• Like
  • Save
Thyroid Disease and Osteoporosis
Upcoming SlideShare
Loading in...5
×
 

Thyroid Disease and Osteoporosis

on

  • 783 views

 

Statistics

Views

Total Views
783
Views on SlideShare
783
Embed Views
0

Actions

Likes
0
Downloads
18
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment
  • Figure 2. Pathogenesis of Graves' Disease. Excess production of thyroid hormone is caused by the activation of thyrotropin receptors by thyroid-stimulating antibodies produced within and outside the thyroid gland. The intrathyroidal inflammatory cells also produce cytokines, such as interleukin-1, tumor necrosis factor {alpha}, and interferon-{gamma}, that induce the expression of adhesion molecules such as CD54, regulatory molecules such as CD40, and HLA class II molecules, which in turn activate local inflammatory cells. These cytokines also induce thyroid cells to synthesize cytokines that may help sustain the intrathyroidal autoimmune process. Antithyroid drugs reduce the production of thyroidal cytokines -- an ability that may explain their immunomodulatory effects (which include a decrease in the production of thyroid-stimulating antibody) -- contributing to remission in some patients.
  • Figure 1. Clinical Manifestations of Graves' Disease. Panel A shows diffuse goiter in a 28-year-old woman with Graves' hyperthyroidism. Panels B and C show ophthalmopathy in a 55-year-old woman with Graves' disease, with periorbital edema, chemosis, scleral injection, and proptosis; the lid retraction in this patient is obscured by periorbital edema. Panel D shows localized dermopathy, occurring as an indurated, noninflamed plaque on the anterolateral aspect of the shin of a 47-year-old woman.
  • Figure 1. Algorithm for the Cost-Effective Evaluation and Treatment of a Clinically Detectable Solitary Thyroid Nodule. In the case of a strong clinical suspicion of cancer, surgery is recommended, regardless of the results of fine-needle aspiration biopsy (FNAB). In the case of a suppressed level of serum thyrotropin, thyroid scintigraphy should be performed, since a functioning nodule almost invariably rules out cancer. In the case of a nondiagnostic FNAB, a repeated biopsy yields a satisfactory aspirate in 50 percent of cases. If ultrasonography reveals additional nodules that are more than 10 mm in diameter, FNAB could be performed on one other nodule, in addition to the one that is clinically detectable. The therapeutic options shown cover both solid and cystic nodules. In the case of a recurrent cyst, the possibilities of treatment are repeated FNAB, surgery, and ethanol injection. I do not recommend levothyroxine therapy for the thyroid nodule.
  • Table 1. Clinical Findings Suggesting the Diagnosis of Thyroid Carcinoma in a Euthyroid Patient with a Solitary Nodule, According to the Degree of Suspicion.
  • Figure 1. Algorithm for the Cost-Effective Evaluation and Treatment of a Clinically Detectable Solitary Thyroid Nodule. In the case of a strong clinical suspicion of cancer, surgery is recommended, regardless of the results of fine-needle aspiration biopsy (FNAB). In the case of a suppressed level of serum thyrotropin, thyroid scintigraphy should be performed, since a functioning nodule almost invariably rules out cancer. In the case of a nondiagnostic FNAB, a repeated biopsy yields a satisfactory aspirate in 50 percent of cases. If ultrasonography reveals additional nodules that are more than 10 mm in diameter, FNAB could be performed on one other nodule, in addition to the one that is clinically detectable. The therapeutic options shown cover both solid and cystic nodules. In the case of a recurrent cyst, the possibilities of treatment are repeated FNAB, surgery, and ethanol injection. I do not recommend levothyroxine therapy for the thyroid nodule.
  • Figure 1. Algorithm for the Cost-Effective Evaluation and Treatment of a Clinically Detectable Solitary Thyroid Nodule. In the case of a strong clinical suspicion of cancer, surgery is recommended, regardless of the results of fine-needle aspiration biopsy (FNAB). In the case of a suppressed level of serum thyrotropin, thyroid scintigraphy should be performed, since a functioning nodule almost invariably rules out cancer. In the case of a nondiagnostic FNAB, a repeated biopsy yields a satisfactory aspirate in 50 percent of cases. If ultrasonography reveals additional nodules that are more than 10 mm in diameter, FNAB could be performed on one other nodule, in addition to the one that is clinically detectable. The therapeutic options shown cover both solid and cystic nodules. In the case of a recurrent cyst, the possibilities of treatment are repeated FNAB, surgery, and ethanol injection. I do not recommend levothyroxine therapy for the thyroid nodule.
  • Hip Fractures Can Lead to Disability, Loss of Independence, and Even Death Half of all victims of a hip fracture will be disabled and 25% will require long-term nursing home care. 1,2 These patients may develop additional complications, including pressure ulcers, pneumonia, urinary tract complications, and severe depression. Thus, hip fractures are the leading cause of morbidity associated with osteoporosis. 2 Within 1 year following a hip fracture, mortality is increased by up to 24% due to complications. 3 The lifetime risk of death resulting from a hip fracture is comparable with the risk due to breast cancer for a white postmenopausal woman 50 years of age. 4 References: 1. Consensus Development Conference: diagnosis, prophylaxis, and treatment of osteoporosis. Am J Med . 1993;94:646–650. 2. Riggs BL, Melton LJ III. The worldwide problem of osteoporosis: insights afforded by epidemiology. Bone . 1995;17:505S–511S. 3. Ray NF, Chan JK, Thamer M, et al. Medical expenditures for the treatment of osteoporotic fractures in the United States in 1995: report from the National Osteoporosis Foundation. J Bone Miner Res . 1997;12(1):24–35. 4. Cummings SR, Black DM, Rubin SM. Lifetime risks of hip, Colles’, or vertebral fracture and coronary heart disease among white postmenopausal women. Arch Intern Med . 1989;149:2445–2448.
  • Risk Factors for Osteoporotic Fracture Several factors have been identified that are associated with an increased risk of osteoporotic fractures. Personal history of fracture as an adult and history of fracture in a first-degree relative are examples of risk factors that cannot be modified by the individual. Other potentially modifiable risk factors include low calcium intake, alcohol intake, smoking, and minimal exercise. Poor health and frailty may or may not be modifiable. Reference: 1. National Osteoporosis Foundation. Physician’s Guide to Prevention and Treatment of Osteoporosis. Belle Mead, NJ: Excerpta Medica, Inc.; 1998.
  • BMD and Fracture Risk Are Inversely Related Significant bone loss at all skeletal sites occurs as women age with an increased rate of loss after menopause. 1 Up to one third of bone mass is lost in the first 5 years after menopause. 1 There is a dramatic increase in the incidence of fracture as women grow older. 2,3 Women over 50 years of age have a 40% chance of suffering an osteoporotic fracture in their remaining years. 4 References: 1. Faulkner KG. Bone densitometry: choosing the proper skeletal site to measure. J Clin Densitom . 1998;1:279–285. 2. Cooper C. Epidemiology and public health impact of osteoporosis. Baillières Clin Rheumatol. 1993;7:459–477. 3. Cooper C, Atkinson EJ, O’Fallon WM, et al. Incidence of clinically diagnosed vertebral fractures: a population-based study in Rochester, Minnesota, 1985-1989. J Bone Miner Res. 1992;7:221–227. 4. Kanis JA. Osteoporosis and its consequences. In: Osteoporosis. Cambridge, MA: Blackwell Science, Ltd; 1994:1–21.
  • Central DXA Measurement Dual x-ray absorptiometry (DXA) can be used to measure BMD at multiple skeletal sites, including spine, proximal femur, forearm, and total body. Uses x-rays of 2 different energy levels to distinguish bone from soft tissue Advantage of being able to measure BMD of the central and most osteoporotic fracture-prone sites, the spine and hip Central DXA can be performed in the office. Scanning time is less than 5 minutes and the radiation dose is considerably lower than that for conventional radiography. Central DXA has good overall accuracy and precision. Reproducible results make it useful for both baseline and follow-up measurements. DXA has been used in most of the prospective epidemiologic studies investigating the BMD/fracture risk relationship.
  • Who Should Be Considered for BMD Testing? The National Osteoporosis Foundation (NOF) has issued recommendations, for the diagnosis of osteoporosis. The guidelines, published in 1998, were developed in collaboration with several professional organizations. These recommendations are intended to serve as a guide for physicians in clinical decision making in the evaluation of individual patients. Who should have BMD testing? Women who are 65 years of age or older regardless of additional risk factors Postmenopausal women under the age of 65 with one or more additional risk factors for osteoporosis, including a personal history of fracture as an adult, history of fracture in a first-degree relative, current cigarette smoking, and low body weight (<127 lbs) Postmenopausal women of any age who have a fracture (to help confirm diagnosis and determine disease severity) Women who are considering therapy for osteoporosis, if BMD testing would facilitate the decision Women who have been on hormone replacement therapy for prolonged periods Reference: 1. National Osteoporosis Foundation. Physician’s Guide to Prevention and Treatment of Osteoporosis. Belle Mead, NJ: Excerpta Medica, Inc.; 1998.
  • Other Populations for Assessment of Osteoporosis Osteoporosis is generally thought of as a disease of postmenopausal women. However, there are other groups at risk, including men and patients on long-term high-dose glucocorticoids.
  • Interpreting BMD Measurement Reports The T-score reports the number of standard deviations by which the patient’s measured bone mass negatively deviates from the mean of the young adult normal reference population (T-score = –1.0 = 1 SD below the mean). A T-score of –1.0 represents a 10% loss of bone mass compared with mean peak bone mass of young normal adults. 1 T-scores can help confirm a diagnosis of low bone mass or osteoporosis. Low bone mass (osteopenia): T-score = –1.0 to –2.0 Osteoporosis: T-score <–2.5 Decrease of 1 SD in spine and hip bone mass increases risk of spine fracture and hip fracture approximately 2-fold. 2 Association between low BMD and fracture risk prediction is stronger than that between systolic blood pressure and stroke, or that between cholesterol and coronary events. 2 References: 1. National Osteoporosis Foundation. Physician’s Guide to Prevention and Treatment of Osteoporosis. Belle Mead, NJ: Excerpta Medica, Inc.; 1998. 2. Marshall D, Johnell O, Wedel H. Meta-analysis of how well measures of bone mineral density predict occurrence of osteoporotic fractures. BMJ. 1996;312:1254–1259.
  • Visualizing a Patient’s T-Score This chart describes the relationship between the T-score and the bone loss curve of a 60-year-old woman. The patient has a T-score of –3.0, or 3 standard deviations below that seen in the young adult female normal reference population. For every standard deviation below the mean, the risk of fracture approximately doubles in the spine and increases about 2.5-fold in the hip. Reference: 1. National Osteoporosis Foundation. Physician’s Guide to Prevention and Treatment of Osteoporosis. Belle Mead, NJ: Excerpta Medica, Inc.; 1998.
  • Recommendations for Treatment Based on BMD Testing Results The NOF has issued recommendations, for the treatment of osteoporosis in women. 1 These recommendations are intended to serve as a guide for physicians in clinical decision making in the evaluation of individual patients. Who should receive pharmacologic treatment for osteoporosis? Postmenopausal women with BMD T-scores of <–1.5 who have at least one additional risk factor Reference: 1. National Osteoporosis Foundation. Physician’s Guide to Prevention and Treatment of Osteoporosis. Belle Mead, NJ: Excerpta Medica, Inc.; 1998.
  • Summary Osteoporosis is a chronic, progressive disease resulting in loss of bone. The reduction in bone mass increases the risk of fracture, potentially leading to disability, loss of independence, and death. The NOF recommends BMD testing for patients with conditions, such as estrogen deficiency and chronic glucocorticoid therapy, that place them at high risk for osteoporotic fracture. T-score is the most clinically relevant measure of fracture risk, but other risk factors should be considered. The NOF recommends initiation of therapy for patients with a T-score of <–1.5 if they have at least one risk factor.

Thyroid Disease and Osteoporosis Thyroid Disease and Osteoporosis Presentation Transcript

  • Thyroid Disease And Osteoporosis Lisa Hays, MD Endocrinology Fellow
  • Outline
    • Signs and symptoms of hyperthyroidism
    • Diagnostic studies for hyperthyroidism
    • Causes and treatments of hyperthyroidism
    • General overview of hypothyroidism
    • Evaluation of thyroid nodules
    • Overview of osteoporosis
  •  
  • Cellular effects of thyroid
  • Hyperthyroidism Symptoms
    • Anxiety/irritability
    • Weakness
    • Tremors
    • Difficulty sleeping
    • Palpitations
    • Increased bowel movements
    • Fatigue
    • Weight loss
    • Hyperkinetic movements
    • Heat intolerance
  • Case Presentation
    • 37 yo male presented to PCP w/ complaint of feeling poorly for past month
    • Also complained of weakness, difficulty sleeping, increased heart rate. 10 stools per day.
    • What else do we need to know before examining?
  • Case Presentation
    • T 99.1, HR 92 irregular, RR 20, BP 153/75
    • Physical examination
      • Mild proptosis
      • Nontender goiter with thyroid bruit present
      • CV: Irregularly irregular rhythm
      • Ext: Brisk DTR’s, mild resting tremor
    • What labs or studies do we need?
  • Laboratory Studies
    • TSH <0.010 uIU/ml (nl 0.47-5.0)
    • Free T4 >6 ng/dl (nl 0.71-1.85)
    • Total T3 >600 ng/dl (nl 72-170)
    • Thyroid Stimulating Antibody 130% (nl 0-125%)
    • Negative Thyroid peroxidase and thyroglobulin antibodies
  • Case Presentation
    • Patient was diagnosed with Graves’ Disease
    • Started on Methimazole 10 mg TID
    • Propranolol for symptom management
    • Anticoagulation for atrial fibrillation
  • Thyroid Antibodies
    • TSH receptor antibodies
      • Can be stimulating or inhibitory
    • Thyroglobulin antibodies
    • Thyroid peroxidase antibodies (formerly known as microsomal)
  •  
  • Anything else?
    • Radioactive Iodine Uptake
      • Measures the amount of iodine taken up by the thyroid in 24 hours
      • Normal 15-30%
    • Thyroid Scan
      • Gives an anatomic view of the thyroid
      • Technetium used to image
  • Differential Diagnosis
    • High uptake
    • Graves’ Disease
    • Multinodular Goiter
    • Toxic solitary Nodule
    • TRH secreting Pituitary Tumor
    • HCG secreting tumor
    • Low uptake
    • Subacute Thyroiditis
    • Silent Thyroiditis
    • Iodine induced
    • Exogenous L-Thyroxine
    • Struma ovarii
    • Amiodarone
  • Graves’ Disease
    • Most common cause of hyperthyroidism
      • 60-80% of cases
    • Autoimmune disease
    • Caused by thyroid stimulating immunoglobulins
      • Bind to TSH receptors on thyroid
      • Cause hypersecrection of thyroid hormone
      • Cause hypertrophy & hyperplasia of thyroid follicles
  • Weetman, A. P. N Engl J Med 2000;343:1236-1248 Pathogenesis of Graves' Disease
  • Clinical Manifestations
    • Symptoms and signs of hyperthyroidism
    • Ophthalmopathy
      • Present in 50% of patients
      • Eyelid retraction
      • Periorbital edema
      • Proptosis (exopthalmos)
      • Diploplia
    • Dermopathy (myxedema)
  • Weetman, A. P. N Engl J Med 2000;343:1236-1248 Clinical Manifestations of Graves' Disease
  • Graves’ Disease
    • Associated Conditions
      • Type I Diabetes Mellitus
      • Addison’s Disease
      • Vitiligo
      • Pernicious anemia
      • Alopecia Areata
      • Myasthenia Gravis
      • Celiac Disease
  • Graves Treatment
    • Antithyroid drugs (Thionamides)
      • Proplythiouracil (PTU) 300-400 mg daily
      • Methimazole 30-40 mg daily
      • Decrease synthesis of hormone, PTU also decreases conversion of T4 to T3
      • Permanent remission in 40-50% of treated patients
      • Risk of agranulocytosis
      • PTU used in pregnancy
    • Beta-Blockers for symptoms
  • Graves Treatment
    • Thyroidectomy
      • Rapid cure but requires thyroid replacement
    • Radioactive Iodine
      • Iodine (131I) is given
      • Effect is typically seen in 3-6 months
      • Hypothyroidism often develops
  • Multinodular Goiter
    • Less common than Graves and effects older individuals
    • Discrete nodules become autonomous and hyperfunction
    • Treatment with thyroidectomy (often poor surgical candidates) or iodine, thionamides
  • Subacute Thyroiditis
    • Etiology is typically viral
    • Known as De Quervain’s thyroiditis or granulomatous thyroiditis
    • Thyroid is often enlarged, tender, painful
    • Very low radioactive iodine uptake
    • Self-resolving within weeks to months
    • Treatment with NSAIDS, steroids, Beta-blockers
  • Silent Thyroiditis
    • Also called painless or lymphocytic thyroiditis
    • Not painful like subacute
    • Transient
    • Low iodine uptake
  • Hypothyroidism
    • Weakness
    • Fatigue
    • Lethargy, sleepiness
    • Slowness of speech and thought
    • “ Puffy” appearance
    • Dry skin, coarse hair
    • Cold intolerance
    • Constipation
  • Physical Findings
    • Puffy features
    • Dry skin
    • Nonpitting edema
    • Hypothermia
    • Bradycardia
    • Slow return of deep tendon reflexes
    • Loss of lateral portion of eyebrows
  •  
  • Causes of Hypothyroidism
    • Primary Hypothyroidism
      • Iodine deficiency
      • Iatrogenic-surgery, radioablation
      • Autoimmune thyroid destruction
      • Drugs interfering with hormone synthesis
      • Infiltrative disease
        • hemochromotosis, sarcoidosis, neoplastic disease
      • Congenital thyroid agensis or defects in hormone synthesis
  • Hashimotos Thyroiditis
    • Most common type of thyroid disease
    • Autoimmune damage
      • Lymphocytic infiltrate, fibrosis, decreased thyroid hormone production
      • Autoantibodies (thyroglobulin and peroxidase)
      • Can also be associated with polyglandular autoimmune disease
        • Adrenal insufficiency, ovarian failure, vitiligo, diabetes
  • Thyroid Replacement
    • Synthetic levothyroxine (T4)
    • Converted to T3 in the body
    • Studies vary on utility of using T3
    • Typical replacement dose is 1.6 micrograms/kg (100-150 mcg typical)
    • Start with reduced dose in elderly and patients with history of heart disease
  • Myxedema Coma
    • Severe untreated hypothyroidism
    • Hypothermia, hypoglycemia, shock, hypoventilation, ileus
    • 50% mortality
    • Treat with IV levothyroxine, steroids
  • Thyroid Nodule
    • 21 yo male w/ no past medical history presents to his PCP complaining of gradually enlarging “knot” in his neck
    • What questions do you have?
    • Examination reveals a firm 3 cm nodule in right lobe of thyroid
    • What is the next step?
  • Thyroid Nodules
    • Lifetime risk of palpable nodule 5-10%
    • 50% of the population has a nodule on autopsy or ultrasound
    • Only 1 in 20 is malignant
  • Differential Diagnosis
    • Malignancy
      • Papillary
      • Follicular
      • Medullary
      • Anaplastic
      • Metastasis
    • Benign follicular adenoma
    • Cyst
    • Colloid Nodule
  • Hegedus, L. N Engl J Med 2004;351:1764-1771 Algorithm for the Cost-Effective Evaluation and Treatment of a Clinically Detectable Solitary Thyroid Nodule
  • Hegedus, L. N Engl J Med 2004;351:1764-1771 Clinical Findings Suggesting the Diagnosis of Thyroid Carcinoma in a Euthyroid Patient with a Solitary Nodule, According to the Degree of Suspicion
  • Evaluation of Nodule
    • Measure TSH
      • If Hyperthyroid (low TSH), do uptake and scan
        • Treat with surgery or I-131 ablation
      • If normal thyroid function, next step is fine needle aspiration (FNA)
    • Check Calcitonin level if family history of MEN2 or medullary carcinoma exists.
  • Hegedus, L. N Engl J Med 2004;351:1764-1771 Algorithm for the Cost-Effective Evaluation and Treatment of a Clinically Detectable Solitary Thyroid Nodule
  • Fine Needle Aspiration
    • FNA is most effective way to distinguish between benign and malignant nodules
    • Inexpensive, performed as outpatient
    • Ultrasound guided FNA if not palpable or less than 1.5 cm in diameter
    • What results will I see?
      • Benign-75% of the time
      • Malignant-4% of cases
      • Suspicious or inadequate-22%
  • Hegedus, L. N Engl J Med 2004;351:1764-1771 Algorithm for the Cost-Effective Evaluation and Treatment of a Clinically Detectable Solitary Thyroid Nodule
  • Management of Nodules
    • Malignant
      • Total thyroidectomy
    • Suspicious
      • Thyroidectomy
    • Benign
      • Discuss with the patient
      • Ultrasound surveillance
      • Surgery
      • Consider levothyroxine suppression (varying results)
  • Case Presentation
    • FNA revealed papillary thyroid carcinoma
    • Patient underwent total thyroidectomy
    • Treatment with I-131 ablation after surgery
  • Osteoporosis
  • Case Presentation
    • 70 year old female asks her PCP if she should have a bone density done.
    • What questions should her PCP ask?
      • No history of fractures
      • Menopause was surgical at age of 55
      • Mother fractured her hip at 74
  • Osteoporosis
    • Definition
      • Microarchitectural deterioration of bone tissue leading to decreased bone mass
      • Bone fragility
      • Susceptibility to fracture
    • A problem of decreased peak bone mass and accelerated bone loss
    • Affects 10 million in the United States
  •  
  • Hip Fractures Can Lead to Disability, Loss of Independence, and Even Death
    • Hip fracture is associated with increased risk of:
      • Disability: 50% never fully recover 1,2
      • Long-term nursing home care required: 25% 2
      • Increased mortality within 1 year due to complications: up to 24% 3
      • Lifetime risk of death: comparable to that of breast cancer 4
    1. Consensus Development Conference. Am J Med . 1993;94:646-650. 2. Riggs BL, Melton LJ III. Bone . 1995;17:505S – 511S. 3. Ray NF et al. J Bone Miner Res . 1997;12(1):24 – 35. 4. Cummings SR et al. Arch Intern Med . 1989;149:2445 – 2448.
  • Osteoporosis
    • Primary osteoporosis
      • Unrelated to chronic illness
      • Related to aging and decreased gonadal function
    • Secondary osteoporosis
      • Secondary to chronic illnesses that cause accelerated bone loss
      • Examples: Glucocorticoid use, celiac sprue, hyperthyroidism
  • Risk Factors for Osteoporotic Fracture Nonmodifiable Potentially Modifiable Gold color denotes risk factors that are key factors for risk of hip fracture, independent of bone density. National Osteoporosis Foundation, Physician’s Guide to Prevention and Treatment of Osteoporosis . Belle Mead, NJ: Excerpta Medica, Inc.; 1998. Personal history of fracture as an adult History of fracture in first-degree relative Caucasian race Advanced age Female sex Dementia Poor health/frailty Current cigarette smoking Low body weight (<127 lbs) Estrogen deficiency, including menopause onset <age 45 Low calcium intake (lifelong) Alcoholism Impaired eyesight despite adequate correction Recurrent falls Inadequate physical activity Poor health/frailty
  • Diagnosis of Osteoporosis
    • History and physical examination to exclude secondary osteoporosis
    • Laboratory studies if suspect secondary osteoporosis
    • Measurement of Bone Mineral Density (BMD)
      • Dual X-ray Absorptiometry (DEXA scan)
        • Provides most reproducible values of bone density
        • g/cm 2
  • BMD and Fracture Risk Are Inversely Related 60 70 80 90 100 30 40 50 60 70 80 90 Age Relative BMD (%) Forearm Spine Hip and Heel 0 1000 2000 3000 4000 35- 39 85+ Colles' Vertebrae Hip Age Annual Fracture Incidence Cooper C. Baillières Clin Rheumatol. 1993;7:459 – 477. Faulkner KG. J Clin Densitom. 1998;1:279 – 285.
  • Central DXA Measurement
    • Measures multiple skeletal sites
      • Spine
      • Proximal femur
      • Forearm
      • Total body
    • Office based
    • Considered the clinical standard
  • Who Should Be Considered for BMD Testing?
    • Women  65 years of age regardless of additional risk factors
    • Postmenopausal women <65 years of age with at least one risk factor for osteoporosis (in addition to menopause)
    • Postmenopausal women  65 years of age with fractures (to confirm diagnosis and determine disease severity)
    • Women considering therapy for osteoporosis, if BMD testing would facilitate the decision
    • Women who have been on HRT for prolonged periods
    National Osteoporosis Foundation, Physician’s Guide to Prevention and Treatment of Osteoporosis . Belle Mead, NJ: Excerpta Medica, Inc.; 1998. National Osteoporosis Foundation Guidelines
  • Other Populations To Consider for Assessment of Osteoporosis
    • Men
    • Patients on long-term high-dose glucocorticoids
  • Interpreting BMD Measurement Reports
    • A clinically relevant value on the BMD report
    • Describes bone mass compared with the mean peak bone mass of healthy young adult women in terms of Standard Deviation (SD)
    • Can help confirm the diagnosis of low bone mass or osteoporosis
    • For every SD below the young adult normal, the risk of fracture approximately doubles
    T-Score Is Key 1. National Osteoporosis Foundation, Physician’s Guide to Prevention and Treatment of Osteoporosis . Belle Mead, NJ: Excerpta Medica, Inc.; 1998. 2. Marshall D. Johnell O, Wedel H. Meta-analysis of how well measures of bone mineral density predict occurrence of osteoporotic fractures. BMJ . 1996;312:1254–1259.
  • Visualizing a Patient’s T-Score
    • T-score = Number of standard deviations (SDs) by which the patient’s bone mass falls above or below the mean peak bone mass for normal young adult women
    • = T-score for patient, a 60-year-old woman; here, T = –3.0
    • Light line: Change in mean bone mass over time in women
    • Heavy line: Mean peak bone mass for young normal adult women
    SD Age (years) 2 1 0 – 1 – 2 – 3 – 4 – 5 – 6 20 30 40 50 60 70 80 90 T-score = –3.0 Peak Bone Mass National Osteoporosis Foundation, Physician’s Guide to Prevention and Treatment of Osteoporosis . Belle Mead, NJ: Excerpta Medica, Inc.; 1998.
  •  
  • Recommendations for Treatment Based on BMD Testing Results National Osteoporosis Foundation, Physician’s Guide to Prevention and Treatment of Osteoporosis . Belle Mead, NJ: Excerpta Medica, Inc.; 1998. T-SCORE ACTION < –2.0 Initiate therapy < –1.5 Initiate therapy (with at least 1 additional risk factor) National Osteoporosis Foundation Guidelines for postmenopausal Women
  • Treatment of Osteoporosis
    • Adequate Calcium (1200 mg elemental)
    • Adequate Vitamin D (at least 400 IU)
    • Weight-bearing exercise
  • Pharmacologic Agents
      • Bisphosphonates
        • Inhibit osteoclastic bone resorption
        • Increased BMD and decreased fractures
        • Ex: alendronate, risedronate
      • Calcitonin
        • Nasal spray or injection
        • Decreased vertebral fractures
        • No hip fracture data
      • Raloxifen
        • SERM
        • Decreased vertebral fracture
  • Osteoporosis Summary
    • Osteoporosis is a disease with serious consequences.
      • Bone loss associated with osteoporosis increases fracture risk, which may lead to disability, loss of independence, and death.
    • Patients at risk for osteoporotic fracture should be considered for BMD testing.
    • T-score is the most clinically relevant measure of fracture risk.
    • According to NOF guidelines, consider therapy in patients with a T-score of < – 2.0 and those with a T-score of < – 1.5 with at least one risk factor.