Elsevier

Joint Bone Spine

Volume 78, Issue 1, January 2011, Pages 41-44
Joint Bone Spine

Review
Glucocorticoid-induced myopathy

https://doi.org/10.1016/j.jbspin.2010.02.025Get rights and content

Abstract

Glucocorticoid-induced myopathy, characterized by muscle weakness without pain, fatigue and atrophy, is an adverse effect of glucocorticoid use and is the most common type of drug-induced myopathy. This muscle disturbance has a frequency of 60%, and it has been most often associated with fluorinated glucocorticoid preparations. Glucocorticoids have a direct catabolic effect on muscle, decreasing protein synthesis and increasing the rate of protein catabolism leading to muscle atrophy. In clinical practice, it is important to differentiate myopathy due to glucocorticoid from muscle inflammatory diseases. The treatment is based on reduction or, if possible, on discontinuation of the steroid. Fluorinated glucocorticoids such as dexamethasone should be replaced with nonfluorinated glucocorticoids such as prednisone. Other experimental treatments may be tried such as IGF-I, branched-chain amino acids, creatine, androgens such as testosterone, nandrolone and dehydroepiandrosterone (DHEA), and glutamine.

Introduction

Glucocorticoid-induced myopathy was first described in 1932 by Harvey Cushing, in Cushing's syndrome [1]. The introduction of glucocorticoids as therapeutic agents, in 1950, made clinicians more aware of glucocorticoid-induced myopathy. Glucocorticoid-induced myopathy, characterized by muscle weakness without pain, fatigue and atrophy, is an adverse effect of glucocorticoid use and is the most common type of drug-induced myopathy. Although glucocorticoid-induced myopathy can affect any individual, cancer patients and the elderly are most at risk for this muscle disorder [2]. The reported incidence of glucocorticoid-induced myopathy is 60% [3], and it has been most often associated with fluorinated glucocorticoid preparations [4].

Section snippets

Pathogenesis

Glucocorticoids have a direct catabolic effect on muscle, decreasing protein synthesis and increasing the rate of protein catabolism, thereby leading to muscle atrophy [5], [6]. The catabolic effect of glucocorticoids might result from different mechanisms: inhibition of amino acid transport within the muscle, affecting protein synthesis; inhibition of the stimulatory action of insulin, insulin-like growth factor I (IGF-I) and amino acids (leucine in particular) in the phosphorylation of two

Clinical manifestations

Glucocorticoid-induced myopathy can occur in an acute form or a chronic form, either at the initiation of or during the maintenance phase of glucocorticoid treatment, the dose being increased in the latter phase due to exacerbation of the underlying disease. The acute form of glucocorticoid-induced myopathy most often occurs in the intensive care unit setting. It is clinically characterized by rapidly progressive weakening of the proximal and distal muscle groups. The respiratory muscles can

Myopathy: glucocorticoid presentation and dose

Glucocorticoid-induced myopathy is more frequently associated with the use of fluorinated glucocorticoid preparations, such as dexamethasone, betamethasone and triamcinolone, than with the use of nonfluorinated preparations, such as prednisone and prednisolone. The glucocorticoid dose that can induce glucocorticoid-induced myopathy varies greatly among patients. Some might present with muscle weakness after a low dose of steroids, whereas others might not suffer from such weakness even if they

Laboratory tests and complementary tests

In patients with glucocorticoid-induced myopathy, muscle enzyme levels are habitually normal or slightly high. The levels of aldolase and aminotransferases are usually within the range of normality. In the acute phase, however, the levels of creatine kinase and aldolase might be quite high. In critical patients, serum creatine kinase levels can rise by approximately 50%. Electroneuromyography results are typically normal in the early stages of the disease, whereas a myopathic pattern, with

Chronic glucocorticoid-induced myopathy versus inflammatory myopathy

When inflammatory myopathies (polymyositis and dermatomyositis) are treated with glucocorticoids, it is difficult to distinguish between exacerbation of the underlying disease and a worsening of the condition (additional muscle weakness) attributable to the glucocorticoid. Some of the factors that can aid in the differential diagnosis are shown in Table 1.

Treatment

In patients with glucocorticoid-induced myopathy, the use of glucocorticoids should be discontinued or reduced, except in cases in which the clinical status of the patient contra-indicates such a change. An increase in muscle strength can be observed within 3 to 4 weeks after discontinuation of the glucocorticoid. In the treatment regimen of such patients, fluorinated glucocorticoids such as dexamethasone should be replaced with non fluorinated glucocorticoids such as prednisone, and the lowest

Conflicts of interest

None of the authors has any conflicts of interest to declare.

Acknowledgments

This work was supported by grants from Conselho Nacional de Desenvolvimento Científico e Tecnológico (305691/2006-6 to RMR Pereira) and Federico Foundation to JF Carvalho.

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