The Experts below are selected from a list of 501 Experts worldwide ranked by ideXlab platform
Jonathan D Adachi - One of the best experts on this subject based on the ideXlab platform.
-
understanding and managing Corticosteroid Induced Osteoporosis
Open Access Rheumatology : Research and Reviews, 2021Co-Authors: Alexandra O Kobza, Alexandra Papaioannou, Deena Herman, Arthur N Lau, Jonathan D AdachiAbstract:Glucocorticoids are effective immunosuppressants used in a wide variety of diseases. Their use results in secondary Osteoporosis in about 30-50% of chronic glucocorticoid users. Glucocorticoids cause a rapid decline in bone strength within the first 3-6 months mostly due to increased bone resorption by osteoclasts. This is followed by a more gradual loss of bone partly due to decreased osteoblastogenesis and osteoblast and osteocyte apoptosis. The loss of bone strength Induced by glucocorticoids is not fully captured by bone mineral density measurements. Other tools such as the trabecular bone score and advanced imaging techniques give insight into bone quality; however, these are not used widely in clinical practice. Glucocorticoid-Induced Osteoporosis should be seen as a widely preventable disease. Currently, only about 15% of chronic glucocorticoid users are receiving optimal care. Glucocorticoids should be prescribed at the lowest dose and shortest duration. All patients should be counselled on lifestyle measures to maintain bone strength including nutrition and weight-bearing exercise. Pharmacological therapy should be considered for all patients at moderate to high risk of fracture as there is evidence for the prevention of bone loss and fractures with a favourable safety profile. Oral bisphosphonates are the current mainstay of therapy, whereas osteoanabolic agents may be considered for those at highest risk of fracture.
-
91 Corticosteroid Induced Osteoporosis a comprehensive review
Principles of Gender-Specific Medicine, 2004Co-Authors: Alexandra Papaioannou, Ann Cranney, Jonathan D AdachiAbstract:It has been accepted that supraphysiologic doses of Corticosteroids cause clinically significant bone loss. Clinically significant bone loss occurs in most men and women exposed to Corticosteroids. Between 30% and 50% of patients taking long-term Corticosteroids experience fractures. With more elderly patients being treated with Corticosteroids for a variety of illnesses, the prevalence of Corticosteroid-Induced Osteoporosis, fractures, and associated morbidity and mortality can only increase unless aggressive intervention is undertaken. If Corticosteroids must be used, then one would hope to be able to prevent fractures by using agents that achieve rapid response and stabilize bone mass. In individuals who are at particular risk for osteoporotic fractures, that risk may be reducedby using the lowest effective Corticosteroid dose and using preventive agents such as the bisphosphonates at the time Corticosteroids are instituted. In those requiting treatment, the bisphosphonates remain the treatment of choice. Vitamin D is a valuable adjunct to the bisphosphonates. Hormone replacement therapy for postmenopausal women and calcitonin are alternatives to bisphosphonate-intolerant persons. Adequate intake of calcium and an exercise program might also be beneficial but it need to be used in conjunction with other therapy.
-
Corticosteroid Induced Osteoporosis a guide to optimum management
Treatments in Endocrinology, 2002Co-Authors: Ann Cranney, Jonathan D AdachiAbstract:Corticosteroid-Induced Osteoporosis is the leading cause of secondary Osteoporosis and a significant cause of morbidity in both men and women. Long-term use of even low-dose Corticosteroids has been associated with increased risk of bone loss. Recent large randomized controlled trials have generated new knowledge on treatment strategies for patients with Corticosteroid-Induced Osteoporosis. However, the majority of individuals receiving Corticosteroids are not receiving prophylaxis for Osteoporosis. Calcium and vitamin D should be recommended to patients initiating therapy with Corticosteroids (and should be adequate for those receiving Corticosteroids for less than 3 months). For those receiving Corticosteroids for greater than 3 months, bisphosphonates are the therapy of choice, with both alendronate (alendronic acid) and risedronate (risedronic acid) approved by the US FDA for use in this indication. Calcitonin can be considered a second-line agent and should be reserved for patients who are intolerant of bisphosphonates or who are experiencing pain from a vertebral fracture. Hormone replacement therapy or testosterone therapy may be offered to those individuals on long-term Corticosteroid treatment who are hypogonadal. Teriparatide (recombinant human parathyroid hormone 1-34) shows promise as a future anabolic agent for the prevention and treatment of patients with Corticosteroid-Induced Osteoporosis.
-
Corticosteroid-Induced Osteoporosis.
International journal of fertility and women's medicine, 2001Co-Authors: Jonathan D AdachiAbstract:Since Harvey Cushing first noted the coexistence of excess cortisol and loss of skeletal mass over 50 years ago, it has been accepted that supraphysiologic doses of Corticosteroids cause clinically significant bone loss. Currently, high-dose oral Corticosteroids are used to treat people with a variety of medical conditions, including: rheumatic diseases, such as rheumatoid arthritis, polymyalgia rheumatica, systemic lupus erythematosus and vasculitis; inflammatory lung diseases, like asthma; gastrointestinal diseases, such as inflammatory bowel disease and chronic liver disease; skin diseases, in particular pemphigus, and more recently those who have undergone transplantation. Clinically significant bone loss occurs in the vast majority of patients exposed to Corticosteroids, and fractures at the spine and hip have been reported with Corticosteroid use. Between 30 and 50 percent of patients taking long-term Corticosteroids will experience fractures. Today, fractures due to Corticosteroid-Induced Osteoporosis may be prevented. A number of well-designed randomized controlled trials have been conducted that demonstrate preservation and, in some instances, actual increases in bone mass with the use of appropriate drug treatment. Some have even demonstrated reductions in fracture risk. As a result, it is extremely important for clinicians to appreciate the very high risk for vertebral fracture, particularly in postmenopausal women on Corticosteroids.
-
Corticosteroid Induced Osteoporosis detection and management
Drug Safety, 2001Co-Authors: Jonathan D Adachi, Alexandra PapaioannouAbstract:Corticosteroid-Induced Osteoporosis is a major cause of morbidity and is the leading secondary cause of Osteoporosis today. Unfortunately, despite this knowledge, patients receiving Corticosteroid therapy are often not offered any preventative treatment. Recent research has focused attention on the critical role the osteoblast has played in the pathophysiology of Corticosteroid-Induced Osteoporosis. In addition to an initial increase in bone resorption, there is evidence that Corticosteroids induce osteoblast and osteocyte apoptosis and as a result are important contributors to bone loss. Interesting work has suggested that the bisphosphonates and calcitonin may help to prevent osteoblast apoptosis from occurring. Large scale randomised controlled trials have also been completed with a variety of therapeutic agents. Of the many different therapies, it is now clear that the bisphosphonates have the greatest evidence to support their use. Increases in bone mineral density when compared with a control group, not only at the spine but also at the hip, have been demonstrated. These studies have shown clinically significant reductions in vertebral fracture rates seen for the most part in postmenopausal women. Other therapies may well be effective, as evidenced by maintenance of bone mass in the spine; however, maintenance of bone mass in the hip and reductions in fracture rate have yet to be demonstrated for many of these therapies. Given our current knowledge and the evidence that is outlined in this review, it is hoped that patients who require therapy with Corticosteroids for more than 3 months will be offered appropriate preventative treatment.
W Bensen - One of the best experts on this subject based on the ideXlab platform.
-
36 month intermittent cyclical etidronate treatment in patients with established Corticosteroid Induced Osteoporosis
The Journal of Rheumatology, 1999Co-Authors: Rolf J Sebaldt, Jonathan D Adachi, W Bensen, Alfred Cividino, George Ioannidis, F Bianchi, M Gordon, E Kaminska, T Scocchia, Annie PetrieAbstract:. Objective. To determine the longterm safety and efficacy of etidronate therapy in patients in whom Corticosteroid Induced bone loss has already occurred. Methods. We performed a 36 month observational cohort study in which all data were obtained from Canadian Database of Osteoporosis and Osteopenia (CANDOO) patients. The etidronate group consisted of 24 patients who received 400 mg of etidronate disodium for 14 days, followed by 76 days of calcium carbonate (500 mg of elemental calcium), repeated every 3 mo; the control group included 37 patients who received calcium carbonate 500 to 1000 mg daily. Outcome measurements included changes within groups from baseline and differences between groups in the bone mineral density (BMD) of the lumbar spine, femoral neck, and trochanter at 12, 24, and 36 months. The incidence of vertebral fractures was also determined. Results. Etidronate therapy resulted in a meaningful percentage increase from baseline in lumbar spine BMD, primarily during the first 24 months of treatment, and this increase was sustained for the remainder of the 36 month study period (5.2%; p = 0.016). Analysis of covariance revealed a significant percentage difference (SD) between groups in lumbar spine BMD at 12 [5.5 (13.5) percent; p = 0.003] and 24 months [6.0 (17.4) percent; p = 0.011] in favor of the etidronate group. After 3 years of therapy, one patient (4%) experienced one vertebral fracture in the etidronate group, whereas 3 patients (8%) experienced 5 vertebral fractures in the control group. Conclusion. Etidronate treatment administered for 36 months reversed lumbar spine bone loss, and appeared to be safe in patients with established Corticosteroid Induced Osteoporosis.
-
Corticosteroid Induced Osteoporosis
Journal of the American Medical Women's Association, 1998Co-Authors: Jonathan D Adachi, W Bensen, Alfred CividinoAbstract:Corticosteroid-Induced Osteoporosis is a serious disorder that results in significant morbidity. A summary of our understanding of the pathophysiology is provided and highlights some of the controversy the exists. Clinical trials for the prevention and treatment of Corticosteroid-Induced Osteoporosis are reviewed.
-
intermittent etidronate therapy to prevent Corticosteroid Induced Osteoporosis
The New England Journal of Medicine, 1997Co-Authors: Jonathan D Adachi, W Bensen, Anthony B Hodsman, Wojciech P Olszynski, David A Hanley, David L Kendler, Jacques P Brown, Robert G Josse, Brian Lentle, Louisgeorge Ste MarieAbstract:Background and Methods Osteoporosis is a recognized complication of Corticosteroid therapy. Whether it can be prevented is not known. We conducted a 12-month, randomized, placebo-controlled study of intermittent etidronate (400 mg per day for 14 days) followed by calcium (500 mg per day for 76 days), given for four cycles, in 141 men and women (age, 19 to 87 years) who had recently begun high-dose Corticosteroid therapy. The primary outcome measure was the difference in the change in the bone density of the lumbar spine between the groups from base line to week 52. Secondary measures included changes in the bone density of the femoral neck, trochanter, and radius and the rate of new vertebral fractures. Results The mean (±SE) bone density of the lumbar spine and trochanter in the etidronate group increased 0.61±0.54 and 1.46±0.67 percent, respectively, as compared with decreases of 3.23±0.60 and 2.74±0.66 percent, respectively, in the placebo group. The mean differences between the groups after one year w...
-
salmon calcitonin nasal spray in the prevention of Corticosteroid Induced Osteoporosis
Rheumatology, 1997Co-Authors: Jonathan D Adachi, W Bensen, Alfred Cividino, Mary J Bell, F Bianchi, G L Craig, W C Sturtridge, Rolf J Sebaldt, M Steele, M GordonAbstract:The objectives were to determine the efficacy and safety of nasal salmon calcitonin 200 IU daily in the prevention of Corticosteroid-Induced Osteoporosis. A minimized, double-blind, placebo-controlled trial was carried out in Corticosteroid-treated patients with polymyalgia rheumatica. The setting was a tertiary care university-affiliated hospital and a total of 31 patients were enrolled. The primary outcome measure was the percentage change in bone mineral density of the lumbar spine in the two treatment groups from baseline to 1 yr of follow-up. The mean +/- S.D. bone mineral density of the lumbar spine in the calcitonin-treated group decreased by 1.29 +/- 6.76% and in the placebo group by 4.95 +/- 3.50% after 12 months. The observed difference of 3.65 +/- 2.10% between groups is statistically significant (P < 0.05). Nasal salmon calcitonin prevented loss of bone in the lumbar spine as measured by dual-energy X-ray absorptiometry.
-
vitamin d and calcium in the prevention of Corticosteroid Induced Osteoporosis a 3 year followup
The Journal of Rheumatology, 1996Co-Authors: Jonathan D Adachi, W Bensen, Alfred Cividino, F Bianchi, Rolf J Sebaldt, M Steele, M Gordon, S Pillersdorf, P Tugwell, Colin E WebberAbstract:Objective. To determine the efficacy and safety of vitamin D 50,000 units/week and calcium 1,000 mg/day in the prevention of Corticosteroid Induced Osteoporosis. Methods. A minimized double blind, placebo controlled trial in Corticosteroid treated subjects in a tertiary care university affiliated hospital. The sample was 62 subjects with polymyalgia rheumatica, temporal arteritis, asthma, vasculitis, or systemic lupus erythematosus. The primary outcome measure was the percentage change in bone mineral density (BMD) of the lumbar spine in the 2 treatment groups from baseline to 36 mo followup. Results. BMD of the lumbar spine in the vitamin D and calcium treated group decreased by a mean (SD) of 2.6% (4.1%) at 12 mo, 3.7% (4.5%) at 24 mo, and 2.2% (5.8%) at 36 mo. In the placebo group there was a decrease of 4.1% (4.1%) at 12 mo, 3.8% (5.6%) at 24 mo, and 1.5% (8.8%) at 36 mo. The observed differences between groups were not statistically significant. The difference at 36 mo was -0.693% (95% CI -5.34, 3.95). Conclusion. Vitamin D and calcium may help prevent the early loss of bone seen in the lumbar spine as measured by densitometry of the lumbar spine. Longterm vitamin D and calcium in those undergoing extended therapy with Corticosteroids does not appear to be beneficial.
H J M Van Rijn - One of the best experts on this subject based on the ideXlab platform.
-
is addition of sodium fluoride to cyclical etidronate beneficial in the treatment of Corticosteroid Induced Osteoporosis
Annals of the Rheumatic Diseases, 1997Co-Authors: W F Lems, J W J Bijlsma, H C M Haanen, H H M L Houben, M I Gerrits, J W G Jacobs, G J M Van Veen, H J M Van RijnAbstract:Objective—To investigate whether administration of sodium fluoride (NaF) in addition to cyclical etidronate has a positive eVect on bone mineral density (BMD) in patients with established Osteoporosis during continued treatment with Corticosteroids. Patients and methods—47 patients who were receiving treatment with Corticosteroids were included in a two year randomised, double blind, placebo controlled trial. Established Osteoporosis was defined as a history of a peripheral fracture or a vertebral deformity, or both, on a radiograph. All patients were treated with cyclical etidronate, calcium, and either NaF (25 twice daily) or placebo. Vitamin D was supplemented in the case of a low serum 25 (OH) vitamin D concentration.BMD of the lumbar spine and hips was measured at baseline and at 6, 12, 18, and 24 months. Results—After two years of treatment, the BMD of the lumbar spine in the etidronate/NaF group had increased by +9.3% (95% confidence intervals (CI): +2.3% to +16.2%, p<0.01), while the BMD in the etidronate/placebo group was unchanged: +0.3% (95% CI: ˛2.2% to +2.8%). The diVerence in the change in BMD between groups was +8.9% (95% CI: +1.9% to +16.0%, p<0.01). For the hips, no significant changes in BMD were observed in the etidronate/NaF group after two years: ˛2.5% (95% CI: ˛6.8% to +1.8%); in the etidronate/placebo group BMD had significantly decreased: ˛4.0% (95% CI: ˛6.6% to ˛1.4%; p<0.01). The diVerence between the groups was not significant: +1.5% (95% CI: ˛3.4% to +6.4%). No significant diVerences in number of vertebral deformities and peripheral fractures were observed between the two groups. Conclusion—The eVect of combination treatment with NaF and etidronate on the BMD of the lumbar spine in Corticosteroid treated patients with established Osteoporosis is superior to that of etidronate alone.
-
effect of sodium fluoride on the prevention of Corticosteroid Induced Osteoporosis
Osteoporosis International, 1997Co-Authors: W F Lems, W G Jacobs, J W J Bijlsma, A Croone, H C M Haanen, H H M L Houben, M I Gerrits, H J M Van RijnAbstract:To investigate whether sodium fluoride (NaF) is able to prevent bone loss in patients treated with Corticosteroids (Cs), we performed a randomized, double-masked, placebo-controlled trial with 44 Cs-treated patients without established Osteoporosis, defined as the absence of previous peripheral fractures and vertebral deformities on radiographs. The effects of NaF (25 mg twice daily) and placebo on the bone mineral density (BMD) of the lumbar spine and hips were compared at baseline and at 6, 12, 18 and 24 months. After 2 years, the BMD of the lumbar spine had decreased in the placebo group by 3.0% (95% CI: −4.9% to −1.0%;p<0.01); in the NaF group there was a statistically insignificant increase in BMD of 2.2% (95% CI: −0.8% to +5.3%). The difference in the changes in BMD between the two groups was +5.2% (95% CI: +1.8% to +8.6%;p<0.01). In the hips, BMD had decreased after 2 years in both groups: in the placebo group by −3.0% (95% CI: −5.0% to −1.0%;p<0.05) and in the NaF group by 3.8% (95% CI: −6.1% to −1.5%;p<0.01). The difference in the changes in BMD between the two groups was not significant: +0.8% (95% CI: −2.1% to +3.8%). Three vertebral deformities were observed in the placebo group and one in the NaF group (insignificant difference), while no peripheral fractures occurred during the study period. It is concluded that in Cs-treated patients without established Osteoporosis NaF prevents bone loss in the lumbar spine but does not have a positive effect on the BMD of the hips.
Frank Buttgereit - One of the best experts on this subject based on the ideXlab platform.
-
calcium vitamin d and etidronate for the prevention and treatment of Corticosteroid Induced Osteoporosis in patients with rheumatic diseases
Clinical and Experimental Rheumatology, 2003Co-Authors: K Loddenkemper, A Grauer, G R Burmester, Frank ButtgereitAbstract:INTRODUCTION Long-term glucocorticoid therapy, a major risk factor for the development of Osteoporosis, is often necessary in chronically ill patients. At present there are no generally accepted guidelines for the prevention or treatment of steroid-Induced Osteoporosis. METHODS In an open prospective study we investigated 99 patients with chronic rheumatic diseases receiving > or = 5 mg/day of prednisolone or the equivalent for at least one year. The objective was to identify Osteoporosis risk factors in addition to glucocorticoid therapy and to evaluate the efficacy of prevention with calcium/vitamin D (group 1--patients with osteopenia) and treatment with cyclical etidronate (group 2--patients with Osteoporosis). Biochemical markers of bone turnover, clinical parameters and bone mineral density (BMD) were measured. RESULTS Increasing age and postmenopausal status were associated with more advanced manifestations of steroid-Induced Osteoporosis (p < 0.05). One year after the start of therapy parameters of bone metabolism increased significantly in group 1, while BMD did not change. In group 2, lumbar spine BMD increased significantly (p < 0.05) whereas femoral neck BMD and bone metabolism parameters remained constant. The intensity of back pain decreased in both groups (p < 0.05). There were fewer new fractures in group 2 than in group 1. CONCLUSION Treatment with etidronate is effective in patients with glucocorticoid-Induced Osteoporosis.
-
ab0173 prevention and treatment of Corticosteroid Induced Osteoporosis in patients with chronic rheumatic diseases
Annals of the Rheumatic Diseases, 2001Co-Authors: K Loddenkemper, Gerdrudiger Burmester, Frank ButtgereitAbstract:Background Long-term glucocorticoid therapy, a major risk factor for the development of Osteoporosis, is often necessary in chronic-rheumatic patients. Generally accepted guidelines for either the prevention of- or the therapy of steroid-Induced Osteoporosis do not exist to date. Objectives In an open prospective study, we examined 99 patients with chronic-rheumatic diseases, who were treated with 5 mg or more equivalent dose of prednisolone/day for at least one year. The study goal was to identify factors which influence the manifestation of Osteoporosis besides glucocorticoid therapy. Additionally, the therapeutic efficacy of a) prevention with either calcium 500 mg/day and vitamin D 1000U/day or b) treatment with intermittent cyclical etidronate (400 mg/day for 14 days followed by 500 mg calcium/day for 76 days) was examined prospectively for one year. Methods Clinical (e.g. rate of fractures, pain intensity), chemical (values of bone mineral metabolism) as well as radiographic parameters (bone mineral density/BMD (DEXA) were measured. Therefore, the patients were divided in two groups: patients with osteopenia (group 1) and patients with Osteoporosis or osteopenia and an increased fracture risk (group 2). Patients in group 1 were given with the above-mentioned “prevention regimen”, and those in group 2, the “treatment regimen”. Results 1. Increasing age was associated with more advanced manifestations of steroid-Induced Osteoporosis (p Conclusion The early treatment with biphosphonates appears effective in long-term glucocorticoid therapy for early Osteoporosis and should be recommended.
Alfred Cividino - One of the best experts on this subject based on the ideXlab platform.
-
36 month intermittent cyclical etidronate treatment in patients with established Corticosteroid Induced Osteoporosis
The Journal of Rheumatology, 1999Co-Authors: Rolf J Sebaldt, Jonathan D Adachi, W Bensen, Alfred Cividino, George Ioannidis, F Bianchi, M Gordon, E Kaminska, T Scocchia, Annie PetrieAbstract:. Objective. To determine the longterm safety and efficacy of etidronate therapy in patients in whom Corticosteroid Induced bone loss has already occurred. Methods. We performed a 36 month observational cohort study in which all data were obtained from Canadian Database of Osteoporosis and Osteopenia (CANDOO) patients. The etidronate group consisted of 24 patients who received 400 mg of etidronate disodium for 14 days, followed by 76 days of calcium carbonate (500 mg of elemental calcium), repeated every 3 mo; the control group included 37 patients who received calcium carbonate 500 to 1000 mg daily. Outcome measurements included changes within groups from baseline and differences between groups in the bone mineral density (BMD) of the lumbar spine, femoral neck, and trochanter at 12, 24, and 36 months. The incidence of vertebral fractures was also determined. Results. Etidronate therapy resulted in a meaningful percentage increase from baseline in lumbar spine BMD, primarily during the first 24 months of treatment, and this increase was sustained for the remainder of the 36 month study period (5.2%; p = 0.016). Analysis of covariance revealed a significant percentage difference (SD) between groups in lumbar spine BMD at 12 [5.5 (13.5) percent; p = 0.003] and 24 months [6.0 (17.4) percent; p = 0.011] in favor of the etidronate group. After 3 years of therapy, one patient (4%) experienced one vertebral fracture in the etidronate group, whereas 3 patients (8%) experienced 5 vertebral fractures in the control group. Conclusion. Etidronate treatment administered for 36 months reversed lumbar spine bone loss, and appeared to be safe in patients with established Corticosteroid Induced Osteoporosis.
-
Corticosteroid Induced Osteoporosis
Journal of the American Medical Women's Association, 1998Co-Authors: Jonathan D Adachi, W Bensen, Alfred CividinoAbstract:Corticosteroid-Induced Osteoporosis is a serious disorder that results in significant morbidity. A summary of our understanding of the pathophysiology is provided and highlights some of the controversy the exists. Clinical trials for the prevention and treatment of Corticosteroid-Induced Osteoporosis are reviewed.
-
salmon calcitonin nasal spray in the prevention of Corticosteroid Induced Osteoporosis
Rheumatology, 1997Co-Authors: Jonathan D Adachi, W Bensen, Alfred Cividino, Mary J Bell, F Bianchi, G L Craig, W C Sturtridge, Rolf J Sebaldt, M Steele, M GordonAbstract:The objectives were to determine the efficacy and safety of nasal salmon calcitonin 200 IU daily in the prevention of Corticosteroid-Induced Osteoporosis. A minimized, double-blind, placebo-controlled trial was carried out in Corticosteroid-treated patients with polymyalgia rheumatica. The setting was a tertiary care university-affiliated hospital and a total of 31 patients were enrolled. The primary outcome measure was the percentage change in bone mineral density of the lumbar spine in the two treatment groups from baseline to 1 yr of follow-up. The mean +/- S.D. bone mineral density of the lumbar spine in the calcitonin-treated group decreased by 1.29 +/- 6.76% and in the placebo group by 4.95 +/- 3.50% after 12 months. The observed difference of 3.65 +/- 2.10% between groups is statistically significant (P < 0.05). Nasal salmon calcitonin prevented loss of bone in the lumbar spine as measured by dual-energy X-ray absorptiometry.
-
vitamin d and calcium in the prevention of Corticosteroid Induced Osteoporosis a 3 year followup
The Journal of Rheumatology, 1996Co-Authors: Jonathan D Adachi, W Bensen, Alfred Cividino, F Bianchi, Rolf J Sebaldt, M Steele, M Gordon, S Pillersdorf, P Tugwell, Colin E WebberAbstract:Objective. To determine the efficacy and safety of vitamin D 50,000 units/week and calcium 1,000 mg/day in the prevention of Corticosteroid Induced Osteoporosis. Methods. A minimized double blind, placebo controlled trial in Corticosteroid treated subjects in a tertiary care university affiliated hospital. The sample was 62 subjects with polymyalgia rheumatica, temporal arteritis, asthma, vasculitis, or systemic lupus erythematosus. The primary outcome measure was the percentage change in bone mineral density (BMD) of the lumbar spine in the 2 treatment groups from baseline to 36 mo followup. Results. BMD of the lumbar spine in the vitamin D and calcium treated group decreased by a mean (SD) of 2.6% (4.1%) at 12 mo, 3.7% (4.5%) at 24 mo, and 2.2% (5.8%) at 36 mo. In the placebo group there was a decrease of 4.1% (4.1%) at 12 mo, 3.8% (5.6%) at 24 mo, and 1.5% (8.8%) at 36 mo. The observed differences between groups were not statistically significant. The difference at 36 mo was -0.693% (95% CI -5.34, 3.95). Conclusion. Vitamin D and calcium may help prevent the early loss of bone seen in the lumbar spine as measured by densitometry of the lumbar spine. Longterm vitamin D and calcium in those undergoing extended therapy with Corticosteroids does not appear to be beneficial.
