steroid induced bone loss

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Steroid induced bone loss

Fracture risk increases as the daily doses of steroids increase. Almost one in three postmenopausal women who routinely take steroids will have a spine fracture. A person on steroids is more than twice as likely to have a spine fracture compared to a person not taking steroids.

Your health care provider determines when you should stop taking your steroids. Once the medication is stopped, it is expected that your fracture risk will lessen. Don't change the way you take your medication until you speak to your health care provider. Are there medications to protect bone during steroid therapy?

The U. Food and Drug Administration FDA approves medications to prevent bone loss and reduce the risk of fractures related to osteoporosis for those who regularly take steroid medications and for long periods of time. Talk to your health care provider to find which medication is appropriate for you. Prevention and treatment also include: Eat a varied, nutrient-rich diet that includes plenty of fruits and vegetables. Choose foods to get the calcium you need and talk to your health care provider about adding a supplement only if necessary.

Get the recommended amount of vitamin D. This often requires taking a supplement. Be physically active every day. These activities are good for you: walking, recreational sports, and dancing. Do not smoke. Quit if you do. Limit drinking alcohol. Improve your strength and balance to prevent falls. Make your home safe from falls. Remove scatter rugs and use grip bars in the shower.

Revised: June Your browser does not support iFrames. Limited data have shown positive results with thiazide diuretics, estrogen, progesterone and nandrolone. When treating patients with corticosteroids, the lowest effective dose should be used, with topical corticosteroids used whenever possible. Auranofin may be considered in patients with corticosteroid-dependent asthma.

It is important to detect and treat hypogonadism in men, if present, and to replace gonadal hormones in postmenopausal women or amenorrhoeic premenopausal women, and to detect and correct cholecalciferol deficiency. High-risk patients and those with established osteoporosis should be treated with bisphosphonates cyclical etidronic acid or intravenous pamidronic acid , nasal calcitonin, or calcifediol or calcitriol. Patients receiving cholecalciferol preparations should be carefully monitored for hypercalciuria and hypecalcaemia.

Abstract Osteoporosis is one of the most serious adverse effects experienced by patients receiving long term corticosteroid therapy. Publication types Review.


In addition to vitamin D 3 , randomised controlled trials DXA dual energy X-ray absorptiometry demonstrated that the hydroxylated derivatives of vitamin D 3 , for example hydroxyvitamin D 3 calcidiol , 1-hydroxyvitamin D 3 alfacalcidol or 1,dihydroxyvitamin D 3 calcitriol administered together with calcium, were superior to calcium alone in reducing bone loss after corticosteroid therapy Table 1.

The risk of hypercalciuria or hypercalcaemia is higher with the hydroxylated vitamin D 3 metabolites than with plain vitamin D 3 , especially when combined with calcium, and this must be monitored. Apart from calcitriol, vitamin D metabolites are not routinely available to Australian prescribers. Studies comparing the vitamin D metabolites in corticosteroid users have not been reported.

Although the effects of corticosteroids on bone formation predominate, antiresorptive drugs appear to reduce fracture risk both by reducing their effects on osteoclast-mediated bone remodelling and preventing the negative effects of corticosteroids on osteoblast and osteocyte viability. The active metabolites of vitamin D3, such as calcitriol 0. Bisphosphonates, such as alendronate and risedronate, also prevent bone loss in these patients and in those already taking chronic therapy.

A meta-analysis attempted to rank various antiresorptive drugs according to their effect on bone mineral density. It found that bisphosphonates had greater efficacy than no therapy or calcium 4. While bisphosphonates are currently the most effective therapies for the management of corticosteroid-induced osteoporosis, few studies have measured fracture outcomes. Further, no study has examined symptomatic vertebral fractures or back pain as a primary end point.

The intravenous bisphosphonates pamidronate and zoledronic acid are often used in patients who are intolerant of oral bisphosphonates. Zoledronic acid is effective in reducing vertebral and hip fractures in postmenopausal osteoporosis, and randomised studies in corticosteroid users are under way. Intermittent injections of parathyroid hormone have a bone anabolic effect.

A randomised clinical trial showed that recombinant human parathyroid hormone injections could override corticosteroid-induced suppression of bone formation and increase bone mass. Postmenopausal women taking oral corticosteroids have the highest risk of bone loss and vertebral fracture so prophylaxis should be considered.

In men and premenopausal women, the decision to intervene is less clear and depends on factors such as the baseline bone mineral density and the anticipated duration and dose of corticosteroid therapy Fig. Oral bisphosphonates, such as alendronate and risedronate, are the drugs of choice for primary prevention of corticosteroid-related osteoporosis. Patients who are intolerant of oral bisphosphonates may be offered calcitriol, or intravenous pamidronate or zoledronic acid.

Although many patients will not qualify for therapy under the Pharmaceutical Benefits Scheme, they should be offered treatment if considered to be at higher risk of fractures. While calcium alone is ineffective in preventing osteoporosis in patients starting high-dose corticosteroids, all patients should receive calcium and those on bisphosphonates should take vitamin D.

Although most clinical trial data are limited to years, it is rational to maintain fracture prophylaxis for as long as corticosteroids are taken at a daily dose of more than 5 mg prednisolone or equivalent. White's lament for the lack of therapy is no longer true.

Patrick White: Letters. Sydney: Random House; ]. Reasonable care is taken to provide accurate information at the time of creation. This information is not intended as a substitute for medical advice and should not be exclusively relied on to manage or diagnose a medical condition.

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This is my first visit. Often e. Occasionally e. Rarely e. Romas E. Corticosteroid-induced osteoporosis and fractures. Aust Prescr ; Article Authors. Subscribe to Australian Prescriber. Summary Corticosteroids can cause fractures by reducing bone formation and the viability of osteoblasts and osteocytes. Introduction 'All they had to offer were calcium and bed rest Mechanisms Bone loss is usually higher at skeletal sites rich in trabecular bone, particularly the vertebral bodies, ribs and distal radius, but it also occurs in cortical bone in the upper femur.

Effects of dosage and timing Short-term studies show that daily doses of prednisolone as low as 5 mg cause markers of bone formation for example osteocalcin to fall rapidly. Risk assessment Each patient's risk factors should be carefully appraised before prescribing corticosteroids Fig. Management The importance of reducing or stopping corticosteroids, whenever possible, cannot be over emphasised.

Calcium and vitamin D Calcium alone is insufficient to prevent rapid bone loss in patients starting corticosteroids. Anabolic drugs Intermittent injections of parathyroid hormone have a bone anabolic effect. Recommendations Postmenopausal women taking oral corticosteroids have the highest risk of bone loss and vertebral fracture so prophylaxis should be considered.

A meta-analysis of prior corticosteroid use and fracture risk. J Bone Miner Res ; Use of oral corticosteroids and risk of fractures. The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis. Osteoporos Int ; Comparison of trabecular bone micro architecture and remodeling in glucocorticoid-induced and postmenopausal osteoporosis.

A simple score for estimating the long-term risk of fracture in patients using oral glucocorticoids. QJM ; Calcium and vitamin D for corticosteroid-induced osteoporosis. Cochrane Database of Systematic Reviews , Issue 1. DOI: Alendronate or alfacalcidol in glucocorticoid-induced osteoporosis. N Engl J Med ; Alendronate versus calcitriol for the prevention of bone loss after cardiac transplantation.

The comparative efficacy of drug therapies used for the management of corticosteroid-induced osteoporosis: a meta-regression. The test is quick and painless. It is similar to an X-ray, but uses much less radiation. Even so, pregnant women should not have this test, to avoid any risk of harming the fetus. This information results in a measure called a T-score. The scoring is as follows:. The risk of fracture most often is lower in people with osteopenia than those with OP.

But, if bone loss continues, the risk of fracture increases. Yet, people taking glucocorticoids seem to be at an increased risk of fracture at higher bone densities than would be expected. As doctors who are experts in diagnosing and treating diseases of the joints, muscles and bones, rheumatologists can help find the cause of osteoporosis.

They can provide and monitor the best treatments for this condition. Anyone taking glucocorticoid medicine must get enough calcium and vitamin D. The American College of Rheumatology recommends you should take at least 1, mg of calcium and to 1, International Units called IU of vitamin D supplements each day. Your doctor may measure the vitamin D level in your blood to find out if you need more vitamin D supplementation.

Some people also will need medication. The decision to start prescription medications will depend on your other risk factors, the dose of glucocorticoid medication you are taking and how long you may be on it, as well as your BMD results by DXA. In a drug class called bisphosphonates, alendronate Fosamax , risedronate Actonel , and zoledronic acid Reclast are FDA approved for both the prevention and treatment of glucocorticoid-induced osteoporosis. Teriparatide Forteo , a different type of drug, also is approved for treatment of glucocorticoid-induced osteoporosis.

This manmade form of parathyroid hormone helps stimulate bone formation. Women planning a pregnancy should talk to their doctor about the pros and cons of using a bisphosphonate or teriparatide. None of the prescription drugs for managing osteoporosis has enough safety data available to recommend using them in women who are pregnant or breastfeeding.

If you take glucocorticoid medicine for any length of time, you should start taking calcium and vitamin D supplements at the doses recommended in the prior section. Work with your doctor to help use the smallest dose of glucocorticoid for the shortest duration possible that will still keep your disease under control. If you have low bone density and a high risk of breaking a bone, your doctor may suggest medicine to prevent your bones from getting weaker. Health care providers now have a tool for estimating the risk of a patient having an osteoporotic fracture in the next ten years.

It can help guide treatment decisions. The most serious health consequence of any type of osteoporosis is a fracture. Spine and hip fractures especially may lead to chronic pain, long-term disability and even death. The main goal of treating glucocorticoid-induced osteoporosis is to prevent fractures. This information is provided for general education only.

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Your health care provider will help you decide whether you need an osteoporosis medication. The decision will depend upon results of your BMD test and personal risk factor assessment. It is often recommended that you get a BMD test before taking steroids for longer than three months. Navigation menu. Steroids - corticosteroids, prednisone and cortisone -- are usually taken by the mouth or through an inhaler. Steroids are used to treat many conditions, such as: asthma, rheumatoid arthritis, lupus, inflammatory bowel diseases, and multiple sclerosis.

Follow your health care provider's recommendations on steroid use because they can harm your bones. What effects do steroids have on bone? Steroids have major effects on how the body uses calcium and vitamin D to build bones. Steroids can lead to bone loss, osteoporosis, and broken bones. When steroid medications are used in high doses, bone loss can happen rapidly. Not all people who take steroid medications lose bone or lose bone at the same rate. The dose, the underlying diseases, and possibly genes all play a part.

For example, postmenopausal women who take steroids for longer than six months have the greatest risk of bone loss. How quickly can bone loss occur when taking a steroids? Bone loss occurs most rapidly in the first 6 months after starting oral steroids. After 12 months of chronic steroid use, there is a slower loss of bone. Inhaled steroids are less likely to cause bone loss than steroids taken by mouth.

However, in higher doses, inhaled steroids may also cause bone loss. Steroids used for only a few days or applied to the skin are not associated with bone loss. The major impact of steroids on bone is fractures broken bones that occur commonly in the spine and ribs. How does taking steroids impact the risk for a fracture broken bones?

Steroid doses taken by mouth equal to or more than 5mg of prednisone daily taken for more than 3 months are considered a risk for fracture. Fracture risk increases as the daily doses of steroids increase. Corticosteroid-induced bone loss in men. The Journal of clinical endocrinology and metabolism. Glucocorticoids suppress bone formation via the osteoclast. The Journal of clinical investigation. Sclerostin-antibody treatment of glucocorticoid-induced osteoporosis maintained bone mass and strength.

Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA. Lems WF. Glucocorticoids: bad or safe for the bones? RMD open. Uncertainties in the prevention and treatment of glucocorticoid-induced osteoporosis. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. Glucocorticoids and osteocyte autophagy.

Bone density threshold and other predictors of vertebral fracture in patients receiving oral glucocorticoid therapy. Oral corticosteroids and fracture risk: relationship to daily and cumulative doses. Rheumatology Oxford, England. Rizzoli R, Biver E. Glucocorticoid-induced osteoporosis: who to treat with what agent? Nature reviews Rheumatology.

Suppression of autophagy in osteocytes does not modify the adverse effects of glucocorticoids on cortical bone. Comparative effects of teriparatide and risedronate in glucocorticoid-induced osteoporosis in men: month results of the EuroGIOPs trial. Calcitonin for the treatment and prevention of corticosteroid-induced osteoporosis. Cochrane Database Syst Rev.

Bachrach BE. Bare-Bones Fact - Children are not small adults. Glucocorticoids: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy. The cumulative incidence of and risk factors for latent beaking in patients with autoimmune diseases taking long-term glucocorticoids and bisphosphonates.

Prevention of glucocorticoid induced-apoptosis of osteoblasts and osteocytes by protecting against endoplasmic reticulum ER stress in vitro and in vivo in female mice. Manolagas SC. Steroids and osteoporosis: the quest for mechanisms. J Pediatr.

Lems WF, Saag K. Bisphosphonates and glucocorticoid-induced osteoporosis: cons. Restoration of the coupling process and normalization of bone mass following successful treatment of endogenous Cushing's syndrome: a prospective, long-term study. A meta-analysis of prior corticosteroid use and fracture risk.

American College of Rheumatology recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis. Frenkel B. Glucocorticoid-induced osteoporosis. Advances in experimental medicine and biology. Bisphosphonates for the prevention and treatment of osteoporosis in patients with rheumatic diseases: a systematic review and meta-analysis. PloS one. Bone formation markers in patients with glucocorticoid-induced osteoporosis treated with teriparatide or alendronate.

Weinstein RS. Glucocorticoid-induced osteoporosis and osteonecrosis. Endocrinol Metab Clin North Am. Fracture risk associated with different types of oral corticosteroids and effect of termination of corticosteroids on the risk of fractures. Calcified tissue international. Use of oral corticosteroids and risk of fractures. Oral glucocorticoid use is associated with an increased risk of fracture. Meta-analysis of tumor necrosis factor inhibitors and glucocorticoids on bone density in rheumatoid arthritis and ankylosing spondylitis trials.

Efficacy of alphacalcidol and calcitriol in primary and corticosteroid-induced osteoporosis: a meta-analysis of their effects on bone mineral density and fracture rate. Glucocorticoid-induced osteoporosis: a systematic review and cost-utility analysis. Health technology assessment Winchester, England.