Post-transplantation osteoporosis.

In the last two decades organ transplantation has become an effective and e stablished therapy for end-stage disease of various organs. The increase in survival has been due to the greater immunosuppressive capacity of regimen s that include cyclosporin. During the first few months after transplantati on cyclosporin is associated with high-dose steroids, which produce deleter ious effects on bone and mineral metabolism. These effects are superimposed on the previous bone lesions produced by the underlying chronic diseases. Rapid bone loss occurs specially during the first 6 to 12 months after tran splantation, when the incidence of fractures is greater. The majority of th e fractures involve the spine. Fracture rates are lower after renal transpl antation (7 to 11% in nondiabetic renal transplant recipients) and higher i n the recipients of other organ transplants: 17.2 to 42% after liver transp lantation, 18 to 50% after cardiac transplantation and 25 to 29% after lung transplantation. No pretransplant densitometric or biochemical parameter c an adequately predict fracture risk in the individual patient. Despite this , patients with low bone mineral density at the hip, particularly in women, tend to have an increased risk of fracture. Patients can have vertebral fr actures despite normal bone mineral density at the spine. Pathogenesis of b one loss is multifactorial. Patients with renal and liver diseases have eit her renal or hepatic osteodystrophy prior to transplantation that predispos e to bone loss, and many patients awaiting pulmonary transplantation alread y have osteoporosis due to the use of corticosteroids for their lung diseas e. Rapid bone loss after transplantation depends, as suggested by prospecti ve biochemical parameters, on a decrease in bone formation (reduction in os teocalcin levels) and an increase in bone resorption. Steroids seem to be t he principal determinants of these derangements, although some role of cycl osporin cannot be excluded. Other factors that contribute to bone loss are secondary hyperparathyroidism and hypogonadism. Calcium supplementation and vitamin D administration as the only preventive measures do not seem to re duce fracture risk. The most promising regimens to prevent bone loss after transplantation seem to be the use of bisphosphonates immediately prior to and during the first year after transplantation.