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 “Silent disease” until complicated by fractures  Most common bone disease in humans  Characterized by:  Low bone mass  Microarchitectural deterioration.

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Presentation on theme: " “Silent disease” until complicated by fractures  Most common bone disease in humans  Characterized by:  Low bone mass  Microarchitectural deterioration."— Presentation transcript:

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2  “Silent disease” until complicated by fractures  Most common bone disease in humans  Characterized by:  Low bone mass  Microarchitectural deterioration  Compromised bone strength  Increased risk for fracture

3 Major  History of fracture as an adult  Fragility fracture in first degree relative  Caucasian/Asian postmenopausal woman  Low body weight (< 127 lb)  Current smoking  Use of oral corticosteroids > 3 mo. Additional  Impaired vision  Estrogen deficiency at early age (< 45 YO)  Dementia  Poor health/frailty  Recent falls  Low calcium intake (lifelong)  Low physical activity  > 2 alcoholic drinks per day

4  COPD  Cushing’s syndrome  Eating disorders  Hyperparathyroidism  Hypophosphatasia  IBS  RA, other autoimmune connective tissue disorders  Insulin dependent diabetes  Multiple sclerosis  Multiple myeloma  Stroke (CVA)  Thyrotoxicosis  Vitamin D deficiency  Liver diseases

5  Aluminum  Anticonvulsants  Cytotoxic drugs  Glucocorticosteroids (oral/high dose inhaled)  Immunosuppresants  Gonadotropin-releasing hormone  Lithium  Heparin (chronic use)  Supraphysiologic thyroxine doses  Aromatase inhibitors  Depo-Provera

6  Common, iatrogenic form of secondary osteoporosis  Associated with corticosteroid use in chronic, noninfectious medical conditions  Asthma  Chronic lung disease  Rheumatologic disorders  Inflammatory bowel disease  Skin diseases

7  Bone remodeling occurs throughout adulthood  Osteoporosis results from an imbalance between osteoclast and osteoblast activity  Two metabolic abnormalities contribute to increased bone resorption  Secondary hyperparathyroidism due to decreased GI absorption and urinary excretion of calcium  Altered gonadal function and decreased adrenal production of androgens

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9  Glucocorticoid-induced osteoporosis predominantly affects regions of the skeleton that have abundant cancellous bone, such as the lumbar spine and proximal femur

10  the loss of bone mineral density is biphasic; it occurs rapidly (6 to 12% loss) within the first year and more slowly (approximately 3% loss yearly) thereafter  increase in the risk of fractures has been reported with the use of inhaled glucocorticoids, as well as with alternate-day and intermittent oral regimens

11  Advanced age  Low body-mass index (<24)  Underlying disease  Prevalent fractures, smoking, excessive alcohol consumption, frequent falls, family history of hip fracture  Glucocorticoid receptor genotype  Increased 11β-HSD1 expression  High glucocorticoid dose (high current or cumulative dose; long duration of therapy)  alternate-day or inhaled therapies also confer risks of glucocorticoidinduced osteoporosis  Low bone mineral density

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13 Glucocorticoid excess

14 osteoblast

15 Glucocorticoid excess osteoblast Decreased osteoblastogenesis

16 Glucocorticoid excess osteoblast Decreased osteoblastogenesis Increased apoptosis

17 Glucocorticoid excess osteoblast Decreased osteoblastogenesis Increased apoptosis Early and continual decrease in

18 Glucocorticoid excess osteoblast Decreased osteoblastogenesis Increased apoptosis Early and continual decrease in *Cancellous osteoblast *Synthetic ability *Bone formation

19 Glucocorticoid excess osteocytes

20 Glucocorticoid excess osteocytes Increased apoptosis

21 Glucocorticoid excess osteocytes Increased apoptosis Decreased canalicular circulation

22 Glucocorticoid excess osteocytes Increased apoptosis Decreased canalicular circulation Decreased bone quality

23 Glucocorticoid excess osteoclasts

24 Glucocorticoid excess osteoclasts Decreased osteoclastogenesis

25 Glucocorticoid excess osteoclasts Decreased osteoclastogenesis Early transient increase in

26 Glucocorticoid excess osteoclasts Decreased osteoclastogenesis Early transient increase in *Osteoclast survival *cancellous osteoclasts *bone resorption

27 Glucocorticoid excess osteoclasts Decreased osteoclastogenesis Early transient increase in *Osteoclast survival *cancellous osteoclasts *bone resorption Osteonecrosis Fracture Osteocytes Increased apoptosis Deceased bone quality Decreased canalicular circulation Osteoblasts Decreased osteoblastogenesis Increased apoptosis Early and continual decrease in *cancellous osteoblasts *synthetic ability *bone formation

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29  Evaluation (side effects )  Patients receiving long-term glucocorticoid therapy should wear medication identification jewelry  Measurement of the patient’s height  Laboratory testing should be performed  Measurement of bone mineral density and plain films

30  Evaluation (side effects )  Patients receiving long-term glucocorticoid therapy should wear medication identification jewelry  Measurement of the patient’s height  Laboratory testing should be performed  Measurement of bone mineral density and plain films

31  Evaluation (side effects )  Patients receiving long-term glucocorticoid therapy should wear medication identification jewelry  Measurement of the patient’s height  Laboratory testing should be performed  Measurement of bone mineral density and plain films

32  Evaluation (side effects )  Patients receiving long-term glucocorticoid therapy should wear medication identification jewelry  Measurement of the patient’s height  Laboratory testing should be performed  Measurement of bone mineral density and plain films

33  Evaluation (side effects )  Patients receiving long-term glucocorticoid therapy should wear medication identification jewelry  Measurement of the patient’s height  Laboratory testing should be performed  Measurement of bone mineral density and plain films

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36  Evaluation (side effects )  Patients receiving long-term glucocorticoid therapy should wear medication identification jewelry  Measurement of the patient’s height  Laboratory testing should be performed  Measurement of bone mineral density and plain films

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38  Persistant hip,knee, shoulder pain especially with movement  MRI needed for diagnosis  Incidence :5-40%  Mechanisms: fat embolism, vascular thrombosis, osteocyte apoptosis

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41  adequate calcium supplementation (1200mg)  adequate vitamin D supplementation (800 to 2000 IU )  Bisphosphonates are considered to be the first-line options for the treatment (alendronate,risedronate,and zoledronic acid)

42  Alendronate, 10 mg/ day or 70 mg/wk  Advantage: Osteoclast inhibition, reduces bone loss and reduces vertebral fractures in patients with glucocorticoid-induced osteoporosis alendronate also prevents glucocorticoid- induced osteocyte apoptosis; if glucocorticoid therapy is discontinued, these drugs can be stopped

43  Disadvantage *Do not directly address the decreased bone formation that is characteristic of glucocorticoid-induced bone disease and have not been shown to reduce hip fractures; *Gastrointestinal side effects *Musculoskeletal discomfort * Osteonecrosis of the jaw, uveitis * Atypical femoral fractures * Bisphosphonates should be avoided in patients with creatinine clearance of ≤30 ml/min

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46  Dose:5 mg/yr, IV Advantage: Osteoclast inhibition reduces bone loss; more rapid onset of skeletal effects Disadvantage :  Acute-phase reaction (flue-like syndrome),can be effectively managed with acetaminophen or ibuprofen

47  Dose :20 μg/day,SC for 2 yrs, followed by bisphosphonate treatment for as long as glucocorticoids are required  directly addresses the increase in osteoblast and osteocyte apoptosis and the decrease in osteoblast number, bone formation,  and bone strength that are characteristic of glucocorticoid-induced osteoporosis and reduces vertebral fractures Teriparatide (forteo)

48 Disadvantage  Costs are greater than with oral or intravenous bisphosphonates  daily injections are required  Response is reduced when teriparatide is given with high-dose glucocorticoids;  it has not been studied in patients with elevated PTH levels Adverse effects include mild hypercalcemia, headache, nausea, legcramps, dizziness; Caution must be taken in patients nephrolithiasis serum calcium should be checked at least once 16 hours or more after injection and oral calcium intake adjusted as needed Teriparatide (forteo)

49 Dose : 60 mg every 6 mo, SC A potent inhibitor of osteoclasts, with ease of administration It can be stopped if glucocorticoids ar discontinued It can be used in patients with creatinineclearance of ≤30 ml/min Denosumab does not address the reduced bone formation caused by glucocorticoid excess Hypocalcemia and vitamin D deficiency must be treated before the use of denosumab

50  More data are needed to predict the risk of fractures among patients taking glucocorticoids and to establish clinical thresholds for intervention  Additional studies are needed to determine the minimum dose of glucocorticoids and duration of therapy thatwarrant interventions to prevent fractures

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53 A 55-year-old woman with severe, persistent asthma requiring glucocorticoid therapy for the past 3 months presents for care. Her medications include albuterol, inhaled fluticasone with salmeterol, montelukast, and prednisone (at a dose of 10 mg/day). In the past, she received several intermittent courses of prednisone at a dose of 15 mg or more. Her weight is 45.5 kg (100 lb), and her height 157.5 cm the body-mass index is 18. Scattered wheezing is heard during expiration. Findings on vertebral percussion and rib-cage compression are unremarkable. How should her case be evaluated and managed to minimize the risk of fractures

54  Slender  Age  taking prednisone at a dose of 10 mg daily for 3 months, and previously received  higher doses of glucocorticoids  Underlying asthma disease  Other asthma therapies should be used as efficiently as possible in an effort to taper the prednisone

55  BMD  Plain film or Vertebral morphometric assessment  Adequate intake of Ca and vit.D  Bisphosphonate  Teriparatide

56 با تشکر از توجه شما


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