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Corticosteroid-induced osteoporosis and fractures - Australian Prescriber
- Prednisone induced osteoporosis
Abstract The first choice for prevention of corticosteroid osteoporosis is a potent oral bisphosphonate—for example, alendronate or risedronate. Statistics from Altmetric. BMD, bone mineral density CS, corticosteroid s HT, hormone therapy PTH, parathyroid hormone bisphosphonates glucocorticoids osteoporosis vitamin D Corticosteroids CS are widely used and effective agents for many inflammatory diseases, but rapid bone loss with subsequent fracture risk is a common problem associated with their long term use.
Calcium and vitamin D Extensive data on the use of calcium have been published, obtained from randomised trials in patients receiving CS where calcium has been used as the control or placebo treatment, indicating that considerable bone loss still occurs.
SUMMARY Several large double blind controlled clinical trials in patients with CS osteoporosis have recently been published which provide new insights into its treatment. Recommendations for the prevention and treatment of glucocorticoid induced osteoporosis, update. Arthritis Rheum ; 44 : — A UK consensus group on management of glucocorticoid induced osteoporosis: an update.
J Intern Med ; : — Guidelines on the prevention and treatment of glucocorticoid induced osteoporosis by the Bone and Tooth Society, National Osteoporosis Society and Royal College of Physicians.
Corticosteroids do not alter the threshold for vertebral fractures. J Bone Miner Res ; 15 : —6. Bone density threshold and other predictors of vertebral fracture in patients receiving oral glucocorticoids therapy. Arthritis Rheum ; 48 : —9. Use of oral glucocorticoids and risk of fractures.
J Bone Miner Res ; 15 : — The comparative efficacy of drug therapies used for the management of corticosteroid induced osteoporosis: a meta regression. J Bone Miner Res ; 17 : — Alendronate for the prevention and treatment of glucocorticoid induced osteoporosis. N Engl J Med ; : —9. Effects of risedronate treatment on bone density and vertebral fracture in patients on corticosteroid therapy.
Calcif Tissue Inter ; 67 : — Vitamin D and calcium in the prevention of corticosteroid-induced osteoporosis: a three year follow up study. J Rheumatol ; 23 : — Calcium and vitamin D3 supplementation prevents bone loss in the spine secondary to low dose corticosteroids in patients with rheumatoid arthritis.
Ann Intern Med ; : —8. Efficacy of alphacalcidol and calcitriol in primary and corticosteroid induced osteoporosis: a meta-analysis of their effects on bone density and fracture rate. Osteoporos Int ; 15 : — Prevention and treatment of glucocorticoid induced osteoporosis: a comparison of calcitriol, vitamin D plus calcium and alendronate plus calcium.
J Bone Miner Res ; 18 : — Testosterone therapy in glucocorticoid-treated men. Arch Int Med ; : —7. Taking a glucocorticoid medication sometimes called corticosteroids for treatment of inflammatory arthritis or other health problems may weaken your bones.
This, in turn, can lead to osteoporosis. The good news is there are ways you can protect your bones while taking glucocorticoid medicine. Glucocorticoid medications have both direct and indirect effects on bone tissue that lead to bone loss. These drugs have a direct negative effect on bone cells, resulting in a reduced rate of forming new bone. Also, they can interfere with the body's handling of calcium and affect levels of sex hormones.
Either of these problems can lead to increased bone loss. Anyone who is taking glucocorticoid medications and has other risk factors for osteoporosis increases their risk of developing glucocorticoid-induced osteoporosis and breaking a bone fracture. You can change some of these risk factors, but not others. You can learn if you have osteoporosis by having a simple test that measures bone mineral density - sometimes called BMD.
BMD - the amount of bone you have in a given area - is measured at different parts of your body. Often the measurements are at your spine and your hip, including a part of the hip called the femoral neck, at the top of the thigh bone femur. 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 Osteoporosis. 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.
NPS MedicineWise disclaims all liability including for negligence for any loss, damage or injury resulting from reliance on or use of this information. Read our full disclaimer. This website uses cookies. Read our privacy policy.
Skip to main content. Log in Log in All fields are required. Log in. Forgot password? 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.
Intermittent treatment with human parathyroid hormone hPTH[] increased trabecular bone volume but not connectivity in osteopenic rats.
Calcium and vitamin D3 supplementation prevents bone loss in the spine secondary to low-dose corticosteroids in patients with rheumatoid arthritis. A randomized, double-blind, placebo-controlled trial. Ann Intern Med ; Efficiency of preventive treatment of glucocorticoid-induced osteoporosis with hydroxyvitamin D3 and calcium in kidney transplant patients.
Transplant Proc ; Prophylactic use of alfacalcidol in corticosteroid-induced osteoporosis. Prevention of corticosteroid osteoporosis. A comparison of calcium, calcitriol, and calcitonin.
❾-50%}Prednisone induced osteoporosis.Corticosteroid-induced osteoporosis and fractures
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 health care provider 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 health care provider 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. Individuals should consult a qualified health care provider for professional medical advice, diagnosis and treatment of a medical or health condition. Do you need help? Glucocorticoid-Induced Osteoporosis Fast Facts Taking a glucocorticoid medication sometimes called corticosteroids for treatment of inflammatory arthritis or other health problems may weaken your bones.
If you take an equivalent doss of prednisone at greater than 2. Daily calcium and vitamin D supplements can help prevent loss of bone mass. Calcium alone is not effective. A rheumatology provider can advise about other treatment options. What Is Glucocorticoid-Induced Osteoporosis? Major risk factors that you cannot change include: Older age children are at risk too Non-Hispanic white or Asian ethnic background Small bone structure Family history of osteoporosis or osteoporosis -related fracture in a parent or sibling Prior fracture due to a low-level injury, particularly after age 50 Risk factors that you may be able to change include: Low levels of sex hormone, mainly estrogen in women e.
Early changes are seen in the lumbar spine. Repeated measurements at year intervals are recommended to monitor bone loss. The T-score can help guide management, but there is no consensus on an appropriate or cost-effective threshold for intervention in patients taking corticosteroids.
T-scores of less than The use of these low intervention thresholds in oral corticosteroid users reflects the fact that fracture rates are considerably higher in corticosteroid users than in non-users. Determining the absolute fracture risk for individual patients is difficult. Scoring systems to ascertain this risk are now emerging, but are not yet in routine use. The importance of reducing or stopping corticosteroids, whenever possible, cannot be over emphasised.
The general practice research database study reported that the excess risk of fracture diminished within one year of stopping therapy and this was most obvious for vertebral fractures.
The risk of hip fracture also fell towards baseline levels after treatment stopped. There are sparse data on the effects of lifestyle interventions in patients using oral corticosteroids.
Patients should be advised not to smoke or abuse alcohol. Although proximal muscle weakness is a complication of oral corticosteroids, the possible effects of physical exercise on muscle mass or fracture rates have not been systematically evaluated.
Calcium alone is insufficient to prevent rapid bone loss in patients starting corticosteroids. However, calcium and vitamin D 3 cholecalciferol may blunt the continuing loss during long-term use of corticosteroids. A Cochrane meta-analysis compared patients taking calcium and vitamin D 3 to patients using calcium alone or placebo.
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. NPS MedicineWise disclaims all liability including for negligence for any loss, damage or injury resulting from reliance on or use of this information.
Read our full disclaimer. This website uses cookies. Read our privacy policy. Skip to main content. Log in Log in All fields are required. Log in. Forgot password? 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.
Taking a glucocorticoid medication sometimes called corticosteroids for treatment of inflammatory arthritis or other health problems may weaken your bones. This, in turn, can lead to osteoporosis. The good news is there are ways you can protect your bones while taking glucocorticoid medicine.
Glucocorticoid medications have both direct and indirect effects on bone tissue that lead to bone loss. These drugs have a direct negative effect on bone cells, resulting in a reduced rate of forming new bone.
Also, they can interfere with the body's handling of calcium and affect levels of sex hormones. Either of these problems can lead to increased bone loss. Anyone who is taking glucocorticoid medications and has other risk factors for osteoporosis increases their risk of developing glucocorticoid-induced osteoporosis and breaking a bone fracture. You can change some of these risk factors, but not others.
You can learn if you have osteoporosis by having a simple test that measures bone mineral density - sometimes called BMD. BMD - the amount of bone you have in a given area - is measured at different parts of your body.
Often the measurements are at your spine and your hip, including a part of the hip called the femoral neck, at the top of the thigh bone femur. 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 Osteoporosis.
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, rheumatology providers 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 Fosamaxrisedronate Actoneland zoledronic acid Reclast are FDA approved for both the prevention and treatment of glucocorticoid-induced osteoporosis.
Teriparatide Forteoa 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 health care provider 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 health care provider 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. Individuals should consult a qualified health care provider for professional medical advice, diagnosis and treatment of a medical or health condition.
Do you need help? Glucocorticoid-Induced Osteoporosis Fast Facts Taking a glucocorticoid medication sometimes called corticosteroids for treatment of inflammatory arthritis or other health problems may weaken your bones.
If you take an equivalent doss of prednisone at greater than 2. Daily calcium and vitamin D supplements can help prevent loss of bone mass. Calcium alone is not effective. A rheumatology provider can advise about other treatment options. What Is Glucocorticoid-Induced Osteoporosis? Major risk factors that you cannot change include: Older age children are at risk too Non-Hispanic white or Asian ethnic background Small bone structure Family history of osteoporosis or osteoporosis -related fracture in a parent or sibling Prior fracture due to a low-level injury, particularly after age 50 Risk factors that you may be able to change include: Low levels of sex hormone, mainly estrogen in women e.
Inflammatory arthritis rheumatoid arthritis, ankylosing spondylitisetc. Patients taking glucocorticoid medicine should: Be physically active and do weight-bearing exercises, like walking, most days each week.
Change lifestyle choices that raise your risk of osteoporosis, such as quitting smoking. Implement strategies to help decrease your risk of falling, which raises the risk of fractures.
Doses as low as mg of prednisone equivalents per day can be a risk factor for fracture, but the risk is clearly greater with higher doses. Many people with joint or muscle pain, breathing or intestinal ailments use corticosteroids (e.g., Prednisone or methylprednisolone). However, long-term use. Glucocorticoid-Induced Osteoporosis (GIO) is a condition in which people who take medicines called glucocorticoids develop osteoporosis. A UK study showed that intermittent use of high-dose glucocorticoids (≥15mg prednisolone) with a cumulative exposure ≤1g may result in a small. Glucocorticoid therapy is associated with an appreciable risk of bone loss, which is most pronounced in the first few months of use. In addition. After treatment stops, the fracture risk rapidly falls towards baseline unless the patient was taking long-term therapy. Statistics from Altmetric. The earliest trial to demonstrate efficacy used oral pamidronate, but studies now exist with all the commonly used bisphosphonates, including etidronate, alendronate, risedronate, and intravenous pamidronate. 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.RIS file. Corticosteroids can cause fractures by reducing bone formation and the viability of osteoblasts and osteocytes. The heightened fracture risk is dose dependent and occurs within months of starting therapy. Daily doses of more than 2. Randomised studies reveal adverse skeletal effects with daily doses as low as 5 mg.
After treatment stops, the fracture risk rapidly falls towards baseline unless the patient was taking long-term therapy. Patients who start corticosteroid therapy should routinely receive calcium and vitamin D supplementation. Those with a higher risk of fracture should also be offered a bisphosphonate. Repeated efforts should be made to reduce the dose of corticosteroids or discontinue long-term therapy if possible.
Fragility fractures are a serious complication of long-term treatment with corticosteroids. The high frequency and rapid onset of corticosteroid-related fractures necessitates prompt identification of at-risk patients. A meta-analysis of more than 42 patients compared outcomes for patients who had taken oral corticosteroids with those who had not.
The relative risk for osteoporotic fracture was 2. For hip fracture the respective relative risks were 4. Overall, the reported fracture risk was similar in men and women, independent of prior fracture, and only partially explained by losses in bone mineral density. In a retrospective study of a general practice database people taking oral corticosteroids were compared with the same number of controls the relative rate was 1.
The fracture risk increased with daily prednisolone doses greater than 2. Importantly, fracture rates decreased rapidly within one year after cessation of oral corticosteroid therapy, indicating reversibility of the risk. 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. The mechanisms of increased bone fragility are not completely understood, but the inhibitory effects of corticosteroids on osteoblasts are likely to be critical.
Corticosteroids inhibit replenishment of osteoblasts, reduce the synthesis of bone collagen and osteocalcin by existing osteoblasts, and promote osteoblast and osteocyte apoptosis. Osteoblast inhibition leads to a reduction in the amount of bone replaced in each remodelling cycle. However, the role of osteoclastic bone resorption in fracture risk is less certain as study results have been inconsistent and markers of bone resorption are often unchanged during short-term corticosteroid treatment.
Corticosteroids reduce intestinal calcium absorption and increase renal calcium excretion. This may contribute to hyperparathyroidism and bone loss. These negative effects on calcium balance can be reversed with oral calcium and vitamin D 3 supplementation, or by treatment with active vitamin D metabolites such as 1,dihydroxyvitamin D 3 calcitriol.
In some patients, corticosteroids also reduce gonadal function, which may further contribute to bone fragility. The role of steroid-induced myopathy on fractures is unknown. The increase over time of both vertebral and non-vertebral fractures without an increase in forearm fractures suggests that the direct effects of corticosteroids on bone strength predominate over any effects on falls.
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. Both the daily dose and treatment duration, and therefore cumulative dose, are considered responsible for the skeletal adverse effects.
However, as fractures often occur rapidly after starting corticosteroids, the effects on fractures are probably more closely related to the daily dose rather than to the duration of therapy or cumulative dose. Bone loss may slow irrespective of whether or not the dose is tapered as the patient's underlying condition improves. The relationship of dose to fracture risk and bone mineral density is different. The daily dose is the single most important determinant of fracture, whereas there is a strong inverse relation between cumulative dose and bone mineral density.
At high doses, trabecular bone connectivity not merely thickness is severely compromised, leading to vertebral fractures. Intermittent oral corticosteroids in men and inhaled corticosteroids increase vertebral fracture risk, but patients taking intermittent corticosteroids are less likely to sustain fractures than those taking continuous therapy.
Taking corticosteroids on alternate days may preserve growth in children, but does not prevent bone loss in children, or in adults.
Pulsed intravenous high dose corticosteroids that is 1 g methylprednisolone are less deleterious to bone mineral density, but increase the risk of osteonecrosis. The rapid reduction in systemic inflammation after pulsed therapy might be protective, as the underlying diseases for which corticosteroids are prescribed for example rheumatoid arthritis, Crohn's disease often contribute to the increased risk of fractures, independently of corticosteroid therapy.
Each patient's risk factors should be carefully appraised before prescribing corticosteroids Fig. Readily identified factors that influence bone loss and fracture risk include the dose, the underlying condition, and factors such as age, female gender, menopausal status and low bone mineral density.
In practice, postmenopausal women are those at highest risk for corticosteroid-induced osteoporosis. The effects of corticosteroids on bone mineral density can be measured precisely and accurately using dual energy X-ray absorptiometry. Early changes are seen in the lumbar spine.
Repeated measurements at year intervals are recommended to monitor bone loss. The T-score can help guide management, but there is no consensus on an appropriate or cost-effective threshold for intervention in patients taking corticosteroids. T-scores of less than The use of these low intervention thresholds in oral corticosteroid users reflects the fact that fracture rates are considerably higher in corticosteroid users than in non-users. Determining the absolute fracture risk for individual patients is difficult.
Scoring systems to ascertain this risk are now emerging, but are not yet in routine use. The importance of reducing or stopping corticosteroids, whenever possible, cannot be over emphasised. The general practice research database study reported that the excess risk of fracture diminished within one year of stopping therapy and this was most obvious for vertebral fractures.
The risk of hip fracture also fell towards baseline levels after treatment stopped. There are sparse data on the effects of lifestyle interventions in patients using oral corticosteroids. Patients should be advised not to smoke or abuse alcohol. Although proximal muscle weakness is a complication of oral corticosteroids, the possible effects of physical exercise on muscle mass or fracture rates have not been systematically evaluated.
Calcium alone is insufficient to prevent rapid bone loss in patients starting corticosteroids. However, calcium and vitamin D 3 cholecalciferol may blunt the continuing loss during long-term use of corticosteroids. A Cochrane meta-analysis compared patients taking calcium and vitamin D 3 to patients using calcium alone or placebo. 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.
NPS MedicineWise disclaims all liability including for negligence for any loss, damage or injury resulting from reliance on or use of this information. Read our full disclaimer. This website uses cookies. Read our privacy policy. Skip to main content. Log in Log in All fields are required. Log in. Forgot password? Romas E. Corticosteroid-induced osteoporosis and fractures. Aust Prescr ; Article Authors.
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