History of Paget’s Disease · 2020-05-15 · Epidemiology: Prevalence of Paget’s Disease in the...
Transcript of History of Paget’s Disease · 2020-05-15 · Epidemiology: Prevalence of Paget’s Disease in the...
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History of Paget’s Disease• Sir James Paget named disease osteitis
deformans in 1876, suspecting basic inflammatory process1,2
• Today predominantly referred to as Paget’s
disease of bone1
Sir James Paget
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Epidemiology: Prevalence of Paget’s Disease in the US
1. Siris ES, Roodman GD. In: Favus MJ, ed. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 6th ed. Washington, DC: ASBMR; 2006:320-330. 2. Altman RD, et al. J Bone Miner Res. 2000;15:461-465.
• Second most common bone disease after osteoporosis1
• Roughly estimated at approximately 2% of the US population over age 55 years1 –Prevalence increases markedly with age,
uncommon before age 401,2 • 15% to 30% of patients have positive family histories1 • Most common in people of Northern European
descent1
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Paget’s Disease: Description
• Chronic, progressive skeletal disorder
• Increased size and number of osteoclasts
• Localized areas of excessive bone resorption and formation – May have only one affected bone or have
pagetic lesions in multiple bones – New lesions rarely develop in previously
unaffected bone after diagnosis
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Copyright ©2005 American Society for Clinical Investigation
Roodman, G. D. et al. J. Clin. Invest. 2005;115:200-208
Osteoclasts in normal bone and in Paget's disease
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ΠΑΘΟΦΥΣΙΟΛΟΓΙΑ
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ΠΑΘΟΦΥΣΙΟΛΟΓΙΑ
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Siris ES, Roodman GD. In: Favus MJ, ed. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 6th ed. Washington, DC: ASBMR; 2006:320-330.
Pagetic Bone and Normal Bone Normal Pagetic
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Paget’s Disease: Clinical Presentation
• Usually mild or asymptomatic1 • Diagnosis is often based on incidental findings1
– Elevated total or bone specific serum alkaline phosphatase
– Radiological findings • Patients may present with symptoms that are nonspecific
or suggestive of other conditions1
– Pain – Fracture – Deformity – Osteoarthritis – Hearing loss
1Siris ES, Roodman GD. In: Favus MJ, ed. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 6th ed. Washington, DC: ASBMR; 2006:320-330.
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Paget’s Disease: Common Sites of Involvement
• Paget’s disease can occur in any bone, but most commonly: – Skull – Vertebrae – Pelvis – Femur – Tibia
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Diagnosing Paget’s Disease: Tests• Laboratory tests1,2
– Alkaline phosphatase, a marker of bone formation – Any level above normal, especially in the absence of
elevated liver enzymes – Bone-specific alkaline phosphatase may be more
reliable. Elevated markers of bone resorption (serum βC-telopeptide of type 1 collagen [CTX], urine N-telopeptide of type I collagen [NTX])
• Radiographs1,2 – Characteristic appearance usually confirms diagnosis
• Bone scan to assess extent of disease1
1. Lyles KW, et al. J Bone Miner Res. 2001;16:1379-1387. 2. Selby PL, et al. Bone. 2002;31:366-373.
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Courtesy of Pierre Delmas, MD.
Early-Stage (Lytic) Paget’s Disease: Tibia
V-shaped “blade of grass” lesion characteristic of lytic phase of Paget’s disease
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Courtesy of Pierre Delmas, MD.
Advanced Paget’s Disease in the Tibia: Sclerotic and Lytic Lesions
Primarily sclerotic changes, with enlargement and thickening of long bones
Secondary osteolytic front
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1976
Paget’s Disease: Progression Over 15 Years in Untreated Patient
Courtesy of Pierre Delmas, MD.1991
Bowing
Cortical thickening
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Courtesy of Pierre Delmas, MD.
Early-Stage (Lytic) Paget’s Disease in the Skull: Known as “Osteoporosis Circumscripta”
Lytic border
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Advanced (Sclerotic) Paget’s Disease: “Cotton Wool” Skull
Lytic lesion
Diffuse sclerotic changes
Courtesy of Pierre Delmas, MD.
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Courtesy of Nuria Guañabens, MD.
Advanced Paget’s Disease in the Pelvis
Bony enlargement
Diffuse sclerotic changes
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Paget’s Disease of Femur
Courtesy of R. Bockman, MD, PhD
X-Ray Bone Scan Pathology
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Paget’s Disease: “Picture Frame” Vertebral Body
Courtesy of Pierre Delmas, MD.
Lytic lesion
Cortical thickening
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A Bone Scan Showing Polyostotic Disease
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Patel M and Bhalla A. N Engl J Med 2008;358:625
A 55-year-old man presented with a 2-year history of painful jaw enlargement and progressively ill-fitting dentures
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Paget’s Disease in the Skull
Courtesy of Pierre Delmas, MD.
Skull enlargement
Dilated scalp veins
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Courtesy of Jacques Brown, MD.
Skeletal Deformities: Bowing of Long Bones
Bowing of humerus
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Skeletal Deformities: Bowing of Lower Limbs
Courtesy of Pierre Delmas, MD.
Bowed femurs
Bowed tibias
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Complications of Paget’s Disease: Complete (Chalk-Stick) Fracture in a Femur
Courtesy of Pierre Delmas, MD.
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Complications of Paget’s Disease: Osteosarcoma in Pagetic Femur
Reproduced with permission from: N. Kelepouris. Clinical manifestations and diagnosis of Paget's disease of bone. In: Rose, BD (Ed), UpToDate (version 13.3), Waltham, MA 2006. Copyright © 2006 UpToDate, Inc.
Sarcomatous degeneration
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Complications of Paget’s Disease: Giant Cell Tumor of Scapula
Courtesy of F. Singer, MD
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Managing Paget’s Disease: Bisphosphonates and Other
Treatment Strategies• Bisphosphonates (gold standard of antipagetic
therapy)1-3 • Subcutaneous calcitonin (rarely used)1,2 • Pain management
–NSAIDs, COX-2 inhibitors, analgesics, opioids1,2
• Surgery1,2 – Fractures, bone deformities, osteoarthritis
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Indications for Treatment of Paget’s Disease
• Bone pain • Preparation for orthopedic surgery • Fracture of pagetic bone • Hypercalcemia and/or hypercalciuria • Neurologic deficit associated with cranial or
vertebral disease • Presence of high-output congestive heart failure • Prevention of future complications
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FDA-Approved Therapies and Dosing Regimens for Paget’s Disease*
Didronel® (etidronate) 5 -10 mg/kg/d or 6 mo 11-20 mg/kg/d 3 mo
3 moSkelid® (tiludronate) 400 mg/dFosamax® (alendronate) 40 mg/d 6 moActonel® (risedronate) 30 mg/d 2 mo
Oral agents
Aredia® (pamidronate) 30 mg/d 4 h on 3 cons. daysIV agents
Agent Dose Duration of Therapy
Reclast® (zoledronic acid)
5 mg Single, 15 min. infusion
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Effect on Serum Alkaline Phosphatase of Alendronate 40 mg/day Vs. Placebo or
Etidronate 400mg/day
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Biochemical Remission Induced by Risedronate Treatment
Risedronate 30 mg/day x 2 mos.
Etidronate 400 mg/day x 6 mos.
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Zoledronic Acid Lowers Alkaline Phosphatase Levels More Than
Risedronate
P < .001
0 10 28 63 91 182Days
0
100
200
300
400
500
Tota
l Alk
alin
e
Phos
phat
ase
(U/L
)
Mean (± SE) Total Alkaline Phosphatase by Visit
P < .001
P < .001
P < .001 P < .001
Reid IR, et al. N Engl J Med. 2005;353:898-908.Copyright © 2003 Massachusetts Medical Society. All right reserved. Adapted with permission, 2007.
Risedronate 30mg/d x 60d (n=80)Zoledronic Acid 5mg IV, 15 min (n=121)
Normal alkaline phosphatase range
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Mean (± SE) of the absolute value and reference ranges are presented. Adapted from Hosking D, et al. J Bone Miner Res. 2007;22:142-148. With permission of the American Society for Bone and Mineral Research.
During Study Extension, Zoledronic Acid Maintained Mean Serum ALP Better Than
Risedronate
Time From Initiation of Therapy (months)
Seru
m A
LP (U
/L)
6 12 18 240
50
100
150
200Start of extended observation period
Risedronate 30mg/d x 60d (n=80)Zoledronic Acid 5mg IV, 15 min (n=121)
Total AlP reference range
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Adverse Events With Zoledronic Acid Comparable to Risedronate After Day 3
Zoledronic Acid (n = 177)
Risedronate (n = 172)
Adverse Events† Patients, n (%) P Value
Total with any AE 117 (66.1) 126 (73.3) .16Pain in arm or leg 13 (7.3) 12 (7.0) .99Arthralgia 9 (5.1) 19 (11.0) .05Dizziness 9 (5.1) 5 (2.9) .41Nasopharyngitis 9 (5.1) 14 (8.1) .29Diarrhea 8 (4.5) 9 (5.2) .81Headache 7 (4.0) 10 (5.8) .46Back pain 4 (2.3) 12 (7.0) .04
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Bisphosphonates
• Adverse effects • UGI intolerance, diarrhea (oral) • Acute phase reaction • Musculoskeletal/bone pain • Hypocalcemia • Renal failure reported with high dose
intravenous bisphosphonates (obtain serum creatinine level before each dose of intravenous bisphosphonate)
• Ocular inflammation (rare) • Osteonecrosis of jaw (ONJ) -rare
• Contraindications • Hypocalcemia • Vitamin D deficiency • Hypoparathyroidism • Severe renal insufficiency
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Bisphosphonates, Vitamin D and Calcium
• Correct vitamin D deficiency before administering a bisphosphonate
• Instruct patients to take 1500 mg of calcium and 800 units of vitamin D
(preferably vitamin D3) daily during the 10 days after an infusion of zoledronic acid
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Patient Follow-Up
Untreated Patients • Annual serum total or bone specific alkaline
phosphatase measurement • Periodic x-rays of osteolytic lesions Treated Patients • Serum total or bone specific alkaline
phosphatase measurement every 3-6 months • Bone resorption markers are optional • Periodic x-rays of osteolytic lesions
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