Skeletal effects of primary hyperparathyroidism: bone mineral density and fracture risk.

Parathyroid hormone (PTH) is associated with anabolic and catabolic skeletal effects that vary according to the kinetics of serum levels and the type of bone. The anabolic effects are manifested in patients with a periodic rapid transient rise in serum PTH, as seen with daily subcutaneous injection of PTH(1-34) and PTH(1-84) in the treatment of osteoporosis. These patients have an increase in bone mineral density (BMD), particularly at skeletal sites with a high trabecular component, such as the lumbar spine, and a reduction in fracture risk. The catabolic effects are typified in patients with primary hyperparathyroidism (PHPT) who have chronic persistently elevated PTH levels. Patients with long-standing PHPT have a reduction in BMD, particularly at predominately cortical skeletal sites, such as the one-third radius, with relative preservation of BMD at the lumbar spine. Some but not all studies have reported an increase in fracture risk with PHPT. Because many patients with PHPT are postmenopausal women at risk for osteoporosis owing to estrogen deficiency, BMD and fracture risk may be a result of multiple factors with variable effects on bone remodeling. The skeletal effects of normocalcemic PHPT have not yet been fully characterized, but may not be the same as hypercalcemic PHPT.