al (2010) sought to determine the prevalence and risk factors of low bone mineral density (BMD) in patients with spondylarthropathies (SpA) at an early stage of disease. In this cross-sectional study, the BMD of lumbar spine and hips was measured in 130 consecutive early SpA patients. The outcome measure BMD was defined as osteoporosis, osteopenia, and normal bone density. Logistic regression Bone Mineral Density Studies Jun 16 9 analyses were used to investigate relations between the following variables: age, gender, disease duration, diagnosis, HLA-B27, erythrocyte sedimentation rate (ESR), Creactive protein (CRP), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI), Bath Ankylosing Spondylitis Metrology Index (BASMI), extra-spinal manifestations and medication, with outcome measure low BMD (osteopenia and/or osteoporosis). The SpA population had a median time since diagnosis of 6.6 months and a disease duration of 6.3 years. In total, 9% of the early SpA patients had osteoporosis, 38% osteopenia, and 53% normal BMD. On univariate analyses, male gender, diagnosis of ankylosing spondylitis, increased CRP, high BASFI, and high BASMI were significantly associated with low BMD. Factors showing a relation with low BMD in the multivariate model were male gender, high BASMI and high BASFI. In early SpA patients, a high frequency (47%) of low BMD in femur as well as in lumbar spine was found. Low BMD was associated with male gender and decreased functional capacity. The authors concluded the findings emphasize the need for more alertness for osteoporosis and osteopenia in spondylarthropathy patients at an early stage of the disease. Alibhai et al (2010) used linked administrative databases in Ontario, Canada, and matched 19,079 men 66 years old or older with prostate cancer with at least 6 months of continuous androgen deprivation therapy or bilateral orchiectomy with men with prostate cancer who had never received androgen deprivation. Matching variables were age, prior cancer treatment, diagnosis year, co morbidity, medication, prior fractures and socioeconomic variables. Primary outcomes were a typical fragility fracture of the spine, hip or wrist and any fracture. Independent predictors of fracture outcomes were assessed with Cox proportional hazards models. At a mean 6.47-year follow-up androgen deprivation therapy was associated with an increased risk of fragility fracture and any fracture. Independent predictors of fragility and any fracture were increasing age, prior bone thinning medications, chronic kidney disease, prior dementia, prior fragility fracture and prior osteoporosis diagnosis or treatment. The authors concluded continuous androgen deprivation therapy for at least 6 months is associated with an increased risk of fracture. Increasing age, prior osteoporotic fracture and dementia are important clinical factors that may warrant greater consideration of anti-osteoporotic therapy in these men. Scientific Rationale – Update September 2009 The advent of potent acid suppressive medications such as proton pump inhibitors (PPI’s) has revolutionized the management of acid-related diseases such as gastroesophageal reflux disease (GERD). However, it is important that PPIs are only given for appropriate indications and that, whenever possible, they are used in the lowest effective dose. Many individuals have been using these medications on a continuous or long-term basis, which could result in untoward symptoms. Proton pump inhibitors may affect bone mineral metabolism. This class of drugs inhibits the production and intragastric secretion of hydrochloric acid, which is believed to be an important mediator of calcium absorption in the small intestine. A significant decreased secretion of hydrochloric acid, known as hypochlorhydria, has been noted, particularly among the elderly population, who may have decreased PPI clearance. These individuals may be more likely to have hypochlorhydria at baseline due to higher prevalence of Helicobacter pylori infection, which could theoretically result in calcium malabsorption. Studies have shown that PPI therapy may decrease insoluble calcium absorption or bone density. The PPI’s may also reduce bone resorption through inhibition Bone Mineral Density Studies Jun 16 10 of osteoclastic vacuolar proton pumps. Long-term PPI therapy, particularly at high doses, may be associated with an increased risk of hip fracture. Recent studies have suggested that the use of proton pump inhibitors for 1 or more years may be associated with hip fracture and other osteoporotic fractures; however, there is limited data on additional risk beyond 4 years exposure. Because proton pump inhibitors are commonly prescribed to control and prevent symptoms of chronic unrelenting conditions, it is likely that many patients will use these medications for more than 4 years. Osteoporosis is a common condition throughout the developed world, affecting up to 16% of women and 7% of men aged 50 years and older. The presence of underlying osteoporosis is a major risk factor for the development of fractures of the hip, proximal femur, spinal vertebra and forearm. In 2000, the estimated number of people with fractures worldwide was 56 million, and about 9 million new osteoporotic fractures occur each year. This number is predicted to increase to 88,124 by the year 2041. Moreover, the case-fatality rate for hip fractures can exceed 20%, and all osteoporosis-related fractures can lead to substantial long-term disability and decreased quality of life. Many risk factors for the development of osteoporosis-related fracture have been identified, including white ethnic background, low body mass index, physical inactivity and female sex. There are also a number of medication classes, including corticosteroids and serotonin selective reuptake inhibitors, whose use has been linked to higher rates of osteoporosis. Studies Insogna (2009) Two recent studies have reported increased hip fracture rates with longterm proton pump inhibitor (PPI) use raising concerns about adverse effects of this class of drugs on mineral metabolism. One plausible mechanism by which PPIs could affect calcium economy and skeletal homeostasis is by impairing intestinal calcium absorption. In the long term, this could potentially lead to a negative whole body calcium balance, resulting in higher rates of bone loss and a greater risk of fragility fractures. Kate et al (2008) performed a two phase matched nested case-control study. Phase 1 identified 4414 case patients (aged 50–79 yrs) with an incident hip fracture between 1995 and 2005. Phase 2 included the 1098 case patients identified as having no major medical risk factors for hip fracture (as assessed in phase 1) and a new set of 10,923 controls without major risk factors for hip fracture. The relative risk (RR) for hip fracture among patients who received any PPI prescription was 0.9 (95% confidence interval 0.7–1.1) compared with those with no PPI prescription. We found no evidence of an increased risk of hip fracture with increased PPI use. The RR estimates were similar in both sexes and in all age subgroups. No specific PPI was associated with an increased risk of hip fracture. Use of PPIs does not increase the risk of hip fracture in patients without major risk factors. The difference in results between our study and that of another, which indicated that PPI use increases the risk of hip fracture, may be due to residual confounding or effect modification in the latter study. Targownik et al (2008) completed a retrospective matched cohort study, using data from Population Health Research Data Repository in Canada. The authors matched 15,792 cases of osteoporosis related fractures with 47,289 controls. No significant association between overall risk of an osteoportic fracture and use of proton pump inhibitors was noted for durations of 6 years or less. However, exposure of 7 or more years was associated with increased risk of an osteoporosis-related fracture. This study Bone Mineral Density Studies Jun 16 11 also found an increased risk of hip fracture after five or more years of exposure to highdose PPI’s. Yang et al (2006) completed a nested case control study using data from the General Practice Research Database (1987-2003), from the U.K. Study included 13,556 hip fracture cases and 135,386 controls. The study noted that risk of hip fracture was increased among patients prescribed long-term, high-dose PPIs, > 5years of medication treatment. Short-term use of PPI’s did not appear to increase the fracture risk. In summary, all of the studies note that additional research is necessary to examine the effect of acid inhibition on calcium absorption and bone mineral metabolism, to determine the effect of acid inhibition on bone mineral density over time. The National Osteoporosis Foundation guidelines do not include PPI therapy as a risk factor for increased bone loss. Scientific Rationale – Update March 2009 According to the National Osteoporosis Foundation (NOF), the decision to perform bone density assessment should be based on an individual’s fracture risk profile and skeletal health assessment. The NOF states that measurement of bone density is not indicated unless the results will influence the patient’s treatment decision. Dual energy x-ray absorptiometry (DXA) is the most widely used method for measuring BMD because it gives very precise measurements at clinically relevant skeletal sites. According to the NOF guidelines, the following bone mass measurement technologies are capable of predicting both site-specific and overall fracture risk. When performed according to accepted standards, these densitometric techniques are accurate and highly reproducible: Central or peripheral dual-energy x-ray absorptiometry (pDXA) Quantitative computed tomography (QCT) and peripheral QCT (pQCT) Quantitative ultrasound densitometry (QUS) According to the NOF, central DXA assessment of the hip or spine is currently the “gold standard” for serial assessment of BMD and may be used to monitor the effectiveness of treatment. QCT, trabecular BMD of the lumbar spine can also be used to monitor age-, disease- and treatment-related BMD changes in men and women. Precision of acquisition should be established by phantom data and analysis precision by re-analysis of patient data. The NOF notes that in postmenopausal women, QCT measurement of spine trabecular BMD can predict vertebral fractures whereas pQCT of the forearm at the ultra distal radius predicts hip, but not vertebral fractures. They note there is lack of sufficient evidence for fracture prediction in men. Quantitative computed tomography (QCT) is based on the differential absorption of ionizing radiation by calcified tissue. Standard CT scanners are used, and attenuation measurements are compared with a standard reference to calculate bone mineral equivalents. Unlike other techniques, 3-dimensional BMD is directly calculated. QCT uniquely allows for the separate estimation of cancellous and cortical bone in the vertebral body. A focused examination of cancellous bone may be useful in assessing response to therapy (e.g., teriparatide therapy). QCT measures volumetric trabecular and cortical bone density at the spine and hip, whereas peripheral QCT (pQCT) measures the same at the forearm or tibia. It is important to note that QCT and pQCT are associated with greater amounts of radiation exposure than central DXA or pDXA. Bone Mineral Density Studies Jun 16 12 Quantitative ultrasound densitometry (QUS) does not measure BMD directly but rather speed of sound (SOS) and/or broadband ultrasound attenuation (BUA) at the heel, tibia, patella and other peripheral skeletal sites. A composite parameter using SOS and BUA may be used clinically. Validated heel QUS devices predict fractures in postmenopausal women (vertebral, hip and overall fracture risk) and in men 65 and older (hip and nonvertebral fractures). QUS is not associated with any radiation exposure. The NOF notes that peripheral skeletal sites (e.g. peripheral DXA, pQCT and QUS) do not respond in the same magnitude as the spine and hip to medications and thus are not appropriate for monitoring response to therapy at this time. Scientific Rationale - Update February 2008 As of February 20, 2008 Medicare has expanded the number of beneficiaries qualifying for BMM by reducing the dosage requirement for glucocorticoid (steroid) therapy from 7.5 mg of prednisone per day to 5.0 mg. It also changed the definition of BMM by removing coverage for a single-photon absorptiometry as it is not considered reasonable and necessary under the Social Security Act (Section 1862 (a)(1)(A)) Finally, it requires in the case of monitoring and confirmatory baseline BMMs, that they be performed with a dual-energy x-ray absorptiometry (axial) test. Medicare also requires a valid ICD-9M diagnosis code indicating the reason for the test is postmenopausal female, vertebral fracture, hyperparathyroidism, or steroid therapy. (MLN Matters MM5847) Initial Scientific Rationale Osteoporosis, or porous bone, is a disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility and an increased susceptibility to fractures of the hip, spine, and wrist. Peak bone mass is reached around age 30; after this age, bone resorption slowly begins to exceed bone formation. Osteoporosis develops when bone resorption occurs too quickly or if replacement occurs too slowly. In women, bone loss is most rapid in the first few years after menopause but persists into the postmenopausal years The National Institute of Health reports that in the in the U.S. today, 10 million individuals already have osteoporosis and 34 million more have low bone mass, placing them at increased risk for this disease. One out of every two women and one in four men over 50 will have an osteoporosis-related fracture in their lifetime. Osteoporosis is responsible for an estimated 300,000 hip fractures annually. More than 2 million American men suffer from osteoporosis, and millions more are at risk. Men account for about 25 percent of hip fractures Bone mineral density (BMD) is a key component used by physicians to determine the need for pharmacologic therapy to treat osteoporosis. The most widely used method to measure bone mineral density is the Dual Energy X-ray Absortiometry, or DEXA scanning. The scanner utilizes two sources of x-ray energy at a set frequency in an alternating fashion which greatly improves the precision and accuracy as compared to the more traditional radioisotope studies (such that would be used for a bone scan). Also, when compared with radiographic absortiometry or single energy x-ray absortiometry, DEXA scanning more precisely documents small changes in bone mass and can be used to examine both the spine and the extremities. DEXA scanning of the spine, hip or the total body requires only one, two or four minutes respectively. Quantitative computed tomography (QCT) is the only technique that can directly measure bone density and volume as well as distinguishing trabecular from cortical Bone Mineral Density Studies Jun 16 13 bone. DEXA scanning is less expensive, exposes the patient to less radiation and is more sensitive and accurate at measuring subtle changes in bone density over time or in response to drug therapy than is QCT. Reports from the various BMD technologies provide a comparison of the patient’s bone mineral density values with those of young normal women (T score) to age matched normal women (Z score). By comparing a patient’s bone density against the peer group, it can be determined if the patient is at risk for fracture and if the bone mass is typical for his/her age and sex. The T-score is expressed in standard deviations (SD). For each standard deviation below the mean, the risk of fracture increases significantly. The World Health Organization (WHO) defines osteopenia as a T score -1 to -2.5 standard deviations below the mean and osteoporosis as -2.5 or more standard deviations below the mean. Each one standard deviation in BMD below the young adult normal represents an increased risk of fracture. Bone mineral density measurements as a method to monitor response to treatment generally do not need to be repeated within two years since changes in bone density occur slowly. In addition, changes in bone mineral density at central sites (i.e., hip and spine) are often not reflected by changes in bone mineral density at peripheral sites, so it is recommended that peripheral measurement not used to monitor treatment response. Review History May 11, 2004 June 28, 2005 August 30,2005 May 2006 July 2006 March 2007 February 2008 September 2008 March 2009 September 2009 October 2010 July 2011 June 2012 June 2013 June 2014 June 2015 June 2016 Medical Advisory Council, initial approval Update Update Update to include Medicare criteria related repeat studies and steroid dose of >= 7.5 mg per day Update – no revisions Coding update Changed glucocortiosteriod dose from 7.5 mgs per day to 5.0 per day. Removed 78350 and G0130 from Medicare covered codes. Updated policy to comply with Medicare criteria related to BMD for monitoring response to treatment and additional indications for more frequent studies. Coding updates. Updated scientific rationale with bone mass measurement technologies accepted by the NOF as capable of predicting both sitespecific and overall fracture risk. Added continuous or long-term therapy ‘Proton Pump Inhibitors’ (PPI’s) (> 5 years), as a criteria for Initial Bone Mineral Density Studies. Revised wording in criteria #1, added criteria #3, 14 and 15. Added Medicare table, links to NCD and benefit policy. Update. Added Revised Medicare Table. No Revisions. Update. No Revisions. Update – no revisions. Code updates. Update – no revisions. Code updates Update – no revisions. Code updates Update – no revisions. Code updates This policy is based on the following evidence-based guidelines: Bone Mineral Density Studies Jun 16 14 1. National Osteoporosis Foundation. Clinician’s Guide to Prevention and Treatment of Osteoporosis. 2008. 2. Hodgson SF, Watts NB, Bilezikian JP, et al. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the prevention and treatment of postmenopausal osteoporosis: 2001 edition, with selected updates for 2003. Endocr Pract 2003 Nov-Dec; 9(6): 544-64. 3. American College of Obstetricians and Gynecologists (ACOG). Osteoporosis. Washington (DC): American College of Obstetricians and Gynecologists (ACOG); 2004 Jan. 14 p. (ACOG practice bulletin; no. 50). 4. Qaseem A, Snow V, Shekelle P. et al. Screening for Osteoporosis in Men: A Clinical Practice Guideline from the American College of Physicians. Ann Intern Med 2008 May 6;148(9):680-4. Available at: http://www.annals.org/content/148/9/680.full 5. National Osteoporosis Foundation (NOF). Clinician’s guide to prevention and treatment of osteoporosis. 2010. 6. American College of Radiology (ACR) Appropriateness Criteria Osteoporosis and bone mineral density. Revised 2010. 7. American Association of Clinical Endocrinologists (AACE) Menopause Guidelines Revision Task Force. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the diagnosis and treatment of menopause. 2010. Available at: https://www.aace.com/files/osteo-guidelines-2010.pdf 8. Nelson H; Haney E, et al. Screening for Osteoporosis: An Update for the U.S. Preventative Services Task Force. Annals of Internal Medicine 2010 July; 153(2):113. 9. U.S. Preventive Services Task Force. Screening for osteoporosis: U.S. preventive services task force recommendation statement. Ann Intern Med. 2011;154(5):356. 10. National Osteoporosis Foundation (NOF). Clinician’s guide to prevention and treatment of osteoporosis. 2013. Update Apr 2014 11. The American Congress of Obstetricians and Gynecologists. Osteoporosis. Practice Bulletin Number 129. Sept 2012. Reaffirmed 2014 References – Update June 2016 1. 2. 3. 4. Chen SJ, Chen YJ, Cheng CH, et al. Comparisons of Different Screening Tools for Identifying Fracture/Osteoporosis Risk Among Community-Dwelling Older People. Medicine (Baltimore). 2016 May;95(20):e3415. Lloyd JT, Alley DE, Hochberg MC, et al. Changes in bone mineral density over time by body mass index in the health ABC study. Osteoporos Int. 2016 Jun;27(6):210916. Pavel OR, Popescu M, Novac L, et al. Postmenopausal osteoporosis - clinical, biological and histopathological aspects. Rom J Morphol Embryol. 2016;57(1):12130. Wu CH, Tung YC, Chai CY, et al. . Increased Risk of Osteoporosis in Patients With Peptic Ulcer Disease: A Nationwide Population-Based Study. Medicine (Baltimore). 2016 Apr;95(16):e3309. References – Update June 2015 1. 2. 3. Benetti-Pinto CL, Ferreira VB, Yela DA. Long-term follow-up of bone density in women with primary ovarian insufficiency. Menopause. 2015 Mar 9. Heidari B, Hosseini R, Javadian Y, et al. Factors affecting bone mineral density in postmenopausal women. Arch Osteoporos. 2015 Dec;10(1):217. López E, Casajús JA, Ibarz E, et al. Application of a model based on dual-energy Xray absorptiometry and finite element simulation for predicting the probability of Bone Mineral Density Studies Jun 16 15 4. osteoporotic hip fractures to a sample of people over 60 years. Proc Inst Mech Eng H. 2015 May;229(5):369-85 Monadi M, Javadian Y, Cheraghi M, et al. Impact of treatment with inhaled corticosteroids on bone mineral density of patients with asthma: related with age. Osteoporos Int. 2015 Apr 10. References – Update June 2014 1. 2. Imai K. Recent methods for assessing osteoporosis and fracture risk. Recent Pat Endocr Metab Immune Drug Discov. 2014 Jan;8(1):48-59. Kurtoglu-Aksoy N, Akhan SE, Bastu E, et al. Implications of premature ovarian failure on bone turnover markers and bone mineral density. Clin Exp Obstet Gynecol. 2014;41(2):149-53. References – Update June 2013 1. Adams JE. Advances in bone imaging for osteoporosis. Nat Rev Endocrinol. 2013 Jan;9(1):28-42 2. Briot K. DXA parameters: Beyond bone mineral density. Joint Bone Spine. 2013 Apr 23. 3. Chevalley T, Bonjour JP, van Rietbergen B, et al. Fracture history of healthy premenopausal women is associated with a reduction of cortical microstructural components at the distal radius. Bone. 2013 May 6. 4. Friis-Holmberg T, Rubin KH, Brixen K, et al. Fracture Risk Prediction Using Phalangeal Bone Mineral Density or FRAX-A Danish Cohort Study on Men and Women. J Clin Densitom. 2013 Apr 23. 5. Ikegami S, Kamimura M, Uchiyama S, et al. Unilateral vs Bilateral Hip Bone Mineral Density Measurement for the Diagnosis of Osteoporosis. J Clin Densitom. 2013 May 15. 6. Liu X, Qian ZY, Feng YS, Li HL, Xu YJ. Comparison of differences between hip and lumbar bone mineral density in dual energy X-ray absorptiometric data. Zhonghua Yi Xue Za Zhi. 2013 Jan 15;93(3):191-4. 7. Rozental TD, Deschamps LN, Taylor A, et al. Premenopausal women with a distal radial fracture have deteriorated trabecular bone density and morphology compared with controls without a fracture. J Bone Joint Surg Am. 2013 Apr 3;95(7):633-42. 8. Runarsdottir RG, Thorsteinsdottir G, Indridason OS, Sigurdsson G. Bone mineral density of young women with history of anorexia nervosa. Laeknabladid. 2012 Oct;98(10):523-9. 9. Tuchendler D, Bolanowski M. Assessment of bone metabolism in premenopausal females with hyperthyroidism and hypothyroidism. Endokrynol Pol. 2013;64(1):404. 10. Ulu MA, Cevik R, Dilek B. Comparison of PA spine, lateral spine, and femoral BMD measurements to determine bone loss in ankylosing spondylitis. Rheumatol Int. 2012 Dec 29. References Update – June 2012 1. 2. 3. Gourlay ML, Fine JP, Preisser JS, et al. Bone-density testing interval and transition to osteoporosis in older women. N Engl J Med 2012; 366:225 Kleerekoper M. Screening for Osteoporosis. UpToDate. March 28 2012. Leslie WD, Morin SN, Lix LM, for the Manitoba Bone Density Program. Rate of Bone Density Change Does Not Enhance Fracture Prediction in Routine Clinical Practice. J Clin Endocrinol Metab 2012. References Update – July 2011 Bone Mineral Density Studies Jun 16 16 1. Jamal SA. Bone mass measurements in men and women with chronic kidney disease. Curr Opin Nephrol Hypertens. 2010;19(4):343-348. References Update – October 2010 1. 2. 3. 4. Abarado C, Mahon SM. Androgen-deprivation bone loss in patients with prostate cancer. Clin J Oncol Nurs. 2010 Apr;14(2):191-8. Alibhai SM, Duong-Hua M, Cheung AM, et al. Fracture types and risk factors in men with prostate cancer on androgen deprivation therapy: a matched cohort study of 19,079 men. J Urol. 2010 Sep;184(3):918-23. Khosla S. Update in male osteoporosis. J Clin Endocrinol Metab. 2010 Jan;95(1):310 van der Weijden MA, van Denderen JC, Lems WF, et al. Low bone mineral density is related to male gender and decreased functional capacity in early spondylarthropathies. Clin Rheumatol. 2010 Aug 10 References Update – September 2009 1. 2. 3. 4. 5. 6. 7. Insogna KL. The Effect of Proton Pump-Inhibiting Drugs on Mineral Metabolism. Am J Gastroenterol 2009; 104:S2–S4. Targownik LE, Lix LM, Metge CJ, et al. Use of proton pump inhibitors and risk of osteoporosis-related fractures. CMAJ. August 12, 2008; 179 (4). doi:10.1503/cmaj.071330. Available at: http://www.cmaj.ca/cgi/content/full/179/4/319 Kaye JA, Jick H. Proton Pump Inhibitor Use and Risk of Hip Fractures in Patients without Major Risk Factors. Pharmacotherapy 2008;28(8):951–959. Vestergaard P, Rejnmark L, Mosekilde L. Proton pump inhibitors, histamine h(2) receptor antagonists, and other antacid medications and the risk of fracture. Calcif Tissue Int. 2006;79:76-83. Yang YX, Lewis JD, Epstein S, et al. Long-term Proton Pump Inhibitor Therapy and Risk of Hip Fracture. JAMA. 2006;296:2947-2953. Available at: http://jama.amaassn.org/cgi/content/full/296/24/2947 O’Connell MB, Madden DM, Murray AM, et al. Effects of proton pump inhibitors on calcium carbonate absorption in women: a randomized crossover trial. Am J Med. 2005;118:778-781. Jacobson BC, Ferris TG, Shea TL, et al. Who is using chronic acid suppression therapy and why? Am J Gastroenterol. 2003;98:51-58. References Update – March 2009 2. 3. 4. 5. Khoo BC, Brown K, Cann C, et al. Comparison of QCT-derived and DXA-derived areal bone mineral density and T scores. Osteoporos Int. 2008 Dec 24. Imai K, Ohnishi I, Matsumoto T et al. Assessment of vertebral fracture risk and therapeutic effects of alendronate in postmenopausal women using a quantitative computed tomography-based nonlinear finite element method. Osteoporos Int. 2008 Sep 18. Zanchetta JR, Bogado CE, Ferretti JL et al. Effects of teriparatide [recombinant human parathyroid hormone (1-34)] on cortical bone in postmenopausal women with osteoporosis. J Bone Miner Res. 2003 Mar; 18(3): 539-43. Lane NE, Sanchez S, Modin GW et al. Parathyroid hormone treatment can reverse corticosteroid-induced osteoporosis. Results of a randomized controlled clinical trial. Clin Invest. 1998 Oct 15; 102(8): 1627-33 References Update – October 2008 Bone Mineral Density Studies Jun 16 17 1. Centers for Medicare & Medicaid Services. LCD for Bone Mineral Density (BMD) Studies (L20800). Effective 1/1/2007. 2. HighMark Medicare Services. Provider bulletin. Effective Jan 2007. 3. Centers for Medicare & Medicaid Services. LCD for Bone Mineral Density (BMD) Studies (L5829) Effective 1/1/2007. References Initial 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. The Relationship Between Bone Mineral Density and Ultrasound in Postmenopausal and Osteoporotic Women, Yeap, SS; Pearson, D; Cawte, SA; Hosking, DJ. Osteoporosis International 1998; 8 (2): 141-146. Bone Densitometry: Patients Receiving Prolonged Steroid Therapy. Health Technology Assessment, No. 9, September 1996, AHCPR Pub. No. 96-0058. Bone Densitometry: Patients with End-Stage Renal Disease. Health Technology Assessment, No. 8, AHCPR Pub. No. 96-0040. Screening for Postmenopausal Osteoporosis, Wallace, Tonner and Atkins, Guide to Clinical Preventive Services, report of the U.S. Preventive Services Task Force, Williams and Wilkins, 1996, pp. 509-516. U.S. Department of Health and Human Services, Center for Medicare and Medicaid Services (CMS). Medicare Program; Medicare Coverage and Payment for Bone Mass Measurements. 42 CFR Part 410, 63 Fed. Reg. 121, pp. 34320-34328; June 24, 1998. No authors listed. Osteoporosis prevention, diagnosis, and therapy. NIH Consens Statement. 2000;17(1):1-45 American Academy of Orthopaedic Surgeons/American College of Obstetricians and Gynecologists/American Geriatrics Society/American College of Radiology/American College of Rheumatology/American Academy of Physical Medicine and Rehabilitation/American Association of Clinical Endocrinologists/National Osteoporosis Foundation/The Endocrine Society/American Society for Bone and Mineral Research. Physician's guide to prevention and treatment of osteoporosis. Belle Mead (NJ): Excerpta Medica, Inc.; 1999. Bone Densitometry, Erlichman and Holohan, in Nuclear Medicine: Diagnosis and Therapy, edited by Harbert, Eckelman and Neurnann; New York: Thieme Medical Publishers, Inc., 1996, pp. 865-880. American College of Obstetricians and Gynecologists, Committee on Gynecologic Practice. Bone density screening for osteoporosis. ACOG Committee Opinion No. 270. Washington, DC: ACOG; 2002. No authors listed. Management of postmenopausal osteoporosis: Position statement of The North American Menopause Society. Menopause. 2002;9(2):84-101. The Effect of Age on the Association Between Body-Mass Index and Mortality, J. Stevens et. Al., New England Journal of Medicine, Volume 338, Number 1; Jan 1, 1998. U.S. Preventive Services Task Force. Screening for Osteoporosis in Postmenopausal Women. In: Guide to Clinical Preventive Services: Report of the U.S. Preventive Services Task Force. 3rd ed. Rockville, MD: Agency for Healthcare Research and Quality, 2000-2002. Available at: http://www.ahrq.gov/clinic/3rduspstf/osteoporosis/osteorr.htm. Accessed May 3, 2004 Miller PD, Njeh CF, Jankowski LG, et al. What are the standards by which bone mass measurement at peripheral skeletal sites should be used in the diagnosis of osteoporosis. J Clin Densitom. 2002;5 Suppl:S39-S45. Cummings SR, Bates D, Black DM. Clinical use of bone densitometry: Scientific review. JAMA. 2002;288(15):1889-1897. Bone Mineral Density Studies Jun 16 18 15. Espallargues M, Sampietro-Colom L, Estrada MD, et al. Identifying bone-massrelated risk factors for fracture to guide bone densitometry measurements: A systematic review of the literature. Osteoporos Int. 2001;12:811-822. 16. Homik J, Hailey D. Selective testing with bone density measurement. Edmonton, Alberta, Canada: Alberta Heritage Foundation for Medical Research; 1999. 17. Bone Mineral Density at Distal Forearm Can Identify Patients with Osteoporosis at Spine or Femoral Neck. Jones T., Davie MW; British Journal Rheumatology, 1998 May; 37 (5): 539-543. 18. Nelson HD, Helfand M. Screening for postmenopausal osteoporosis. Rockville, MD: Agency for Healthcare Research and Quality (AHRQ); 2002. 19. Agency for Healthcare Research and Quality (AHRQ).Osteoporosis in postmenopausal women: Diagnosis and monitoring. Rockville, MD: AHRQ; 2001. 20. Kanis JA, Brazier JE, Stevenson M, et al. Treatment of established osteoporosis: A systematic review and cost-utility analysis. Health Technol Assess. 2002;6(29). Institute for Clinical Systems Improvement (ICSI) 21. Densitometry as a diagnostic tool for the identification and treatment of osteoporosis in women. Bloomington, MN: ICSI; 2000. Canadian Coordinating Office for Health Technology Assessment (CCOHTA). 22. Bone mineral density screening. Ottawa, Canada: CCOHTA; 2003. International Society of Clinical Densitometry (ISCD). Bone mineral density testing. Official Positions. West Hartford, CT: ISCD; November 1, 2003. 23. Miller PD. Bone mass measurements. Clin Geriatr Med. 2003;19(2):281-297, vi. 24. Review of Bone Density Measurement; Evidence that Radiographic Osteopenia Predicts Low Bone Mass. Ahmed Al: Ilic, D; Blake, GM; Ryner, JM; Fogel, I. Radiology 1998 Jun; 207 (3): 619-624. Important Notice General Purpose. Health Net's National Medical Policies (the "Policies") are developed to assist Health Net in administering plan benefits and determining whether a particular procedure, drug, service or supply is medically necessary. The Policies are based upon a review of the available clinical information including clinical outcome studies in the peer-reviewed published medical literature, regulatory status of the drug or device, evidence-based guidelines of governmental bodies, and evidence-based guidelines and positions of select national health professional organizations. 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