Salmon calcitonin nasal spray in the prevention of corticosteroid- induced osteoporosis

Adachi, Jonathan D.; Bensen, W.; Bell, Mary; Bianchi, F; Cividino, Alfred; Craig, Gary L.; Sturtridge, W. C.; Sebaldt, R. J.; Steele, Marjorie; Gordon, Matt; Themeles, Ellison; Tugwell, Peter; Roberts, Robin S.; Gent, M.J. van

doi:10.1093/rheumatology/36.2.255

Cited by 141 publications

(83 citation statements)

References 12 publications

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“…A 2-year randomized clinical trial demonstrated the effi cacy of combined calcium and vitamin D supplementation in preventing bone loss in patients with rheumatoid arthritis treated with low doses of GCs [202] . These fi ndings were not reproduced in a 3-year follow-up study, where the same combination did not show any benefi t [203] . Randomized clinical trials and meta-analyses have shown that active metabolites of vitamin D ( ␣ -calcidiol and calcitriol) are more effective than vitamin D in maintaining bone density during medium-to-high dose GC treatment [204][205][206] .…”

Section: Therapeutic Optionsmentioning

confidence: 83%

Glucocorticoid-Induced Osteoporosis: From Basic Mechanisms to Clinical Aspects

Alesci

Martino

Ilias

et al. 2005

Neuroimmunomodulation

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Glucocorticoid (GC)-induced osteoporosis (GCOP) is the most common cause of osteoporosis in adults aged 20–45 years as well as the most common cause of iatrogenic osteoporosis. GC excess, either endogenous or exogenous, induces bone loss in 30–50% of cases. Indeed, bone loss leading to fractures is perhaps the most incapacitating, sometimes partially irreversible, complication of GC therapy. Nevertheless, GCOP is often underdiagnosed and left untreated. The following article provides an update on the cellular and molecular mechanisms implicated in the pathophysiology of GC-induced bone loss, as well as some guidelines on diagnostic, preventive and therapeutic strategies for this medical condition, in an effort to promote a better knowledge and greater awareness of GCOP by both the patient and the physician.

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Section: Therapeutic Optionsmentioning

confidence: 83%

Glucocorticoid-Induced Osteoporosis: From Basic Mechanisms to Clinical Aspects

Alesci

Martino

Ilias

et al. 2005

Neuroimmunomodulation

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“…It should be noted, however, that many of the patients in that study were vitamin D deficient. Adachi et al (73) have recently re-examined the effect of calciferol (50 000 U/week) plus calcium (1000 mg/day) in a randomised controlled trial. At the end of 3 years, they found no suggestion of any beneficial effect from the use of this intervention.…”

Section: Vitamin D and Its Metabolitesmentioning

confidence: 99%

Glucocorticoid osteoporosis--mechanisms and management

Reid

1997

European Journal of Endocrinology

252

148

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Glucocorticoids are potent osteopenic agents, producing negative calcium and bone balance via actions at many sites. The most significant adverse effects of glucocorticoid drugs on the skeleton are probably a direct inhibition of matrix synthesis by the osteoblast, reductions in calcium absorption in both the gut and the renal tubule, and the production of hypogonadism, particularly in men. Reductions in bone density of 10-40% result, the loss being more marked in trabecular bone and in patients receiving a high cumulative dose of the steroid. Fractures occur in about 30% of individuals who take these drugs for an average of 5 years. Bone loss is reversible when glucocorticoid treatment is withdrawn. Bone density can also be increased by sex hormone replacement in those with demonstrable deficiency, by bisphosphonates, and possibly by vitamin D metabolites. All patients treated with glucocorticoids for more than 6 months should be considered for bone densitometry and be offered appropriate drug treatment if values are towards the lower end of the young normal range or if there is already evidence of fractures occurring after minimal trauma. With this approach, the significant morbidity associated with steroid osteoporosis might be substantially avoided.

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“…Proposed treatments include bisphosphonates, hormone replacement therapy, vitamin D (cholecalciferol or calciferol) and calcium, calcitriol, calcidiol, alfacalcidol, calcitonin, fluoride, testosterone, and anabolic steroids (Adachi et al 1996, Ringe et al 1999, Eastell et al 2000, Boutsen et al 2001, Å strand & Aspenberg 2002, Crandall 2002, Sambrook 2007). In addition, several alternative therapeutic approaches have been considered in recent years.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of genistein aglycone on the development of osteonecrosis of the femoral head and secondary osteoporosis induced by methylprednisolone in rats

Bitto¹,

Polito²,

Burnett³

et al. 2009

Journal of Endocrinology

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Glucocorticoid (GC)-induced osteoporosis (GIO) is the most important secondary cause of bone loss. Clinical evidence suggests a role for genistein (GEN) aglycone in the prevention of osteoporosis. We investigated whether GEN could prevent GIO as well as the development of osteonecrosis in the femoral head using an experimental rat model. A total of 28 female SpragueDawley rats were used in the study. GIO and osteonecrosis were induced by daily s.c. injections of 30 mg/kg of methylprednisolone (MP; nZ7). Another group of animals (MPCGEN; nZ7) concomitantly received MP (30 mg/kg per s.c.) and GEN aglycone (5 mg/kg per i.p.) for 60 days. Control animals were administered daily with vehicle (VEH) or GEN (5 mg/kg per i.p.) only. At the beginning and end of the treatment, animals were examined for bone mineral density (BMD) and bone mineral content (BMC). After killing, serum was collected to determine bone-alkaline phosphatase (b-ALP), carboxyterminal collagen crosslink (CTX) and osteoprotegerin (OPG) levels. Femurs were removed and tested for breaking strength and bone histology analyzed for structural quality of the femoral neck. GEN aglycone prevented bone loss as measured by BMD and BMC. Moreover, GEN significantly increased the bone formation markers b-ALP and OPG, reduced the bone resorption marker CTX and statistically maintained comparable strength versus the VEH only group. Finally, histological scoring revealed a protective effect of GEN on bone structure statistically comparable with the VEH control animals. Results suggest that the GEN aglycone might be a preventive treatment for GIO and complications of osteonecrosis with long-term GC treatment.

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Salmon calcitonin nasal spray in the prevention of corticosteroid- induced osteoporosis

Cited by 141 publications

References 12 publications

Glucocorticoid-Induced Osteoporosis: From Basic Mechanisms to Clinical Aspects

Glucocorticoid-Induced Osteoporosis: From Basic Mechanisms to Clinical Aspects

Glucocorticoid osteoporosis--mechanisms and management

Protective effect of genistein aglycone on the development of osteonecrosis of the femoral head and secondary osteoporosis induced by methylprednisolone in rats

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