Glucocorticoid-induced osteoporosis

Abstract

Glucocorticoid induced osteoporosis (GC-OP) is the most important form of all secondary osteoporoses. Mainly from in vitro and animal studies a lot of information exists concerning the underlying pathogenetic mechanisms. Some findings are still controversial but it is generally accepted that the three most important mechanisms are inhibition of osteoblastic matrix formation, stimulation of osteoclastic bone resorption and deterioration of intestinal calcium resorption with consecutive mild secondary hyperparathyroidism. In the individual patients the time between the beginning of corticoid therapy and clinical manifestation of osteoporosis varies considerably. If there is really a threshold dosage of corticoids is still debated. Besides dosage and duration of steroids age, sex, other risk factors of osteoporosis and underlying disease may be important factors. In contrast to the clinical prominence of GC-OP only little experience exists in counteracting the detrimental effects of corticoids on bone tissue. For pure prevention it seems reasonable to overcome intestinal calcium malabsorption by calcium or vitamin D. Concerning treatment of manifest GC-OP we studied the effect of salmon calcitonin (sCT) in patients with chronic obstructive lung disease. 18 patients injected themselves 100 U sCT every second day subcutaneously while 18 randomized patients served as untreated controls. There was a significant pain reduction in the sCT group and after six months the mineral content of the distal radius had increased by 2.7% despite a daily mean intake of 16.2 mgs prednisone during that time. In the control group (mean daily prednisone dose 16.8 mgs) the mineral content decreased with 3.5% on the average (p less than 0.001).