Missed opportunities in physician management of glucocorticoid‐induced osteoporosis?

Glucocorticoids, prescribed for their antiinflammatory and immunosuppressive features, are the most common cause of secondary osteoporosis. Used to treat a variety of diseases affecting almost every bodily system, glucocorticoids can result in bone loss irrespective of the disease being treated or the age or sex of the person receiving the drug. A detailed discussion of the pathogenesisofboneloss inglucocorticoid-inducedosteoporosis (GIOP) is beyond the scope of this editorial, but recent reviews are available on this topic (1,2). Community survey data estimate the frequency of oral use of glucocorticoids as 0.5% of the general population and 1.75% of women older than age 55 (3). The estimated incidence of GIOP is 50% in patients treated for 6 months (4,5), and fractures occur in approximately one-third of those patients undergoing long-term oral glucocorticoid therapy ( 1 year) (6,7). Bone loss and fractures ensue most commonly in postmenopausal women (8), but men and menstruating women are not spared these complications (2,9). There is rapid onset of trabecular bone loss (10–20%) as early as 3 months after initiation of therapy, followed by a slower rate of 2% per year thereafter. In contrast, bone loss in the femoral neck proceeds more slowly (2–3% in the first year), but continues over time (10). In the year prior to initiation of glucocorticoid treatment, the incidence of nonvertebral fractures was 1.6 per 100 person-years, and it increased to 2.0 per 100 person-years within 3 months of starting therapy and then remained constant thereafter (8). In this same study, similar patterns of increasing fracture rates were noted for hips, vertebrae, and forearms. Parallel trends in loss of bone mineral density (BMD) equivalent to 1 SD or doubling of the fracture risk in postmenopausal women (11) and an increased risk of hip (22%) and vertebral (51%) fractures were documented in individuals receiving inhaled glucocorticoids compared with nonusers (12). Low BMD and subsequent fracture are related in part to dosage of glucocorticoid (8). The relative rate of vertebral fractures increased from 1.55 to 5.18 in patients receiving low doses ( 2.5 mg daily) compared with patients in the high-dose ( 7.5 mg daily) group. Even the relative rates of nonvertebral fractures increased from 1.17 to 1.36 from the lowest to the highest dose groups. These data suggest that even low doses of glucocorticoids are associated with an increased risk of fracture. However, other factors may be important in determining fracture risk in patients exposed to glucocorticoids. Bone loss may also be accelerated when the underlying disease process compromises bone architecture, either from the inflammation process itself or from immobility due to the disease, such as in rheumatoid arthritis (RA), systemic lupus erythematosus, inflammatory bowel disease, or asthma (7,13–15). Advancing age is also a risk factor for both men and women taking oral glucocorticoids (16), as is the risk of falling (8). The possibility of decreased fracture risk and recovery back to baseline levels within 2 years after Supported by NIH/NIAMS grants P60-AR-30692 and K2402138, an Arthritis Foundation Clinical Science Grant, the Arthritis Foundation Greater Chicago Chapter, the Illinois Lupus Foundation, and research grants from PG accepted in revised form July 26, 2002. Arthritis & Rheumatism