Calcitonin for preventing and treating corticosteroid induced osteoporosis [Review]

Rheumatology, Ottawa Civic Hospital, 737 Parkdale Ave, Ottawa.
Cochrane database of systematic reviews (Online) (Impact Factor: 6.03). 02/2000; 2(2):CD001983. DOI: 10.1002/14651858.CD001983
Source: PubMed


Corticosteroid-induced osteoporosis is a cause of morbidity in patients with chronic obstructive lung disease, asthma, and rheumatologic disorders. Corticosteroid treatment causes bone loss by a variety of complex mechanisms. It has been shown that bone mineral loss at the hip averages 14% in the first year after starting corticosteroid therapy.
To review the efficacy of calcitonin (subcutaneous or nasal) for the treatment and prevention of corticosteroid-induced osteoporosis.
We conducted a search of Medline, the Cochrane Controlled Trials Register and Embase using the Cochrane Musculoskeletal Group search strategy for randomized controlled trials (RCTs) up to May 1998. We also searched bibliographic references and consulted content experts.
Two independent reviewers selected RCTs which met predetermined inclusion criteria.
Two reviewers independently extracted data using predetermined forms and assessed methodological quality of randomization, blinding and dropouts. For dichotomous outcomes, relative risks (RR) were calculated. For continuous data, weighted mean differences (WMD) of the percent change from baseline were calculated. We decided a priori to use random effects models for all outcomes, because of uncertainty about whether a consistent true effect exists in such different populations.
Nine trials met the inclusion criteria, including 221 patients randomized to calcitonin and 220 to placebo. The median methodologic quality was two out of a maximum of five points. Calcitonin was more effective than placebo at preserving bone mass at the lumbar spine after six and 12 months of therapy with a WMD of 2.8% (95% CI: 1.4 to 4.3) and 3.2% (95% CI: 0.3 to 6.1). At 24 months, lumbar spine BMD was not statistically different between groups: WMD 4.5% (95% CI: -0.6 to 9.5)]. Bone density at the distal radius was also higher with calcitonin after six months of therapy, but bone density at the femoral neck was not different between placebo and calcitonin treated groups. The relative risk of fractures was not significantly different between calcitonin and placebo with a relative risk (RR) of 0.71 (95% CI: 0.26 to 1.89) for vertebral and 0.52 (95% CI: 0.14 to 1.96) for nonvertebral fractures. The subgroup analyses of methodological quality and duration of corticosteroid therapy were confounded. Trials of patients who had been taking steroids for greater than three months (which were of low methodologic quality) demonstrated a larger effect of calcitonin on spine bone density (about 6%) than prevention trials (about 1%). There was no consistent effect of different dosages (50-100 IU compared to 200-400 IU). However, subcutaneous calcitonin showed substantially greater prevention of bone loss. Withdrawals due to side effects were higher in the calcitonin-treated groups: RR 3.19 (95%CI: 0.66 to 15.47). Important side effects included nausea and facial flushing.
Calcitonin appears to preserve bone mass in the first year of glucocorticoid therapy at the lumbar spine by about 3% compared to placebo, but not at the femoral neck. Our analysis suggests that the protective effect on bone mass may be greater for the treatment of patients who have been taking corticosteroids for more than three months. Efficacy of calcitonin for fracture prevention in steroid-induced osteoporosis remains to be established.

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    • "The improvement seemed to be most prominent when calcitonin was used in patients with established glucocorticoid use, rather than as primary prevention, and when administered subcutaneously. There was no improvement in femoral neck BMD or in the relative risk of vertebral or nonvertebral fractures [Cranney et al. 2000]. Another, more recent, systemic review found similar results with no effect on fracture risk for both vertebral and nonvertebral fractures [Kanis et al. 2007]. "
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    ABSTRACT: Glucocorticoid-induced osteoporosis (GIO) is a serious consequence of glucocorticoid therapy leading to fractures in 30-50% of patients. A wide range of protective medications have been studied in this condition including calcium, vitamin D, vitamin D analogs, oral and intravenous bisphosphonates, sex hormones, anabolic agents and calcitonin. The mechanism of action, and evidence for these therapies, are reviewed - focusing on important trials and new evidence. Recently published guidelines are also reviewed and compared. Bisphosphonates are currently the recommended first-line therapy for the prevention and treatment of GIO. They have been shown to increase bone mineral density (BMD) at the spine and hip and to decrease the incidence of vertebral fractures (especially in postmenopausal women). Testosterone therapy and female hormone replacement therapy (HRT) have been found to increase lumbar spine BMD in hypogonadal patients on glucocorticoid therapy, but effects on hip BMD have not been consistent and there is no fracture data in the GIO population. Similarly, calcitonin increases lumbar spine BMD but has no proven fracture efficacy. The effect of selective estrogen receptor modulators, the oral contraceptive pill and strontium on GIO is relatively unknown. Parathyroid hormone (PTH 1-34) and zoledronic acid have emerged as exciting new options for the treatment of GIO. Both therapies have been found to result in gains in BMD at the spine and hip that are either noninferior or superior to those seen with oral bisphosphonate therapy. PTH 1-34 has also been found to decrease the incidence of new vertebral fractures and may be an option in high-risk patients established on long-term glucocorticoid therapy.
    Therapeutic advances in musculoskeletal disease 04/2009; 1(2):71-85. DOI:10.1177/1759720X09343729
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    • "Richy et al.17 also reported that activated vitamin D (alfacalcidol and calcitriol) maintained lumbar spine BMD, but did not reduce the incidence of vertebral fractures. Cranney et al.18 reported that calcitonin preserved BMD at the lumbar spine with an increase of about 3% compared to the placebo, but did not preserve BMD at the hip, and did not reduce the incidence of vertebral fractures in the first year of corticosteroid therapy. The researchers also suggested that the protective effect of calcitonin on BMD might be greater in patients who have been taking corticosteroids for more than three months. "
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    ABSTRACT: Osteoporosis is one of the most serious complications of corticosteroid treatment. Loss of bone mineral density (BMD) and fractures occur early in the course of corticosteroid treatment, and thus early recognition of fracture risk and effective intervention based on evidence-based-medicine (EBM) are needed. A study of meta-analysis representing the highest level in a hierarchy of evidence showed that when the outcome measure of interest was limited to changes in lumbar spine BMD, bisphosphonates were the most effective of the agents studied in comparison with no therapy or treatment with calcium, and were also more efficacious than either vitamin D or calcitonin; the efficacy of bisphosphonates was enhanced when used in combination with vitamin D. Randomized controlled trials (RCTs) representing the second level in a hierarchy of evidence showed that bisphosphonates stabilized BMD not only in the lumbar spine, but also in the hip, and that parathyroid hormone (PTH) markedly increased lumbar spine BMD. According to the EBM, bisphosphonates and possibly PTH are suggested to be the most efficacious for preserving BMD. The efficacy of these agents in reducing the incidence of vertebral fractures in patients exposed to corticosteroids remains to be established in meta-analysis studies, although some RCTs have demonstrated the anti-fracture effects of etidronate, alendronate, and risedronate in the spine. Further RCTs of fracture prevention conducted on a large number of patients and their meta-analysis are needed to confirm the efficacy of bisphosphonates, PTH, or other agents in preventing vertebral and nonvertebral fractures.
    Yonsei Medical Journal 09/2005; 46(4):456-63. DOI:10.3349/ymj.2005.46.4.456 · 1.29 Impact Factor
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    ABSTRACT: Osteoporosis is a systemic disease characterized by an increased risk of fracture and is usually provoked by an alteration of bone metabolism of multiple pathogenic causes. Exogenous risk factors are important, mainly drugs. The present article reviews several commonly used drugs that can induce osteoporosis. La osteoporosis (OP) es una enfermedad sistémica que se caracteriza por aumento del riesgo de fractura. Generalmente se produce por una alteración del metabolismo óseo de diferentes causas patogénicas. Los factores exógenos son importantes, fundamentalmente los fármacos. A continuación se revisan diferentes fármacos que se utilizan frecuentemente y que pueden inducir OP.
    Seminarios de la Fundación Española de Reumatología 10/2009; DOI:10.1016/j.semreu.2009.09.002
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