A paradoxical observation has been the strong association of certain microbial organisms with autoimmune diseases. For example, Klebsiella pneumoniae and coxsackievirus B have been strongly correlated with ankylosing spondylitis and diabetes mellitus type 1 , respectively. This has been explained by the tendency of the infecting organism to produce super-antigens that are capable of polyclonal activation of B-lymphocytes , and production of large amounts of antibodies of varying specificities, some of which may be self-reactive (see below).
Glucocorticoid therapy is associated with an appreciable risk of bone loss, which is most pronounced in the first few months of use. In addition, glucocorticoids increase fracture risk, and fractures occur at higher bone mineral density (BMD) values than occur in postmenopausal osteoporosis. The increased risk of fracture has been reported with doses of prednisone or its equivalent as low as to mg daily [ 1 ]. Thus, glucocorticoid-induced bone loss should be treated aggressively, particularly in those already at high risk for fracture (older age, prior fragility fracture). In other individuals, clinical risk factor and bone density assessment may help guide therapy. The prevention and treatment of glucocorticoid-induced bone loss will be reviewed here. The clinical features are reviewed separately. (See "Clinical features and evaluation of glucocorticoid-induced osteoporosis" .)
Depending on timing, intra-tympanic steroid injection is also offered (dexamethasone 10-24mg/cc). Intra-typmpanic steroid injection is performed by inserting a needle through the eardrum and injecting about of highly concentrated steroids directly into the middle ear space. The patient is than instructed to keep the affected ear up for 30 minutes without swallowing, yawning, or popping the ear. After injection, the patient is allowed to immediately resume normal activities. This steroid injection has also been used to treat Meniere's Disease flare-ups.