Prevention and Treatment of Glucocorticoid-Induced Osteoporosis

Osteoporosis is a disease state resulting in decreased bone mineral density (BMD) and increased risk of fracture, specifically of the vertebrae, spine and hip. Risk factors and high risk populations for developing osteoporosis include low BMD, long-term glucocorticoid therapy, genetics, diet, postmenopausal women and patients with inflammatory or chronic disease states. A variety of signaling pathways involving hormones, cytokines and other signaling molecules are involved in bone formation and are affected by long-term glucocorticoid therapy, leading to the development of glucocorticoid-induced osteoporosis (GIO). There are a variety of drugs that work efficaciously to prevent and treat GIO. Alendronate is a potent bisphosphonate that has shown efficacy in increasing BMD and decreasing bone turnover. Risedronate, another potent bisphosphonate, has demonstrated similar effects in patients suffering from GIO and has been observed to decrease fractures. Zoledronic acid is another bisphosphonate option that has proven efficacy and noninferiority to oral bisphosphonates in GIO, but it is unique in that it is given intravenously once a year. Additionally, teriparatide is a recombinant human parathyroid hormone (PTH) which is a newer therapy for the treatment of GIO and is beginning to replace older therapies such as testosterone and estrogen. The once daily administration of teriparatide induces bone formation, which allows for increase in bone mass thus reducing the risk of vertebral and nonvertebral fractures. Furthermore, calcium and vitamin D are usually seen as prophylaxis and adjunctive therapy. At the initiation of therapy, pharmacists should recommend bone density tests to evaluate if medication is appropriate for the patient. Subsequent action includes patient education and monitoring of initiated therapy and disease progression