SYMPTOMATIC AND SCINTIGRAPHIC IMPROVEMENT AFTER INTRAVENOUS PAMIDRONATE TREATMENT OF PAGET'S DISEASE OF BONE IN PATIENTS WITH NORMAL SERUM ALKALINE PHOSPHATASE LEVELS

2003 ◽  
Vol 9 (4) ◽  
pp. 280-283 ◽  
Author(s):  
George Ang, MD ◽  
David Feiglin, MD ◽  
Arnold M. Moses, MD, FACE
Keyword(s):  
Alkaline Phosphatase ◽  
Serum Alkaline Phosphatase ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Normal Serum ◽  
Paget’S Disease Of Bone ◽  
Paget's Disease Of Bone ◽  
Intravenous Pamidronate

Paget’s disease of bone

2013 ◽  
Author(s):  
Stuart H. Ralston
Keyword(s):  
Bone Turnover ◽  
Viral Infections ◽  
Serum Alkaline Phosphatase ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Bisphosphonate Therapy ◽  
Paget’S Disease Of Bone ◽  
Bone Architecture ◽  
Paget's Disease Of Bone ◽  
Disease Extent

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.

Pharmacotherapy of Paget's Disease of Bone: Focus on Zoledronic Acid

2009 ◽  
Vol 1 ◽  
pp. CMT.S1095
Author(s):  
Konstantinos Tziomalos ◽  
Vasilios G. Athyros ◽  
Asterios Karagiannis
Keyword(s):  
Zoledronic Acid ◽  
Serum Alkaline Phosphatase ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Paget’S Disease Of Bone ◽  
Principal Characteristic ◽  
Paget's Disease Of Bone ◽  
Osteoclastic Activity ◽  
Therapeutic Decisions ◽  
Increased Risk

Paget's disease of bone (PDB) affects 1%-3% of the population and is associated with increased risk for bone fracture and deformity. Increased osteoclastic activity is the principal characteristic of PDB. Bisphosphonates inhibit osteoclastic activity and represent the mainstay of treatment of PDB. Zoledronic acid, a potent member of this class, normalizes serum alkaline phosphatase (ALP) levels in the majority of patients with PDB and induces sustained disease remissions. It appears to be more effective than both risedronate and pamidronate. However, it is not clear whether bisphosphonates, including zoledronic acid, improve the clinical outcome of patients with PDB. Zoledronic acid was associated with increased risk for atrial fibrillation and osteonecrosis of the jaw in some studies in patients with osteoporosis and cancer, respectively, but not in patients with PDB. Until we have data on the effects of bisphosphonates on clinical outcomes in PDB such as fracture, deformity and osteosarcoma, we must base therapeutic decisions on the data regarding the effects of these agents on disease activity markers (such as serum ALP levels) and bone pain.

Plasma Calcitonin in Paget's Disease of Bone

1977 ◽  
Vol 52 (3) ◽  
pp. 329-332 ◽  
Author(s):  
J. A. Kanis ◽  
G. Heynen ◽  
R. J. Walton
Keyword(s):  
Alkaline Phosphatase ◽  
Plasma Levels ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Paget’S Disease Of Bone ◽  
Paget's Disease Of Bone ◽  
Control Subjects ◽  
Plasma Alkaline Phosphatase ◽  
And Control ◽  
Age And Sex

1. Plasma levels of immunoreactive calcitonin were measured in 22 patients with untreated Paget's disease of bone and in 22 control subjects matched for age and sex. 2. No significant differences in plasma calcitonin were found between patients and control subjects, and hormone levels did not correlate significantly with activity of plasma alkaline phosphatase. 3. These results suggest that Paget's disease of bone is not due to deficient secretion of endogenous calcitonin.

scholarly journals Treatment of Paget's disease of bone with single dose intravenous pamidronate.

1993 ◽  
Vol 52 (8) ◽  
pp. 616-618 ◽  
Author(s):  
R A Watts ◽  
S J Skingle ◽  
M M Bhambhani ◽  
G Pountain ◽  
A J Crisp
Keyword(s):  
Single Dose ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Paget’S Disease Of Bone ◽  
Paget's Disease Of Bone ◽  
Intravenous Pamidronate

Paget’s disease of bone

2013 ◽  
pp. 1237-1244
Author(s):  
Stuart H. Ralston
Keyword(s):  
Bone Turnover ◽  
Viral Infections ◽  
Serum Alkaline Phosphatase ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Paget’S Disease Of Bone ◽  
Bone Architecture ◽  
Paget's Disease Of Bone ◽  
Disease Extent ◽  
Bone Scans

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.

Paget’s disease of bone

2016 ◽  
Author(s):  
Stuart H. Ralston
Keyword(s):  
Bone Turnover ◽  
Viral Infections ◽  
Serum Alkaline Phosphatase ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Bisphosphonate Therapy ◽  
Paget’S Disease Of Bone ◽  
Bone Architecture ◽  
Paget's Disease Of Bone ◽  
Disease Extent

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.

Plasma α2 HS-glycoprotein Concentration in Paget's Disease of Bone: its Possible Significance

1980 ◽  
Vol 58 (5) ◽  
pp. 435-438 ◽  
Author(s):  
B. A. Ashton ◽  
R. Smith
Keyword(s):  
Alkaline Phosphatase ◽  
Plasma Concentration ◽  
Bone Formation ◽  
Alkaline Phosphatase Activity ◽  
Paget’S Disease ◽  
Paget's Disease ◽  
Paget’S Disease Of Bone ◽  
Paget's Disease Of Bone ◽  
Plasma Alkaline Phosphatase ◽  
Normal Adults

1. The plasma concentration of the α2HS-glycoprotein has been measured in 58 normal adults and in patients with Paget's disease of bone before (24) and during treatment (16). 2. The average plasma α2HS-glycoprotein was lower in the patients with Paget's disease than in the normal adults and was inversely related to plasma alkaline phosphatase activity (r = −0.55, n = 24, P<0.001). 3. When the patients with Paget's disease were treated with either diphosphonate or calcitonin, the plasma α2HS-glycoprotein concentration increased towards normal. In those patients treated with calcitonin, this increase was too rapid to be entirely accounted for by a cessation of bone formation.

Sign in / Sign up

Export Citation Format

Share Document