Reduced bone mineral density in men after heart transplantation

Anijar, José Ricardo; Szejnfeld, Vera Lúcia; Almeida, Dirceu Rodrigues; Fernandes, Artur da Rocha Corrêa; Ferraz, Marcos Bosi

doi:10.1590/s0100-879x1999000400006

Cited by 13 publications

(7 citation statements)

References 33 publications

(28 reference statements)

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“…The form of osteoporosis post‐cardiac transplant is one that produces much morbidity with fracture risk in cross‐sectional studies varying between 18% and 50% at the spine (78,83–94) . By the time of transplantation, most patients have lost substantial bone density at both the spine and femur.…”

Section: Post‐transplant Bone Diseasementioning

confidence: 99%

“…By the time of transplantation, most patients have lost substantial bone density at both the spine and femur. When applying World Health Organization (WHO) criterion for osteoporosis, 8–10% patients suffer from osteoporosis, and 40–50% have osteopenia (83,84) . Risk factors are similar to the other transplant groups, except for the osteodystrophy in renal transplant patients, and include lifestyle excesses of tobacco and alcohol, loop diuretics, inactivity, hypogonadism, and anorexia.…”

Section: Post‐transplant Bone Diseasementioning

confidence: 99%

“…Cardiac transplantation: The form of osteoporosis postcardiac transplant is one that produces much morbidity with fracture risk in cross-sectional studies varying between 18% and 50% at the spine. (78,(83)(84)(85)(86)(87)(88)(89)(90)(91)(92)(93)(94) By the time of transplantation, most patients have lost substantial bone density at both the spine and femur. When applying World Health Organization (WHO) criterion for osteoporosis, 8 -10% patients suffer from osteoporosis, and 40 -50% have osteopenia.…”

Section: Acute Rapid Severe Bone Lossmentioning

confidence: 99%

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Disorders Associated With Acute Rapid and Severe Bone Loss

Epstein

Inzerillo

Caminis

et al. 2003

Journal of Bone and Mineral Research

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We describe a constellation of bone diseases characterized by the common feature of acute, rapid, and severe bone loss accompanied by dramatic fracture rates. These disorders are poorly recognized, resulting mainly from systemic diseases, frailty, immobilization, and immunosuppressive drugs, such as glucocorticoids and the calcineurin inhibitors. The opportunity to prevent or treat fractures is commonly missed because they are often not detected. Ideally, patients need to be identified early and preventative therapy initiated promptly to avoid the rapid bone loss and fractures. The most effective therapy at present seems to be the bisphosphonates, particularly when bone resorption is predominant. However, more severe forms of bone loss that result from an osteoblastic defect and reduced bone formation may benefit potentially more from newer anabolic agents, such as recombinant human parathyroid hormone (rhPTH).

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Section: Post‐transplant Bone Diseasementioning

confidence: 99%

Section: Post‐transplant Bone Diseasementioning

confidence: 99%

Section: Acute Rapid Severe Bone Lossmentioning

confidence: 99%

See 1 more Smart Citation

Disorders Associated With Acute Rapid and Severe Bone Loss

Epstein

Inzerillo

Caminis

et al. 2003

Journal of Bone and Mineral Research

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“…Hepatic congestion and prerenal azotemia may cause mild secondary hyperparathyroidism and further contribute to abnormal mineral metabolism. Although many patients awaiting cardiac transplantation may have normal bone density, approximately 4-10% fulfill World Health Organization (WHO) criteria for osteoporosis (Table 56.3) [19,76,[139][140][141][142], and one study reported a prevalence of 23% [85].…”

Section: Skeletal Status Before Transplantationmentioning

confidence: 99%

“…In cross-sectional studies, the prevalence of vertebral fractures (Table 56.4) ranges between 18% and 50%. Moderate-to-severe bone loss occurs in a substantial proportion of subjects at both LS and the FN [124,[139][140][141][143][144][145][146][147][148][149][150][151][152][153]. In a cross-sectional study, osteopenia or osteoporosis (T score < −1.0) were found in 26% of long-term cardiac transplant recipients at the LS and 66% at the FN [154].…”

Section: Prevalence Of Osteoporosis In Heart Transplant Recipientsmentioning

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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Transplantation Osteoporosis

Stein¹,

Shane²

2009

Osteoporosis

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In the past two decades, there has been a rapid increase in the number of organ transplanted worldwide, including Brazil, along with an improvement in survival and quality of life of the transplant recipients. Osteoporosis and a high incidence of fragility fractures have emerged as a complication of organ transplantation. Many factors contribute to the pathogenesis of osteoporosis following organ transplantation. In addition, most patients have some form of bone disease prior to transplantation, which is usually related to adverse effects of end-stage organ failure on the skeleton. This chapter reviews the mechanisms of bone loss that occur both in the early and late post-transplant periods, as well as the features specific to bone loss after kidney, lung, liver, cardiac and bone marrow transplantation. Prevention and treatment for osteoporosis should be instituted prior and in the early and late phase after transplantation, and will also be addressed in this article. RESUMOOsteoporose Pós Transplante. Nas últimas décadas houve um grande aumento no número de transplantes realizados no Brasil e no mundo, o que proporcionou uma melhora na sobrevida e qualidade de vida dos pacientes transplantados. A osteoporose e o aumento da prevalência de fraturas por fragilidade óssea têm se mostrado como uma complicação do transplante. Muitos fatores contribuem para a patogênese da osteoporose relacionada ao transplante. Além disso, a maioria dos pacientes apresenta doença óssea antes do transplante, a qual é secundária à doença grave de base. Este artigo revisa os mecanismos da perda óssea que ocorre tanto na fase precoce quanto na fase tardia após o transplante, como também os fatores específicos envolvidos na perda óssea relacionados ao transplante renal, pulmonar, cardíaco, hepático e de medula óssea. A prevenção e o tratamento da osteoporose em todas as fases do transplante também são abordados neste artigo.

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Reduced bone mineral density in men after heart transplantation

Cited by 13 publications

References 33 publications

Disorders Associated With Acute Rapid and Severe Bone Loss

Disorders Associated With Acute Rapid and Severe Bone Loss

Osteoporosis in Organ Transplant Patients

Transplantation Osteoporosis

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