The utility of bone turnover markers in Paget's disease of bone

2014 ◽  
Author(s):  
Mark J Hannon ◽  
Isolda M Frizelle ◽  
Mark Kilbane ◽  
Malachi J McKenna
Bone ◽  
2004 ◽  
Vol 35 (1) ◽  
pp. 224-230 ◽  
Author(s):  
Ian R Reid ◽  
James S Davidson ◽  
Diana Wattie ◽  
Fiona Wu ◽  
Jenny Lucas ◽  
...  

Author(s):  
Stuart H. Ralston

Paget’s disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal increases in disorganized bone remodelling which disrupt normal bone architecture, causing the affected bones to enlarge and become weakened. This can lead to various complications including pain, deformity, fracture, nerve compression syndromes, and osteoarthritis. Genetic factors play a key role in the pathogenesis of PDB. This is mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which have additive effects on disease susceptibility. Suggested environmental factors for PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are a more sensitive method of defining disease extent. Serum total alkaline phosphatase levels are usually raised in patients with metabolically active disease and are often used as a measure of disease activity. Bisphosphonates are the treatment of choice for PDB; they reduce the elevations in bone turnover that are characteristic of the disease and are an effective treatment for bone pain. Among the bisphosphonates, zoledronic acid is most likely to give a favourable pain response. Bisphosphonate treatment should not be given with the primary aim of normalizing elevated biochemical markers of bone turnover since there is no evidence that this is beneficial. Although potent bisphosphonates can normalize elevated bone turnover in many patients with PDB, it unclear as yet whether this prevents complications of the disease.


Author(s):  
Stuart H. Ralston

Paget's disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.


Rheumatology ◽  
1992 ◽  
Vol 31 (1) ◽  
pp. 35-39 ◽  
Author(s):  
J. Y. REGINSTER ◽  
A. M. JEUGMANS-HUYNEN ◽  
M. WOUTERS ◽  
N. SARLET ◽  
H. D. MCINTYRE ◽  
...  

1990 ◽  
Vol 78 (2) ◽  
pp. 215-219 ◽  
Author(s):  
D. P. O'Doherty ◽  
D. R. Bickerstaff ◽  
E. V. McCloskey ◽  
R. Atkins ◽  
N. A. T. Hamdy ◽  
...  

1. We studied the acute effects of intranasal and subcutaneous calcitonin in 40 patients with active Paget's disease of bone. Patients received a single dose of either 400 units of calcitonin delivered as a nasal spray, or 1, 10 or 100 units of subcutaneous calcitonin, or placebo. 2. Subcutaneous salmon calcitonin, administered at doses of 1, 10 and 100 units to nine patients with Paget's disease of bone, induced a dose-dependent fall in the serum calcium. This calcium-lowering effect was not seen with a second group of nine patients receiving placebo. 3. The lower doses of calcitonin had significant effects, and these were more pronounced in patients with lower rates of bone turnover. 4. Four hundred units of calcitonin administered as a nasal spray induced effects qualitatively similar to those seen with subcutaneous calcitonin, with an efficacy equivalent to approximately 30 units of subcutaneous calcitonin. 5. We conclude that the bioequivalence of calcitonin given by intranasal insufflation is low compared with its parenteral administration. The intranasal route may be more appropriate for managing patients with disorders associated with low bone turnover.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Richa Patel ◽  
Ana Ramirez Berlioz ◽  
Bhavana Chinnakotla ◽  
Lilamani Romayne Goonetilleke Kurukulasuriya

Abstract Introduction: Paget’s disease of the bone is characterized by excessive osteoclastic bone resorption followed by formation of disorganized bone; which is often focal. Bone pain and deformities are common features and it often leads to complications such as pathological fractures, deafness or neurologic deficits. Elevated bone turnover markers and alkaline phosphatase reflect ongoing exaggerated bone resorption and osteoblastic activity. We present an unusual scenario of post-menopausal osteoporosis and Paget’s disease occurring in the same patient. Clinical Case: 86-year-old female with history of Type 2 Diabetes Mellitus, Hypertension, Hypothyroidism, degenerative joint disease of lumbar spine with prior interbody fusion and laminectomy was referred to our clinic by Orthopedics for evaluation of newly diagnosed Paget’s disease. 2 months ago, she noticed severe right hip pain limiting daily activities. She denied any history of falls, fractures or family history of Paget’s. Physical exam was notable for tenderness to right sacro-iliac joint and right femoral trochanteric region. Work up included MRI of Lumbar spine and Pelvis, Pelvis X-ray, DEXA scan and routine blood work. Interestingly, her DEXA scan showed T score of +2.9 in Right hip and -3.1 in Left hip. On Pelvis X-ray cortical thickening, coarse trabecula and osteoarthritic changes were noted in right femur and hip, consistent with Paget’s disease. Left femur showed strikingly thinner cortices compared to the right, due to underlying osteoporosis. MRI of lumbar spine and pelvis was consistent with polyostotic Paget’s involving L3-L5, Sacrum and Right femur. Nuclear bone scan showed areas of uptake including anterior calvarium, lumbar spine, right hip, right femur, 8th rib, left mid tibia and 1st metatarsal of left foot. Since the distribution of uptake seemed atypical for Paget’s, a skeletal survey was obtained which was negative for bone lesions suggestive of malignancy. Laboratory testing revealed serum calcium 9.8mg/dL(8.4–10.2), 25-Hydroxy Vitamin D 30ng/dL(20–30), PTH 45.6pg/mL (15–65), Alkaline Phosphatase 370U/L (35–104), Procollagen I intact N-terminal 516mcg/L (16–96) and N-Terminal Telopeptide (NTX) 126.4 nM BCE (6.2–19). Patient received one dose of IV Zoledronic acid with modest improvement in hip and lower back pain. She continues to take Calcium carbonate 600mg twice daily and vitamin D3 1000IU once daily. We plan to see her in follow up in 3 months with repeat levels bone turnover markers. Conclusion: This is a unique case of Paget’s disease and osteoporosis, two very different diseases of metabolic bone disorder spectrum found in one patient. Treatment of Paget’s disease is indicated for pain reduction, prevention of fractures and deformities and to prevent disease progression in weight bearing areas. Bisphosphonates can target pathology of both diseases by reducing osteoclastic bone resorption.


Author(s):  
Stuart H. Ralston

Paget’s disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.


Author(s):  
Stuart H. Ralston

Paget’s disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.


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