REVIEW - Steroids and osteoporosis

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Vnitr Lek. 2007 Jul-Aug;53(7-8):831-40.

Glucocorticoids and osteoporosis

Zikán V.

III. Interní klinika 1. lékarské fakulty UK a VFN Praha.

Treatment with glucocorticoids (GC) has no alternative in many medical

disciplines for their anti-inflammatory and immunosuppressive effect.

However, osteoporosis and the related fractures are a serious

complication brought about by long-term GC therapy. The risk of

fractures, especially of the vertebras and the ribs, becomes higher as

early as in the first months of oral GC therapy. It grows in

proportion to the daily dose of GC, and is present even if low doses

are administered (2.5-7.5 mg of prednisone per day). Decreasing bone

density (BMD) is not accountable for the higher risk of fractures in

GC therapy and fractures occur with higher values of BMD than in

primary osteoporosis. There is still no tool that we could use to

quantify the changes in the bone quality and the increased risk of

fracture in clinical practice. The principal mechanism by which GC

induces osteoporosis is inhibition of bone formation caused by the

suppression of osteoblastogenesis as well as the activity of

functional osteoblasts, with accelerated osteocyte and osteoblast

apoptosis. There are significant differences between individuals in

terms of GC sensitivity, the reasons of which have not yet been

explained. Prior to planned long-term GC therapy (> 3 months) with

daily doses higher than 2.5 mg of prednisone p.o. (or higher doses of

inhaled GC), it is recommended to perform a densitometry exam using

dual-energy X-ray absorptiometry (DXA) in the lumbar region of the

spine and femoral collum to evaluate additional risk factors of

osteoporosis and fractures for a more precise estimate of the risk of

fracture in the specific patient. Sufficient intake of calcium

(1,000-1,500 mg of elementary calcium per day) and of the vitamin D

(800 IU per day) should be assured in all patients treated by GC.

Endogenous production of sexagens should be evaluated and possible

substitution therapy should be considered in premenopausal women and

younger men. Today, bisphosphonates can be given to patients with a

high risk of fracture, the effects of which in preventing the decrease

of BMD and vertebral fractures have been documented in randomised

clinical studies, even though the evaluation of the risk of fractures

was not the primary endpoint of those studies. However, in view of the

antiremodelling effect of bisphosphonates, it is clear that this

therapy does not eliminate the cause of GC induced osteoporosis and

drugs with stimulating effect on osteoblasts will certainly be

preferred in the future. Very promising are the first clinical studies

of injection parathormone (PTH 1-34) which stimulated bone formation

in a continuing GC treatment.

PMID: 17915428

http://www.ncbi.nlm.nih.gov/pubmed/17915428?ordinalpos=9 & itool=EntrezSystem2.PEn\

trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Not an MD