Glucocorticoid-induced osteoporosis.

Glucocorticoids, in supraphysiologic doses, exert both anti-inflammatory and immunosuppressive actions which have made them useful in the treatment of rheumatoid arthritis, asthma, and systemic lupus erythematosus (SLE). Unless these conditions can be prevented, we will continue to depend on glucocorticoids and related compounds to alleviate symptoms and to slow down the progression of the disease. Unfortunately, long-term administration of these compounds often leads to untoward effects involving cardiovascular, gastrointestinal, and musculoskeletal systems. The most disabling of these adverse effects is the development of osteopenia. Bone loss secondary to glucocorticoid administration is known to have a characteristic distribution. It is more severe in the regions with high trabecular bone content (spine and ribs), and less striking in predominantly cortical bone areas (Hann et al, 1979). Consequently, rib fractures and compression deformities of the vertebrae frequently occur.