INFO - Overview of steroid-induced osteoporosis

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Overview of glucocorticoid induced osteoporosis

Glucocorticoids are widely used in the treatment of patients with chronic,

noninfectious, inflammatory diseases. These include asthma, pulmonary

disease, rheumatoid arthritis and other connective tissue diseases,

inflammatory bowel disease, and organ transplantation. However, these agents

are double-edged swords: Despite their beneficial anti-inflammatory and

immunosuppressive effects, adverse effects are frequent.

Glucocorticoids have a profound effect on bone metabolism and are the major

cause of secondary osteoporosis. Skeletal wasting is most rapid during the

first 6 months of glucocorticoid therapy, with trabecular bone more affected

than cortical bone. Daily prednisone doses of 7.5 mg often result in

significant bone loss and increased fracture risk. Laan et al.[ 1 ]

demonstrated an average loss of 8% of trabecular bone density and a 2% of

cortical bone density in the lumbar spine over a 20-week period in people

treated with a mean dose of prednisone of 7.5 mg/day. A corresponding

increase in early fracture risk has been described, even independent of

changes in BMD, as quickly as 3 months after beginning glucocorticoid

therapy[ 2 ],[ 3 ].

Bone density in steroid-treated individuals, studied cross-sectionally, is

related both to the duration of their glucocorticoid treatment and to the

dose of these drugs. Scientists do not yet know whether there is a threshold

dose of glucocorticoid below which osteopenia does not occur; alternate-day

glucocorticoid regimens have not been shown to produce less bone loss than

daily regimens. Even inhaled steroids appear to increase bone loss when used

chronically[ 4 ],[ 5 ],[ 6 ]. However, inhaled steroids pose less risk than

oral glucocorticoids. Regardless of the form of administration, using the

lowest dose of glucocorticoids needed to control symptoms will help minimize

bone loss.

Initial rapid bone loss of 5% to 15% within the first 6 to 12 months

Trabecular bone preferentially affected

Bone loss potentially reversible with lowering of dose or cessation of

steroid

According to the American College of Rheumatology (ACR) Task Force on

Osteoporosis Guidelines, the magnitude of GIOP suggests that the majority of

patients receiving long-term glucocorticoid therapy have low bone mineral

density (BMD), and that over one-fourth sustain osteoporotic fractures. The

prevalence of vertebral fractures in asthma patients receiving

glucocorticoid therapy for at least 1 year is 11%, and

glucocorticoid-treated patients with rheumatoid arthritis have an increased

incidence of fractures of the hip, rib, spine, leg, ankle, and foot. Thus,

GIOP is an important clinical problem that involves both prevention and

treatment.

http://www-cme.erep.uab.edu/onlineCourses/giop_rev1/contents1of1.asp

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Mayo Clinic in Rochester

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s Hopkins Medicine

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