Timing and quantification of bone loss in cardiac transplant recipients

Cleemput, Johan Van; Daenen, Wim; Nijs, J; Geusens, Piet; Dequeker, Jan; Vanhaecke, Johan

doi:10.1007/bf00336537

Cited by 27 publications

(27 citation statements)

References 17 publications

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“…Their incidence (18.2%) in the untreated group, in the first 2 years of follow-up, is similar to rates previously reported. 18,19,21,22 Although this study's small population precludes broader assertions, it is reasonable to suggest that prophylactic calcitonin administration could be most effective in the early period after cardiac transplantation, whereas extended administration does not seem to provide a benefit and could be discontinued.…”

Section: Discussionmentioning

confidence: 90%

Effect of Long-Term Calcitonin Administration on Steroid-Induced Osteoporosis after Cardiac Transplantation

Kapetanakis¹,

Antonopoulos²,

Antoniou³

et al. 2005

The Journal of Heart and Lung Transplantation

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Section: Discussionmentioning

confidence: 90%

Effect of Long-Term Calcitonin Administration on Steroid-Induced Osteoporosis after Cardiac Transplantation

Kapetanakis¹,

Antonopoulos²,

Antoniou³

et al. 2005

The Journal of Heart and Lung Transplantation

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“…Many patients already have a low bone mass at the time of the graft, due to cigarette smoking, prolonged physical inactivity, extensive use of loop diuretics and poor nutritional status [4]. In addition, bone mass decreases dramatically after the transplant, at trabecular sites as well as cortical sites [4][5][6][7][8][9][10]. This bone loss is explained by the relatively high doses of glucocorticoids given during the months following the graft, and by the negative effect of cyclosporin A, which probably increases bone turnover [10][11][12][13][14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Intravenous Pamidronate as Treatment for Osteoporosis after Heart Transplantation: A Prospective Study

Seydoux²,

Sandini

et al. 2001

Osteoporosis International

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Fractures due to osteoporosis are one of the major complications after heart transplantation, occurring mostly during the first 6 months after the graft, with an incidence ranging from 18% to 50% for vertebral fractures. Bone mineral density (BMD) decreases dramatically following the graft, at trabecular sites as well as cortical sites. This is explained by the relatively high doses of glucocorticoids used during the months following the graft, and by a long-term increase of bone turnover which is probably due to cyclosporine. There is some evidence for a beneficial effect on BMD of antiresorptive treatments after heart transplantation. The aim of this study was to assess prospectively the effect on BMD of a 3-year treatment of quarterly infusions of 60 mg of pamidronate, combined with 1 g calcium and 1000 U vitamin D per day, in osteoporotic heart transplant recipients, and that of a treatment with calcium and vitamin D in heart transplant recipients with no osteoporosis. BMD of the lumbar spine and the femoral neck was measured by dual-energy X-ray absorptiometry in all patients every 6 months for 2 years and after 3 years. Seventeen patients, (1 woman, 16 men) aged 46+/-4 years (mean +/- SEM) received only calcium and vitamin D. A significant decrease in BMD was observed after 6 months following the graft, at the lumbar spine (- 6.6%) as well as at the femoral neck (-7.8%). After 2 years, BMD tended to recover at the lumbar spine, whereas the loss persisted after 3 years at the femoral neck. Eleven patients (1 woman and 10 men) aged 46+/-4 years (mean +/- SEM) started treatment with pamidronate on average 6 months after the graft, because they had osteoporosis of the lumbar spine and/or femoral neck (BMD T-score below -2.5 SD). Over the whole treatment period, a continuous increase in BMD at the lumbar spine was noticed, reaching 18.3% after 3 years (14.3% compared with the BMD at the time of the graft). BMD at the femoral neck was lowered in the first year by -3.4%, but recovered totally after 3 years of treatment. In conclusion, a 3-year study of treatment with pamidronate given every 3 months to patients with existing osteoporosis led to a significant increase in lumbar spine BMD and prevented loss at the femoral neck. However, since some of these patients were treated up to 14 months after the transplant, they may already have passed through the phase of most rapid bone loss. In patients who were not osteoporotic at baseline, treatment with calcium and vitamin D alone was not able to prevent the rapid bone loss that occurs immediately after transplantation.

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“…Longitudinal studies have documented rates of bone loss ranging from 2.5% to 11%, predominantly during the first 3-12 months after transplantation (Table 56.4) [49,[156][157][158][159][160][161][162][163]. Bone loss at the hip is equal to or greater than bone loss at the LS [19,160].…”

Section: Bone Loss After Heart Transplantationmentioning

confidence: 99%

Osteoporosis in Organ Transplant Patients

Stein

Shane

2013

Osteoporosis

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As transplantation osteoporosis results from alterations in the bone remodeling system, a review of normal bone remodeling is helpful to understanding the pathogenesis of this disease. The bone remodeling cycle is an orderly progression of events in which old, microdamaged bone is replaced by new, mechanically stronger bone. The complete remodeling cycle at each remodeling site requires approximately 3-6 months. Bone remodeling occurs by two main processes, resorption [1] followed by formation [2], which take place on both cancellous and cortical bone surfaces. Resorption begins with activation of macrophage precursors to form osteoclasts, giant multinucleated cells that excavate a cavity on the bone surface. Osteoclasts express receptors for receptor activator of receptor activator of nuclear factor-kappaB ligand (RANKL), which is produced by osteoblasts and osteocytes, and for calcitonin, prostaglandins (PGs), calcium, and vitronectin (integrin α 1 β 3 ). Approximately 0.05 mm 3 of bone tissue is resorbed by each osteoclast, leaving small resorption pits on the bone surface called Howship's lacunae in a process that takes approximately 2-3 weeks. A brief rest period called the reversal phase follows. Next, local mesenchymal bone marrow stem cells differentiate into osteoblasts that are attracted to the empty resorption pits where they accumulate as clusters of plump cuboidal cells along the bone surface. Osteoblasts produce the collagenous and noncollagenous proteins that constitute the matrix of the newly formed bone and are responsible for mineralization of the matrix or osteoid after a period of maturation that lasts approximately 20 days. Osteoblasts express receptors for several hormones (thyroid and parathyroid hormones, estrogens, vitamin D 3 ), cell adhesion molecules (integrins), and cytokines. RANKL, receptor activator of nuclear factor-kappaB (RANK), and osteoprotegerin (OPG) are three members of the tumor necrosis factor (TNF) ligand and receptor-signaling family that are final mediators of bone resorption [3,4]. RANKL is expressed in osteoblasts, osteocytes, and bone marrow stromal cells. When sufficient concentrations of macrophage colony stimulating factor (M-CSF) are present, RANKL binds to RANK, which is expressed on the surface of osteoclast lineage cells. This binding results in rapid differentiation of osteoclast precursors in bone marrow to mature osteoclasts, increased osteoclast activity, and reduced apoptosis of mature osteoclasts. RANKL is neutralized by binding to OPG, which is secreted by cells of the osteoblast lineage. Competitive binding of RANKL to either RANK or OPG regulates bone remodeling by increasing (RANK) or decreasing (OPG) osteoclastogenesis. Immunosuppressants exert their effects on bone remodeling by interacting with the RANK/RANKL/ OPG system [5].In healthy adults, declines in bone mass as a result of remodeling imbalance occur, but are small. When bone remodeling becomes "uncoupled," such that the rate of resorption exceeds the rate of formation, bone loss will occur...

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Timing and quantification of bone loss in cardiac transplant recipients

Cited by 27 publications

References 17 publications

Effect of Long-Term Calcitonin Administration on Steroid-Induced Osteoporosis after Cardiac Transplantation

Effect of Long-Term Calcitonin Administration on Steroid-Induced Osteoporosis after Cardiac Transplantation

Intravenous Pamidronate as Treatment for Osteoporosis after Heart Transplantation: A Prospective Study

Osteoporosis in Organ Transplant Patients

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