Skip to main content
. Author manuscript; available in PMC: 2013 Sep 1.
Published in final edited form as: Endocrinol Metab Clin North Am. 2012 May 23;41(3):595–611. doi: 10.1016/j.ecl.2012.04.004

Table 1.

Risk Factors for Glucocorticoid-Induced Osteoporosis.

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.