Alendronate In Glucocorticoid-induced Osteoporosis Research Articles

PartII: Interactive case:Drug‐inducedendocrine disorders

Part<scp>II</scp>: Interactive case:<scp>Drug‐induced</scp>endocrine disorders

Glucocorticoid-induced osteoporosis in men

Osteoporosis and fractures are a common consequence of glucocorticoid therapy for inflammatory disorders. Men fracture approximately 10 yr later in life than women and receive less attention as regards osteoporosis risk, including in glucocorticoid-induced osteoporosis (GIOP). In addition, while men are less likely to have certain rheumatologic disorders often treated with glucocorticoids, men are more likely to have chronic obstructive pulmonary disease, inflammatory bowel disease, and organ transplantation as reasons for use of oral glucocorticoids. Attempts to improve recognition of GIOP in general have not been successful, and since men are considered less at risk for osteoporosis in general, attention to men with GIOP is even less. Evaluation of GIOP is similar in men and women, and most modern treatment studies of GIOP have included men. Thus, alendronate, risedronate, and zoledronic acid are Food and Drug Administration (FDA)-approved bisphosphonates for GIOP in men. Teriparatide is also FDA-approved for GIOP. In one 36-month trial of teriparatide vs alendronate for GIOP in men and women, the anabolic agent led to a greater increase in bone density and was associated with a lower incidence of morphologic vertebral fractures. Thus, while good management is available for GIOP, recognition of men at risk is the most important step in improving outcomes.

Teriparatide or Alendronate in Glucocorticoid-Induced Osteoporosis

Bisphosphonates are, at present, recommended for patients who have-or are at risk of developing-glucocorticoid-induced osteoporosis. Effective treatment, however, remains challenging. One alternative is once-a-day anabolic therapy with teriparatide, recombinant human parathyroid hormone (1-34), which stimulates bone formation, increases bone mass, and lowers the risk of vertebral and other fractures. Teriparatide directly stimulates osteoblastogenesis and inhibits osteoblast apoptosis, both of which are important mechanisms by which glucocorticoids promote bone loss. This 18-month randomized, double-blind, controlled trial compared teriparatide (20 μg once a day) with the bisphosphonate alendronate (10 mg daily) in 428 women and men with osteoporosis who had received glucocorticoids for at least 3 months in a minimal daily prednisone-equivalent dose of 5 mg. The primary outcome was change in bone mineral density (BMD) at the lumbar spine. When last measured, mean BMD at the lumbar spine had increased more in patients receiving teriparatide than in those receiving alendronate (7.2% versus 3.4%). The difference became statistically significant within 6 months. BMD at the total hip had increased more in the teriparatide group after a year of treatment. New vertebral fractures were less frequent in this group (0.6% versus 6.1%), but there was no significant difference in the frequency of nonvertebral fractures. Semiquantitative grading indicated that preexisting vertebral fractures did not progress during the 18-month study period. Markers of bone formation (N-terminal propeptide of type I collagen) and resorption (C-telopeptide of type I collagen) were increased in patients taking teriparatide but suppressed in those given alendronate. Significantly more teriparatide-treated patients had at least one serum calcium level exceeding 10.5 mg/dL, but no patient in either group had sustained levels of 11 mg/dL or higher. The investigators conclude from these findings that, given what is known of the pathophysiology of glucocorticoid-induced osteoporosis, teriparatide is a valid treatment option for patients with this disorder who are at high risk of fracture.

Teriparatide or Alendronate in Glucocorticoid-Induced Osteoporosis

Background Bisphosphonate therapy is the current standard of care for the prevention and treatment of glucocorticoid-induced osteoporosis. Studies of anabolic therapy in patients who are receiving long-term glucocorticoids and are at high risk for fracture are lacking. Methods In an 18-month randomized, double-blind, controlled trial, we compared teriparatide with alendronate in 428 women and men with osteoporosis (ages, 22 to 89 years) who had received glucocorticoids for at least 3 months (prednisone equivalent, 5 mg daily or more). A total of 214 patients received 20 μg of teriparatide once daily, and 214 received 10 mg of alendronate once daily. The primary outcome was the change in bone mineral density at the lumbar spine. Secondary outcomes included changes in bone mineral density at the total hip and in markers of bone turnover, the time to changes in bone mineral density, the incidence of fractures, and safety. Results At the last measurement, the mean (±SE) bone mineral density at the lumbar spin...

Teriparatide or Alendronate in Glucocorticoid-Induced Osteoporosis

Teriparatide or Alendronate in Glucocorticoid-Induced Osteoporosis

Teriparatide or Alendronate in Glucocorticoid-Induced Osteoporosis

Teriparatide or Alendronate in Glucocorticoid-Induced Osteoporosis

Teriparatide or Alendronate in Glucocorticoid-Induced Osteoporosis

Bisphosphonate therapy is the current standard of care for the prevention and treatment of glucocorticoid-induced osteoporosis. Studies of anabolic therapy in patients who are receiving long-term glucocorticoids and are at high risk for fracture are lacking. In an 18-month randomized, double-blind, controlled trial, we compared teriparatide with alendronate in 428 women and men with osteoporosis (ages, 22 to 89 years) who had received glucocorticoids for at least 3 months (prednisone equivalent, 5 mg daily or more). A total of 214 patients received 20 microg of teriparatide once daily, and 214 received 10 mg of alendronate once daily. The primary outcome was the change in bone mineral density at the lumbar spine. Secondary outcomes included changes in bone mineral density at the total hip and in markers of bone turnover, the time to changes in bone mineral density, the incidence of fractures, and safety. At the last measurement, the mean (+/-SE) bone mineral density at the lumbar spine had increased more in the teriparatide group than in the alendronate group (7.2+/-0.7% vs. 3.4+/-0.7%, P<0.001). A significant difference between the groups was reached by 6 months (P<0.001). At 12 months, bone mineral density at the total hip had increased more in the teriparatide group. Fewer new vertebral fractures occurred in the teriparatide group than in the alendronate group (0.6% vs. 6.1%, P=0.004); the incidence of nonvertebral fractures was similar in the two groups (5.6% vs. 3.7%, P=0.36). Significantly more patients in the teriparatide group had at least one elevated measure of serum calcium. Among patients with osteoporosis who were at high risk for fracture, bone mineral density increased more in patients receiving teriparatide than in those receiving alendronate. (ClinicalTrials.gov number, NCT00051558 [ClinicalTrials.gov].).