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Determining causation--a case study: adrenocorticosteroids and osteoporosis. Should the fear of inducing clinically important osteoporosis influence the decision to prescribe adrenocorticosteroids?

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TLDR
The available evidence does not substantiate a causal role of exogenous adrenocorticosteroids in producing clinically important osteoporosis, and does not support withholding steroid therapy on the basis of fears of osteop orosis induced pain and disability.
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This article is published in Journal of Chronic Diseases.The article was published on 1984-01-01. It has received 29 citations till now.

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Citations
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The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis.

TL;DR: It is concluded that oral corticosteroid treatment using more than 5 mg (of prednisolone or equivalent) daily leads to a reduction in bone mineral density and a rapid increase in the risk of fracture during the treatment period.
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Guidelines for reading literature reviews.

TL;DR: New guidelines that will help readers assess the scientific quality of the review are proposed and will allow clinicians to spend their valuable reading time on high-quality material and to judge the validity of an author's conclusions.
Journal ArticleDOI

Glucocorticoid-Induced Osteoporosis

TL;DR: The most disabling of these adverse effects is the development of osteopenia, which is more severe in the regions with high trabecular bone content (spine and ribs), and less striking in predominantly cortical bone areas (Hann et al, 1979).
Journal ArticleDOI

Fractures after rheumatoid arthritis. A population-based study

TL;DR: The incidence of osteoporotic fractures in patients who have been diagnosed as having rheumatoid arthritis was found to be increased, though not dramatically so: the relative risk for hip fracture, for example, was 1.5.
References
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Journal ArticleDOI

Steroid-Induced Fractures and Bone Loss in Patients with Asthma

TL;DR: It is concluded that long-term steroid therapy in asthmatic patients is associated with decreased trabecular bone density and an increased prevalence of rib and vertebral fractures.
Journal ArticleDOI

Glucocorticoid-Induced Osteoporosis

TL;DR: The most disabling of these adverse effects is the development of osteopenia, which is more severe in the regions with high trabecular bone content (spine and ribs), and less striking in predominantly cortical bone areas (Hann et al, 1979).
Journal ArticleDOI

Altered mineral metabolism in glucocorticoid-induced osteopenia. Effect of 25-hydroxyvitamin D administration.

TL;DR: It is concluded that treatment with 25-OHD and calcium can significantly improve parameters of mineral and bone metabolism in patients with glucocorticoid-induced osteopenia.
Journal ArticleDOI

Intestinal Calcium Absorption in Exogenous Hypercortisonism: ROLE OF 25-HYDROXYVITAMIN D AND CORTICOSTEROID DOSE

TL;DR: It is suggested that calcium malabsorption in the corticosteroid-treated patients is due to a dose-related abnormality of vitamin D metabolism and not to a direct effect of Corticosteroids on depressing transmucosal intestinal absorption of calcium.
Journal ArticleDOI

Histomorphometric profile, pathophysiology and reversibility of corticosteroid-induced osteoporosis

TL;DR: The results indicate that CS's induce bone rarefaction mainly by decreasing osteoblastic activity at the cell level, however, the bone loss is probably magnified by secondary hyperparathyroidism which increases the birthrate of basic multicellular bone remodelling units.
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