Usually no treatment is necessary. Spontaneous remission occurs in
VIRA-A (vidarabine) parenterally is teratogenic in rats and rabbits. Ten percent VIRA-A (vidarabine) ointment applied to 10% of the body surface during organogenesis induced fetal abnormalities in rabbits. When 10% VIRA-A (vidarabine) ointment was applied to 2% to 3% of the body surface of rabbits, no fetal abnormalities were found. This dose greatly exceeds the total recommended ophthalmic dose in humans. The possibility of embryonic or fetal damage in pregnant women receiving VIRA-A (vidarabine) Ophthalmic Ointment, 3%, is remote. The topical ophthalmic dose is small, and the drug relatively insoluble. Its ocular penetration is very low. However, a safe dose for a human embryo or fetus has not been established. There are no adequate and well-controlled studies in pregnant women. VIRA-A (vidarabine) should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
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" .)