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

Kapetanakis, Emmanouil I.; Antonopoulos, Athanassios; Antoniou, Theofani; Theodoraki, Kassiani; Zarkalis, D.; Sfirakis, Peter D.; Chilidou, Despina A.; Alivizatos, Peter A.

doi:10.1016/j.healun.2004.02.016

Cited by 18 publications

(4 citation statements)

References 34 publications

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“…This partial recovery of BMD has been reported previously for patients treated with pamidronate, alendronate, clodronate, etidronate, calcitonin, calcitriol, and calcidiol. [6][7][8][9][10][11] In our study, alendronate therapy was associated with lower bone loss at femoral sites and even with a relative increase in lumbar BMD in comparison with the rest of the studied groups.…”

Section: Discussionsupporting

confidence: 49%

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Bone Loss after Heart Transplant: Effect of Alendronate, Etidronate, Calcitonin, and Calcium plus Vitamin D3

et al. 2012

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Section: Discussionsupporting

confidence: 49%

“…The first one is the small number of patients, similar to other studies. [6][7][8][9]12,26 Second, antiresorptive therapy was not blinded, neither was there a control group. Third, transient hypogonadism is often seen after heart transplant.…”

Section: Discussionmentioning

confidence: 99%

Bone Loss after Heart Transplant: Effect of Alendronate, Etidronate, Calcitonin, and Calcium plus Vitamin D3

et al. 2012

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“…A trial of 23 patients were randomized to calcitonin or no therapy, all patients received calcium and vitamin D supplementation. Follow-up occurred over 7 years with annual BMD scan and there was a statistically significant difference with higher BMD in the calcitonin group seen as early as 1-year [53]. In another trial of 18 patients randomized to calcitonin or calcitonin plus exercise immediately post-transplant there was a marginal increase in BMD at 8-months, although this was within the error limits for the DEXA scan used [54].…”

Section: Osteoporosismentioning

confidence: 89%

Non-Immunosuppressant Medication Use in Heart Transplant Patients: A Guide for Pharmacists

Egan¹,

Pearson²

2014

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For heart transplant patients, there are a number of non-immunosuppressant medications that are routinely prescribed to mitigate the side-effects of immunosuppression, treat the related complications, and improve long-term survival. This review focuses on the medications used to prevent and manage cardiac allograft vasculopathy (CAV), hypertension, dyslipidemia and osteoporosis. The rationale and evidence supporting their use are summarized and the immunosuppressant drugs are only discussed briefly, as they relate to each of these medical issues. Pharmacy practitioners are likely to encounter patients post-cardiac transplant in a variety of clinical settings; therefore, a concise appreciation of the principles for the long-term medical management of these patients is important when providing collaborative care.

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“…While both injectable and inhaled calcitonin have been used successfully to treat GC-induced bone loss in humans [249], calcitonin is not consistently useful in preventing bone loss and fractures after transplantation. Most studies have not found a benefit [204,250,251], although one retrospective study found that patients who received intranasal calcitonin after cardiac transplant had less LS bone loss during the first 3 years than those who had not [252].…”

Section: Calcitoninmentioning

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

Cited by 18 publications

References 34 publications

Bone Loss after Heart Transplant: Effect of Alendronate, Etidronate, Calcitonin, and Calcium plus Vitamin D3

Bone Loss after Heart Transplant: Effect of Alendronate, Etidronate, Calcitonin, and Calcium plus Vitamin D3

Non-Immunosuppressant Medication Use in Heart Transplant Patients: A Guide for Pharmacists

Osteoporosis in Organ Transplant Patients

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