Nasal administration of salmon calcitonin for prevention of glucocorticoid-induced osteoporosis in children with nephrosis

Nishioka, Tadashi; Kurayama, Hideaki; Yasuda, Toshiyuki; Udagawa, Junko; Matsumura, Chieko; Niimi, Hiroo

doi:10.1016/s0022-3476(05)80030-7

Cited by 50 publications

(16 citation statements)

References 14 publications

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“…There is no agreement on the effective dose of calcitonin in osteoporosis. Experiments with cultures of neonatal mouse calvaria and fetal rat long bones (27) and other evidence (49)(50)(51) show that inhibition of bone resorption by calcitonin is transient and, after some time, an escape from inhibition can be observed. This transient remodelling asynchrony may produce an initial increase in bone mass.…”

Section: Discussionmentioning

confidence: 99%

Effect of medication on biomechanical properties of rabbit bones: Heparin induced osteoporosis

et al. 1997

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The aim of this controlled study is to investigate the effect of heparin on osteoporosis initiation and of calcitonin and tamoxifen on the progress of osteoporosis induced by heparin through biomechanical means and, thus, to assist in clinical usage of these drugs. 32 four-month-old female New Zealand white rabbits were divided into four different experimental groups. The animals in group A were administered heparin (Liquemine) intraperitoneally at the dosage of 1000 IU/kg/day. The animals in group B were injected the same amount of heparin as those of group A, and in addition, were given calcitonin at the dosage of 100 IU/kg/day. The animals in group C were medicated the same way as group B but 2 mg/kg/day tamoxifen (Nolvadex) was orally added into their intestine via cannula, one side connected to the injector. The animals in group D were the control. The experiment lasted 8 weeks. The animals in all experimental groups showed the same growth pattern as that of the control group. Whole-bone femur, humerus and tibia specimens were subjected to 3-point bending tests while sections from the proximal ends of the same specimens were subjected to compression tests. The data, recorded as load vs deflection, were converted into stress vs strain using the strength of materials formulae. The data obtained from the bending and the compression experiments were treated separately. The stiffness of the bones of the medicated groups were compared with those of the control groups. Our data indicated that the tamoxifen treated humera, femora and tibiae attained the largest bending stiffness in all cases investigated. However, this was not the case for compression. None of the drug administered groups attained the stiffness of the control group except for the case of tamoxifen treated femora which attained stiffness close to that of the controls. The results show that heparin altered the mechanical properties of bones indicating osteoporosis, tamoxifen was effective in reducing the effect of heparin while calcitonin yielded no conclusive result.

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Section: Discussionmentioning

confidence: 99%

Effect of medication on biomechanical properties of rabbit bones: Heparin induced osteoporosis

et al. 1997

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“…Unlike in adults, medical intervention for GC-induced osteoporosis in children remains virtually unchartered in the literature to date, with studies of calcitonin [77], alendronate [78], pamidronate [79,80,81], and growth hormone [82] restricted to small numbers of patients, observational studies, and case-control trials. The greatest experience with osteoporosis treatment in children comes from the use of intravenous, cyclical pamidronate in children with osteogenesis imperfecta (OI, a congenital bone fragility condition).…”

Section: Approach To Diagnosis and Treatmentmentioning

confidence: 99%

Osteoporosis due to Glucocorticoid Use in Children with Chronic Illness

Ward

2005

Horm Res Paediatr

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Osteoporosis is increasingly recognized as a complication of chronic childhood illnesses, particularly when glucocorticoids (GCs) are necessary for treatment. Elucidation of the mechanisms leading to bone fragility in these settings requires disentanglement of the relative contributions of myriad risk factors, including disease activity, muscle weakness, immobilization, delayed growth and puberty, compromised nutrition, and osteotoxic medications. Over the years, bone mass and density evaluations by dual energy X-ray absorptiometry (DXA) have become popular for assessing bone health in children; however, such measurements are difficult to interpret because of the confounding effect of bone size and the lack of DXA-based densitometric criteria for defining osteoporosis in childhood. Recently, a new diagnostic approach for evaluation of densitometric data in children has been suggested, driven by Frost’s mechanostat theory. A diagnostic algorithm based on the mechanostat theory of bone-muscle development is proposed for the characterization of bone disease in children with chronic illness. In addition to DXA-based assessments, techniques such as peripheral quantitative computerized tomography and ilial histomorphometry, for which there are pediatric reference data, are gaining ground in the characterization of skeletal changes due to chronic illness. Although these diagnostic techniques expand our understanding of osteoporosis in children, they do not replace clinical assessment. Concrete clinical evidence for GC-induced bone fragility can be seen in spinal changes due to vertebral compression, with spinal morphometry emerging as an essential, but frequently overlooked, tool in the evaluation of children’s bone health. Presently, osteoporosis treatment in the chronic illness setting remains experimental and should be restricted to clinical studies. Following an understanding of the natural history of GC-induced osteoporosis in children, randomized, placebo-controlled prevention and intervention trials will be the next step toward the development of clinical practice guidelines.

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“…This seems particularly pertinent to corticosteroid-dependent NS, since a proportion of these patients may eventually develop renal insufficiency and ESRD [19,30], with consequent renal osteodystrophy [20], and eventually may require renal transplantation with further exposure to corticosteroid therapy and risk of fractures [51]. Reports on the use of growth hormone [52], bone-sparing corticosteroids like deflazacort [53], calcitonin, and vitamin D [54], and more recently bisphosphonates [55] are encouraging. However, long-term longitudinal studies evaluating peak bone mass and possibly bone histomorphometry in patients with prolonged NS are needed.…”

Section: Discussionmentioning

confidence: 99%

Bone histology in steroid-treated children with non-azotemic nephrotic syndrome

Freundlich

Jofe

Goodman

et al. 2004

Pediatric Nephrology

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Patients with nephrotic syndrome (NS) and normal glomerular filtration rate (GFR) frequently exhibit abnormalities of calcium and vitamin D homeostasis, mainly hypocalcemia and reduced circulating vitamin D metabolites. These abnormalities have been linked to alterations of bone histology in adults with non-azotemic NS, particularly osteomalacia and excessive bone resorption. Whether similar abnormalities of bone histology occur in children and adolescents with NS, particularly in those requiring prolonged treatment with corticosteroids, remains largely unknown. Thus, bone histomorphometry and selected bone-modulating hormones were studied in eight children (aged 2-16 years) with normal GFR (range 85-169 ml/min per 1.73 m(2)) and NS. All patients received corticosteroids for at least 12 months prior to bone biopsy. At the time of bone biopsy, the urine protein/creatinine ratio was elevated (2.1+/-3.6), while the average concentrations of parathyroid hormone (36+/-13 pg/ml), 25-hydroxyvitamin D [25(OH) D] (22+/-14 ng/ml), and 1,25(OH)(2)D (59+/-22 pg/ml) were normal. Bone histomorphometry displayed focal osteomalacia (OM) and mild increased bone resorption in most patients. The mineralization lag time, an indicator of the degree of osteomalacia, correlated with the time elapsed since the original diagnosis of NS ( r=0.93, P<0.0005). Overt hyperparathyroidism was not evident, but increased eroded perimeter and elevated bone formation rate (BFR) were evident in two patients, suggesting high-turnover bone disease. The BFR was inversely correlated with the administered dose of prednisone at the time of biopsy ( r=-0.78, P<0.05) and one patient exhibited low bone turnover changes. The growth velocity standard deviation score (SDS) at time of biopsy ranged from -1.6 to 3.2, resulting in a height SDS range of -1.9 to 0.6. The height SDS at time of bone biopsy correlated inversely with the dose of administered glucocorticoid ( r=-0.71, P<0.05) and with the duration of the disease ( r=-0.7, P=0.05). These data, albeit preliminary, demonstrate that children with NS treated with prolonged corticosteroid therapy exhibit bone histopathological changes without a concomitant impairment in GFR. While the OM appears to be related to the disease process, the alterations of bone formation and the adynamic changes are likely the result of the corticosteroid therapy. The potential consequences of these findings on adult bone mass and ultimate height deserve further studies.

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Nasal administration of salmon calcitonin for prevention of glucocorticoid-induced osteoporosis in children with nephrosis

Cited by 50 publications

References 14 publications

Effect of medication on biomechanical properties of rabbit bones: Heparin induced osteoporosis

Effect of medication on biomechanical properties of rabbit bones: Heparin induced osteoporosis

Osteoporosis due to Glucocorticoid Use in Children with Chronic Illness

Bone histology in steroid-treated children with non-azotemic nephrotic syndrome

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