Corticosteroid osteoporosis.
Glucocorticoids produce osteoporosis via a number of mechanisms, the most important of which is probably inhibition of bone formation. This results in reduction in bone mass of 10-20% at commonly assessed sites, but the bone loss is 30-40% when predominantly trabecular bone is measured. The dosage and duration of steroid treatment influence the extent of bone loss, but other factors are not predictive. At the present time, a patient who has demonstrable sex hormone deficiency should receive appropriate replacement therapy. Optimization of calcium intake is advisable. If bone loss is severe or continues in spite of these measures, the addition of a bisphosphonate, calcitonin, fluoride or a vitamin D metabolite may be appropriate, according to local availability. Thiazide diuretics can be combined with all of these regimens. If combined with vitamin D or its metabolites, careful monitoring of serum calcium levels should be undertaken. Bone density should be monitored annually until such time as it is stable.
Reid
I R
IR
City Hospital, Aberdeen, UK.
Grey
A B
AB
D000305:Adrenal Cortex Hormones / Q000009:adverse effects* / Q000627:therapeutic use; D015519:Bone Density / Q000187:drug effects; D005260:Female; D050723:Fractures, Bone / Q000453:epidemiology / Q000209:etiology; D006801:Humans; D015994:Incidence; D010024:Osteoporosis / Q000139:chemically induced* / Q000188:drug therapy / Q000517:prevention & control
D000305:Adrenal Cortex Hormones