Bone loss after glucocorticoid therapy

Cascio, Vincenzo Lo; Bonucci, E.; Imbimbo, Bruno P.; Ballanti, P.; Tartarotti, D.; Galvanini, G.; Fuccella, L. M.; Adami, Silvano

doi:10.1007/bf02405356

Cited by 91 publications

(27 citation statements)

References 15 publications

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“…More side effects were reported in the placebo group in comparison with the treatment group, but these differences were not statistically significant. Other side effects reported by the placebo group included severe headache (1), facial "fullness" (1), muscle spasms (1), transient body rash (1), arthralgias (1), and lowgrade fevers (1). The treatment group also reported insomnia (1) and bruising (1).…”

Section: Effects Of Low-dose Prednisone On Bone Metabolismmentioning

confidence: 99%

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Effects of Low-Dose Prednisone on Bone Metabolism

Ton

Gunawardene

Lee

et al. 2005

Journal of Bone and Mineral Research

191

106

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Prednisone 5 mg/day suppresses multiple indices of bone formation in a randomized placebocontrolled trial in healthy postmenopausal females. This suggests that even low doses of prednisone may reduce bone repair or renewal and may have adverse effects on bone mass and/or bone strength.Introduction: High doses of chronic glucocorticoids are known to have adverse effects on bone, and measures to prevent bone loss are well established for doses >7.5 mg daily, because these doses can cause premature or exaggerated osteoporosis. However, it is unclear if chronic prednisone doses of 5 mg daily have the same effects on bone. There are no established recommendations for preventing glucocorticoid-induced osteoporosis in people taking prednisone 5 mg daily, a dose used frequently in medical practice to treat diseases of the lungs, joints, skin, muscles, eyes, nerves, etc. Our primary objective was to test whether prednisone 5 mg daily affects serum and urine indices of bone metabolism in healthy postmenopausal women. Our secondary objectives were to determine if prednisone 5 mg affected systolic or diastolic blood pressure or causes side effects. Materials and Methods: A double-blinded randomized placebo-controlled 8-week trial in 50 healthy postmenopausal women was conducted at the Massachusetts General Hospital Outpatient General Clinical Research Center. Patients were randomly assigned to prednisone 5 mg daily or matching placebo for 6 weeks, followed by a 2-week recovery phase. Markers of bone formation and resorption were determined at weeks 0, 2, 4, 6, and 8. Indices of osteoblast activity included serum propeptide of type I N-terminal procollagen (PINP), propeptide of type I C-terminal procollagen (PICP), osteocalcin, and bone-specific alkaline phosphatase (BSALP). Indices of osteoclast activity included urine and serum type I collagen N-telopeptide (NTX) and free urinary deoxypyridinoline (DPD). Results and Conclusions: Prednisone rapidly and significantly decreased serum PINP (p < 0.01), PICP (p < 0.01), and osteocalcin (p < 0.01) and free urinary deoxypyridinoline (p ‫ס‬ 0.017). These changes were largely reversed during the recovery period. Side effects were indistinguishable in the two groups. Neither systolic nor diastolic blood pressure changed significantly throughout the study between the two groups. In conclusion, low-dose prednisone significantly decreases indices of bone formation and may decrease indices of bone resorption in postmenopausal women. Further studies are needed to assess the effects of low-dose prednisone on BMD and fracture risk.

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Section: Effects Of Low-dose Prednisone On Bone Metabolismmentioning

confidence: 99%

“…(1) The loss is most marked in trabecular bone, probably because bone formation and resorption are normally highest there. (2) Pharmacologic doses of glucocorticoids cause bone loss by suppressing bone formation (3) without concomitantly suppressing bone resorption.…”

mentioning

confidence: 99%

Effects of Low-Dose Prednisone on Bone Metabolism

Ton

Gunawardene

Lee

et al. 2005

Journal of Bone and Mineral Research

191

106

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“…Longitudinal studies have shown that bone loss begins after a few weeks of GC treatment, is rapid in the fi rst few months, and reaches 5-15% after 1 year. Afterwards, loss continues at a slower rate, probably because of GC dose attenuation or development of some degree of tolerance [12] .…”

Section: Epidemiologymentioning

confidence: 99%

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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“…Thus studies have demonstrated less marked hypercalciuria (85,86), lesser effects on intestinal calcium absorption (85), reduced bone loss (87)(88)(89)(90) and less growth retardation in children treated with deflazacort (91,92). However, all these studies assumed that the potency of prednisone relative to deflazacort was 1.2.…”

Section: Bone-sparing Glucocorticoidsmentioning

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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Bone loss after glucocorticoid therapy

Cited by 91 publications

References 15 publications

Effects of Low-Dose Prednisone on Bone Metabolism

Effects of Low-Dose Prednisone on Bone Metabolism

Glucocorticoid-Induced Osteoporosis: From Basic Mechanisms to Clinical Aspects

Glucocorticoid osteoporosis--mechanisms and management

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