The most common joint involved is the hip and the most common cause of the disorder is trauma. his 1932 presentation to the Johns Hopkins Medical Society. Eighteen years later, only one year after the introduction of cortisone for the treatment of rheumatoid arthritis, clinicians became aware of the rapidly injurious skeletal effects of glucocorticoid administration (2,3). At first, it was uncertain whether the hip fractures that had occurred were the result of falls due to steroid myopathy or merely coincidental with cortisone therapy because vertebral fractures and radiographic osteoporosis had not yet been observed. However, within just a few more years, osteoporosis and fractures were clearly recognized as skeletal complications of treatment with cortisone, prednisolone, and prednisone (4). Collapse of the femoral and humeral heads after high-dose therapy was described shortly thereafter (5,6). Today, we know that glucocorticoid administration is the most common cause of secondary osteoporosis and the leading cause of nontraumatic osteonecrosis. In patients receiving long-term therapy, glucocorticoids induce fractures in 30 to 50% and osteonecrosis in 9 to 40% (7,8). Sadly, patients are seldom warned about these side effects and as a result, adverse skeletal events are the most common glucocorticoid-related complications associated with successful litigation (9). GLUCOCORTICOID-INDUCED OSTEOPOROSIS (GIO) RISK FACTORS Bone loss in GIO is usually biphasic, with a relatively rapid reduction in bone mineral density (BMD) of 6C12% within the first year, followed by a slower annual loss of about 3% for as long as the glucocorticoids are administered (10). However, the relative risk of fracture escalates by as much as 75% within the first 3 months after initiation of glucocorticoid therapy and this often occurs before a significant decline in BMD (11). There is also a remarkable decrease in the risk of fractures within the first 3 months after the glucocorticoids are discontinued, well before any improvement in BMD. The rapid onset and offset of the fracture risk suggest a qualitative defect in bone material properties not captured by bone densitometry (11). Furthermore, more than one third of postmenopausal women receiving long-term glucocorticoid therapy may have one or more asymptomatic vertebral fractures without abnormal results on calcaneal ultrasound or lumbar and hip BMD determinations (12). Thus, the disparity between bone quantity and quality in glucocorticoid-induced osteoporosis makes ultrasound or BMD measurements inadequate for identifying who is at risk of fractures (13). Several large case-controlled studies show clear and strong associations between glucocorticoid exposure and fracture (11,14). An increase in vertebral and hip fractures occurs with as little as 2.5 to 7.5 mg/day of prednisolone (equivalent to 3.1 to Cefuroxime sodium 9.3 mg of prednisone). In a cohort study of patients aged 18 to 64 years receiving glucocorticoids for a variety of disorders, the combination of higher dose, longer duration and continuous use had the greatest effect on the incidence of fractures (14). Continuous treatment with 10 mg/day of prednisone for more Cefuroxime sodium than 90 days was associated with a 7-fold increase in hip fractures and a 17-fold increase in vertebral fractures (14). At present, evidence Cefuroxime sodium suggests that the risk of fracture is usually small and intervention is not required with single dose-pack prescriptions, intermittent oral therapy with a cumulative exposure of less than 1 gram per year, or replacement therapy for patients with hypopituitarism, adrenal insufficiency, or congenital adrenal hyperplasia, provided that the replacement doses are not excessive and the recommendations for increased dosage during periods of stress are not supraphysiologic or inappropriate (e.g. as with mental stress as opposed to febrile or gastrointestinal illnesses) (7,15). The risk of glucocorticoid-induced osteoporosis is probably the same in men and women of all ethnicities (20). Risk factors include advancing age, prolonged duration of treatment, increased daily dosage and cumulative dose (multiple courses of high-dose oral Rabbit Polyclonal to EKI2 or intravenous therapy on a baseline of relatively low doses also increase risk), low body mass index, prevalent fractures, frequent falls, underlying disease (especially organ transplant recipients, inflammatory bowel disease and the accompanying malabsorption, rheumatoid arthritis,.