作者: Adina E. Schneider , Mone Zaidi , Solomon Epstein
DOI: 10.1016/B978-012183502-6/50006-7
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摘要: Publisher Summary This chapter reviews the cellular and molecular mechanisms that have recently been discovered regarding bone loss associated with calcineurin inhibitors. Calcineurin inhibitors are widely used in management of auto-immune disorders revolutionized organ transplantation. A direct causative role for has difficult to demonstrate clinical studies as a result concomitant use glucocorticoids. The rapid severe occurs after transplant is likely be attributable not only glucocorticoids, but also inhibitors, CsA FK506. These agents block T-cell proliferation by inhibiting Ca++++-calmodulin-sensitive phosphatase calcineurin. drugs shown cause high-turnover both human animal studies. Animal demonstrated acute increases remodeling, consisting osteoclast activation and, some circumstances, osteoblastic formation. There limited persuasive evidence T cells may mediate action FK506, again, this needs further confirmation.