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Lewiecki E.M.,New Mexico Clinical Research and Osteoporosis Center
Current Osteoporosis Reports | Year: 2010

Measurement of bone mineral density (BMD) is used to diagnose osteoporosis, assess fracture risk, and monitor response to therapy. Of the different methods for measuring BMD, dual-energy X-ray absorptiometry (DXA) is the only technology for classifying BMD according to criteria established by the World Health Organization (WHO) and the only technology that is validated for BMD input with the WHO fracture risk assessment algorithm, FRAX. Vertebral fracture assessment (VFA) by DXA provides an image of the thoracic and lumbar spine for the purpose of detecting vertebral fracture deformities. Identification of a previously unrecognized vertebral fracture may change diagnostic classification, assessment of fracture risk, and treatment decisions. In comparison with standard radiographs of the spine, the correlation for detecting moderate and severe vertebral fractures is good, with a smaller dose of ionizing irradiation, greater patient convenience, and lower cost. Optimal performance of DXA and VFA requires training and adherence to quality standards. © 2010 Springer Science+Business Media, LLC. Source

Lewiecki E.M.,New Mexico Clinical Research and Osteoporosis Center
Nature Reviews Rheumatology | Year: 2011

Postmenopausal osteoporosis is a disease of high bone remodeling, with an imbalance of bone resorption over bone formation, resulting in decreased bone mineral density and disruption of bone microarchitecture. With our improved understanding of the molecular and cellular regulators and mediators of bone remodeling, new targets for therapeutic intervention have been identified. Receptor activator of nuclear factor κB ligand (RANKL) is the principal regulator of osteoclast differentiation, activity, and survival; denosumab, a fully human monoclonal antibody to RANKL, inhibits bone resorption and is approved for the treatment of women with postmenopausal osteoporosis at high risk of fractures. Cathepsin K is a protease produced by activated osteoclasts that degrades the protein matrix of bone. An inhibitor of cathepsin K, odanacatib, is in phase III clinical trials for the treatment of postmenopausal osteoporosis; it decreases bone resorption while seeming to suppress bone formation less than other antiresorptive agents. Sclerostin is a cytokine produced by osteocytes that inhibits osteoblastic bone formation; investigational monoclonal antibodies to sclerostin, such as AMG 785, have osteoanabolic properties with the potential to improve clinical outcomes in patients with osteoporosis. These and other novel interventions that target newly recognized regulators of bone remodeling are promising agents for the treatment of osteoporosis. © 2011 Macmillan Publishers Limited. All rights reserved. Source

Lewiecki E.M.,New Mexico Clinical Research and Osteoporosis Center
Expert Opinion on Biological Therapy | Year: 2010

Importance of the field: Osteoporosis is a common skeletal disease that is associated with an imbalance in bone remodeling. Denosumab is an investigational fully human monoclonal antibody to receptor activator of NF-κB ligand (RANKL), a cytokine member of the TNF family that is the principal mediator of osteoclastic bone resorption. Areas covered in this review: The efficacy and safety of denosumab in the management of postmenopausal osteoporosis is evaluated by reviewing the published literature and presentations at scientific meetings through 2009. What the reader will gain: This review focuses on the data on fracture risk reduction and safety endpoints of denosumab in the treatment of postmenopausal osteoporosis. Take home message: In postmenopausal women with osteoporosis, denosumab (60 mg by subcutaneous injection every 6 months) increased bone mineral density, reduced bone turnover markers, and reduced the risk of vertebral, hip and non-vertebral fractures. Denosumab was well tolerated with a safety profile generally similar to placebo. It is a promising emerging drug for the prevention and treatment of postmenopausal osteoporosis. © 2010 Informa UK Ltd. Source

Lewiecki E.M.,New Mexico Clinical Research and Osteoporosis Center
Journal of Clinical Densitometry | Year: 2010

Asymptomatic primary hyperparathyroidism (PHPT) may cause adverse skeletal effects that include high bone remodeling, reduced bone mineral density (BMD), and increased fracture risk. Parathyroid surgery, the definitive treatment for PHPT, has been shown to increase BMD and appears to reduce fracture risk. Current guidelines recommend parathyroid surgery for patients with symptomatic PHPT or asymptomatic PHPT with serum calcium >1. mg/dL above the upper limit of normal, calculated creatinine clearance <60. mL/min, osteoporosis, previous fracture, or age <50. yr. The type of operation performed (parathyroid exploration or minimally invasive procedure) and localizing studies to identify the abnormal parathyroid glands preoperatively should be individualized according to the skills of the surgeon and the resources of the institution. In patients who choose not to be treated surgically or who have contraindications for surgery, medical therapy should include a daily calcium intake of at least 1200. mg and maintenance of serum 25-hydroxyvitamin D levels of at least 20. ng/mL (50. nmol/L). Bisphosphonates and estrogens have been shown to provide skeletal benefits that appear to be similar to parathyroid surgery. Cinacalcet reduces serum calcium in PHPT patients with intractable hypercalcemia but has not been shown to improve BMD. It is not known whether any medical intervention reduces fracture risk in patients with PHPT. There are insufficient data on the natural history and treatment of normocalcemic PHPT to make recommendations for management of this disorder. © 2010 The International Society for Clinical Densitometry. Source

Lewiecki E.M.,New Mexico Clinical Research and Osteoporosis Center
Reviews in Endocrine and Metabolic Disorders | Year: 2010

Osteoporosis is a common disease characterized by low bone strength that increases the risk of fractures. The consequences of fractures include increases in morbidity, mortality, and healthcare costs. Randomized clinical trials have shown that pharmacological therapy can reduce the risk of fractures. In clinical practice, however, failure to achieve optimal therapeutic benefit is common for reasons that include taking medication incorrectly, stopping it prematurely, malabsorption, and the presence of unrecognized diseases or conditions with adverse skeletal effects. Monitoring for anti-fracture effectiveness in individual patients is limited by the absence of clinical tools to directly measure bone strength. It is therefore necessary to monitor therapy with biomarkers such as bone mineral density and bone turnover markers. This is a review of the utility of these tools in the care of individual patients. © Springer Science+Business Media, LLC 2010. Source

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