Table 1.
Risk Factor | Explanation |
---|---|
Advancing age | Elderly patients receiving glucocorticoid therapy have a 26- fold higher risk of vertebral fractures than younger patients and a shorter interval between initiation of treatment and the occurrence of fracture (14) |
Low body mass index | Significant risk factor for GIO and probably fractures as well (13). |
Underlying disease | Rheumatoid arthritis, polymyalgia rheumatica, inflammatory bowel disease, chronic pulmonary disease, and transplantation are independent risk factors (7) |
Family history of hip fracture, prevalent fractures, smoking, excessive alcohol consumption, frequent falls. |
All are independent risk factors for osteoporosis but have not been well studied in patients receiving glucocorticoids. |
Glucocorticoid receptor genotype | Individual glucocorticoid sensitivity may be regulated by polymorphisms in the glucocorticoid receptor gene (16). |
11β-HSD isoenzymes | 11β-HSD1 expression increases with aging and glucocorticoid administration and thereby enhances glucocorticoid activation (17) |
Glucocorticoid dose (peak, current, or cumulative, duration of therapy, interval) |
There may be no safe dose, although this is somewhat controversial. However, the risk of fracture unarguably escalates with increased doses and duration of therapy. Alternate day or inhalation therapy does not spare the skeleton (7,15). |
LowBMD | Glucocorticoid-induced fractures occur independently of a decline in bone mass but patients with very low bone density may be at higher risk (7,13). |
11β-HSD, 11β-hydroxysteroid dehydrogenase; BMD, bone mineral density.