Written by Thomas J. Schnitzer, M.D., Ph.D.

Do most patients receiving glucocorticoids - at either high or low doses - get any preventive treatment for osteoporosis? Are rheumatologists more diligent than other physicians in treating such patients? Two papers examined different cohorts of patients receiving glucocorticoid therapy and came to similar conclusions: physicians in general are not thinking about preventive treatment for their patients on glucocorticoids. [1] [abstract below] [2] [abstract below] Despite extensive data supporting the efficacy of bisphosphonates (alendronate and risedronate) in preventing bone loss and reducing the risk of fractures in such patients, these drugs are used in only 20% to 30% of patients, and this appeared to be independent of dose.

Calcium and vitamin D are prescribed more often, but still are used in no more than half the patients on glucocorticoids. BMD measurements were seldom obtained (<20% of patients in one study and <40% in the other). Recent American College of Rheumatology guidelines [3] [abstract below] support the use of vitamin D and calcium in all patients on chronic glucocorticoid therapy and the addition of a bisphosphonate for those with low BMD (T score < -1).

Rheumatologists were more likely than other physicians to both diagnose and treat patients, but they still failed to treat the majority of at-risk patients. Therefore, this population of patients remains under-served, and physicians need to pay greater attention to bone health in this vulnerable group of patients on glucocorticoids.

AUTHORS: Yood RA, Harrold LR, Fish L, Cernieux J, Emani S, Conboy E, Gurwitz JH.

BACKGROUND: Treatment with glucocorticoids is the leading cause of drug-induced osteoporosis. Currently available guidelines indicate that patients receiving long-term glucocorticoid therapy should receive measures to prevent osteoporosis.

OBJECTIVES: To examine whether patients receiving long-term glucocorticoid therapy in a managed care setting received preventive therapy or prescribed medications for osteoporosis and to identify patient and provider characteristics associated with treatment.

SUBJECTS AND METHODS: A cohort of 224 health plan enrollees 20 years and older who were dispensed at least 1 oral glucocorticoid prescription per quarter during the period October 1997 through September 1998 was identified from administrative data. Medical charts and administrative data were reviewed to determine use of preventive therapy and prescribed medications for osteoporosis.

RESULTS: Of the 224 patients, 62% had at least 1 documented intervention aimed at osteoporosis prevention (counseling about calcium or vitamin D or weight-bearing exercise; prescription for estrogen, calcitonin, or bisphosphonate; or a bone mineral density study). Women were more likely than men to receive intervention (76% vs 44%; prevalence odds ratio, 4.41; 95% confidence interval, 2.17-9.10). Patients receiving a mean daily prednisone dose of 10 mg or more or 5 to less than 10 mg were no more likely to receive intervention than those receiving 5 mg or less prednisone daily. Sixty-two (90%) of 69 patients who were prescribed glucocorticoid therapy by rheumatologists had at least 1 intervention documented compared with 29 (48%) of 60 for internists, 26 (55%) of 47 for pulmonologists, and 22 (46%) of 48 for all other physicians. In a multiple logistic regression model, including patient age, sex, mean daily glucocorticoid dose, and physician specialty, women and patients prescribed glucocorticoids by a rheumatologist were significantly more likely to receive intervention aimed at osteoporosis prevention.

CONCLUSIONS: A substantial proportion of patients receiving long-term glucocorticoid therapy do not receive preventive therapy for osteoporosis. Efforts should be made to reduce barriers to such treatment and increase the proportion of patients given preventive therapy.

[2] TITLE: Variations in glucocorticoid induced osteoporosis prevention in a managed care cohort. AUTHORS: Mudano A, Allison J, Hill J, Rothermel T, Saag K. AUTHOR AFFILIATION: Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Alabama at Birmingham, 625 MEB, 1813 Sixth Ave. South, Birmingham, AL 35213, USA. SOURCE: J Rheumatol 2001 Jun;28(6):1298-305 CITATION IDS: PMID: 11409123

ABSTRACT: OBJECTIVE: To characterize glucocorticoid use and patterns of osteoporosis prevention therapies among a large US national cohort.

METHODS: Health maintenance organization (HMO) members who were receiving chronic glucocorticoid therapy (> 90 day supply) within a 3 year observation period were identified along with their prescribing physicians. Receipt of anti-osteoporotic prescription therapies and bone mass measurement was determined. Multivariable analyses were used to define significant predictors of these preventive interventions.

RESULTS: We identified 2378 HMO members who filled prescriptions for at least a 90 day supply of glucocorticoids, but had not filled a glucocorticoid prescription in the prior 90 days. In women over age 50, use of anti-osteoporotic therapies and bone mass measurement was 41% and 16%, respectively. Glucocorticoid-prescribing physicians were identified for 878 (37%) of these glucocorticoid users, and internal medicine specialists (39%) and rheumatologists (20%) wrote the majority of the prescriptions for glucocorticoids. Women age 50 and over were most likely to receive a prescription anti-osteoporotic preventive therapy (OR 4.0; 95% CI 1.5-10.8). Patients with a rheumatologist prescribing their glucocorticoids were more likely than those of internists to have a bone mass measurement (OR 2.2; 95% CI 1.3-3.6) and receive bisphosphonates (OR 1.9; 95% CI 1.1-3.1), but were not more likely to receive preventive treatment overall.

CONCLUSION: Although better than in several prior studies, we identified low levels of selected preventive care measures for chronic glucocorticoid users in a large population based cohort. Significant demographic and practice pattern variation suggests opportunities for targeted preventive interventions.

[3] TITLE: Recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis: 2001 update. AUTHORS: American College of Rheumatology Ad Hoc Committee on Glucocoritcoid-Induced Osteoporosis. SOURCE: Arthritis Rheum 2001 Jul;44(7):1496-503 CITATION IDS: PMID: 11465699

ABSTRACT: Glucocorticoid-induced bone loss should be prevented, and if present, should be treated (Table 2). Supplementation with calcium and vitamin D at a dosage of 800 IU/day, or an activated form of vitamin D (e.g., alfacalcidiol at 1 microg/day or calcitriol at 0.5 microg/day), should be offered to all patients receiving glucocorticoids, to restore normal calcium balance. This combination has been shown to maintain bone mass in patients receiving long-term low-to-medium-dose glucocorticoid therapy who have normal levels of gonadal hormones. However, while supplementation with calcium and vitamin D alone generally will not prevent bone loss in patients in whom medium-to-high-dose glucocorticoid therapy is being initiated, supplementation with calcium and an activated form of vitamin D will prevent bone loss. There are no data available to support any conclusion about the antifracture efficacy of the combination of calcium supplementation plus an activated form of vitamin D. Antiresorptive agents are effective in the treatment of glucocorticoid-induced bone loss. All of these agents either prevent bone loss or modestly increase lumbar spine bone mass and maintain hip bone mass. While there are no randomized controlled trials of prevention of glucocorticoid-induced bone loss or radiographic vertebral fracture outcomes with HRT or testosterone, patients receiving long-term glucocorticoid therapy who are hypogonadal should be offered HRT. The bisphosphonates are effective for both the prevention and the treatment of glucocorticoid-induced bone loss. Large studies have demonstrated that bisphosphonates also reduce the incidence of radiographic vertebral fractures in postmenopausal women with glucocorticoid-induced osteoporosis. Treatment with a bisphosphonate is recommended to prevent bone loss in all men and postmenopausal women in whom long-term glucocorticoid treatment at > or =5 mg/day is being initiated, as well as in men and postmenopausal women receiving long-term glucocorticoids in whom the BMD T-score at either the lumbar spine or the hip is below normal. While there is little information on the prevention or treatment of bone loss in premenopausal women, these women, too, may lose bone mass if they are being treated with glucocorticoids, so prevention of bone loss with antiresorptive agents should be considered. If bisphosphonate therapy is being considered for a premenopausal woman, she must be counseled regarding use of appropriate contraception. The therapies to prevent or treat glucocorticoid-induced bone loss should be continued as long as the patient is receiving glucocorticoids. Data from large studies of anabolic agents (e.g., PTH) and further studies of combination therapy in patients receiving glucocorticoids are eagerly awaited so additional options will be available for the prevention of this serious complication of glucocorticoid treatment.  

Corticosteroid osteoporosis

Philip Sambrook, Nancy E. Lane
p 401-413, Volume 15, Number 3, July 2001

Abstract

Corticosteroids are widely used and effective agents for the control of many inflammatory diseases, but corticosteroid osteoporosis is a common problem associated with their long term high dose use. Prevention of corticosteroid osteoporosis is preferable to treatment of established corticosteroid bone loss.

Several large double-blind controlled clinical trials in patients with corticosteroid osteoporosis have recently been published that provide new insights into its treatment.

Based upon available evidence, the rank order of choice for prophylaxis would be a bisphosphonate followed by a vitamin D metabolite or an oestrogen type medication. Calcium alone appears to be unable to prevent rapid bone loss in patients starting corticosteroids, especially with prednisolone doses at 10 mg a day or greater.

If an active vitamin D metabolite is used, calcium supplementation should be avoided unless dietary calcium intake is low. Hormone replacement therapy should be considered if hypogonadism is present. Since vertebral fracture is a common and important complication of high dose corticosteroid therapy, these findings suggest that rapid bone loss and hence fractures, can be prevented by prophylactic treatment. Although the follow-up data is limited, it is likely that such therapy needs to be continued beyond 12 months whilst patients continue significant doses of corticosteroid therapy.

Copyright 2001 Harcourt Publishers Ltd