Within the past 2 decades, organ transplantation has become established as effective therapy for @entity8 . Regimens to prevent rejection after transplantation commonly include high-dose glucocorticoids and calcineurin-calmodulin phosphatase inhibitors (the @entity38721 and @entity1140 ), which are detrimental to bone and mineral homeostasis, and are associated with rapid @entity604 that is often superimposed upon an already compromised skeleton. The incidence of @entity174 ranges from 8% to 65% during the first year after transplantation. In general, @entity174 rates are lowest in renal transplant recipients and highest in @entity1 who receive a liver transplant for @entity2835 . Rates of @entity604 and @entity174 are greatest during the first 6 to 12 months after transplantation. Postmenopausal @entity1 and @entity6126 @entity1 appear to be at increased risk. Although no pretransplant densitometric or biochemical parameter has yet been identified that adequately predicts @entity174 risk in the individual @entity1 , low pretransplant bone mineral density does tend to increase the risk of @entity174 , particularly in @entity1 . However, @entity1 may sustain @entity174 despite normal pretransplant bone mineral density. Although the pathogenesis of the rapid @entity604 is multifactorial, prospective biochemical data suggest that uncoupling of bone formation from resorption may be in part responsible, at least during the first 3 to 6 months. Prevention of transplantation @entity170 should begin well before transplantation. @entity1 awaiting transplantation should be evaluated with spine radiographs, bone densitometry, thyroid function tests, serum @entity460 , @entity560 , @entity461 , and @entity251 (in @entity1 ). Therapy for @entity170 , low bone mass, and potentially reversible biochemical causes of @entity604 should be instituted during the waiting period before transplantation. In @entity1 with normal pretransplant bone density, therapy to prevent early posttransplant @entity604 should be instituted immediately following transplantation. Most pharmacologic agents available for therapy of @entity170 have not been subject to prospective controlled studies in organ transplant recipients. However, antiresorptive drugs, such as biphosphonates, appear to hold therapeutic promise.

XXXX after organ transplantation.

@entity1 :: ('9606', 'Species') :: ['women', 'Patients', 'patients', 'patient', 'men'] @entity2835 :: ('MESH:D008105', 'Disease') :: ['primary biliary cirrhosis'] @entity8 :: ('MESH:D007674', 'Disease') :: ['endstage renal, hepatic, cardiac, and pulmonary disease'] @entity251 :: ('MESH:D013739', 'Chemical') :: ['testosterone'] @entity38721 :: ('MESH:D003524', 'Chemical') :: ['cyclosporines'] @entity174 :: ('MESH:D050723', 'Disease') :: ['fractures', 'fracture'] @entity604 :: ('MESH:D016301', 'Disease') :: ['bone loss'] @entity170 :: ('MESH:D010024', 'Disease') :: ['osteoporosis'] @entity460 :: ('MESH:D002118', 'Chemical') :: ['calcium'] @entity1140 :: ('MESH:D016559', 'Chemical') :: ['tacrolimus'] @entity6126 :: ('MESH:D007006', 'Disease') :: ['hypogonadal'] @entity461 :: ('5741', 'Gene') :: ['parathyroid hormone'] @entity560 :: ('MESH:D014807', 'Chemical') :: ['vitamin D']
@entity170 :: (MESH:D010024,Disease) :: ['Osteoporosis']
