
Corticosteroids are a class of drugs that are widely used to treat various conditions, including asthma, chronic obstructive pulmonary disease, and autoimmune diseases. While corticosteroids can be effective in managing these conditions, their use has been associated with a range of side effects, including muscle weakness, also known as corticosteroid-induced myopathy or steroid myopathy. This muscle weakness typically affects the proximal muscles of the upper and lower limbs and the neck flexors, leading to difficulty in performing daily activities such as rising from a chair or climbing stairs. The development of corticosteroid-induced myopathy is believed to be related to the duration of corticosteroid treatment, the dosage, and individual sensitivity, with high doses and long-term use increasing the risk. In addition to discontinuing or reducing the dosage of corticosteroids, physical therapy, including resistance and aerobic exercises, has been shown to be beneficial in preventing and treating corticosteroid-induced myopathy.
| Characteristics | Values |
|---|---|
| Cause | Excess endogenous corticosteroid production or excess exogenous corticosteroid use |
| Risk factors | Age, gender, obesity, dose, duration of therapy, individual sensitivity |
| Symptoms | Weakness (especially proximal muscle weakness), CK levels are normal, muscle atrophy |
| Treatment | Reduce or discontinue steroids, switch to non-fluorinated glucocorticoids, physical therapy, adequate protein intake |
| Prognosis | Usually reversible within 3-4 weeks of tapering steroids, recovery may take weeks to months |
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What You'll Learn

Fluorinated corticosteroids
The development of muscle weakness due to fluorinated corticosteroids can occur rapidly, sometimes within days or weeks of starting treatment, and may be more prevalent with higher doses. However, it is important to note that the relationship between dose, duration of therapy, and the development of myopathy is not fully understood. Individual sensitivity plays a significant role, and some patients may experience muscle weakness even with low doses or short-term use.
The mechanism by which fluorinated corticosteroids induce myopathy is not entirely clear. It is believed that these drugs may inhibit protein synthesis, particularly in type II muscle fibers, leading to reduced expression of the insulin-like growth factor-1, which may increase muscle cell apoptosis. Additionally, fluorinated corticosteroids are thought to impair muscle protein and carbohydrate metabolism, contributing to muscle weakness.
Treatment for corticosteroid-induced myopathy aims to reduce the corticosteroid dose as much as possible. In some cases, switching from fluorinated to non-fluorinated glucocorticoids, such as replacing dexamethasone with prednisone or hydrocortisone, may be recommended. Physical therapy, including resistance and aerobic exercises, has been shown to prevent and treat steroid-induced myopathy effectively.
It is worth noting that while fluorinated corticosteroids can cause muscle weakness, they are also used to treat certain muscle conditions. For example, in the case of an autoimmune blistering disease (AIBD), glucocorticoids are used as a treatment, but they can also induce myopathy as a side effect. Therefore, it is crucial to carefully consider the benefits and risks of using fluorinated corticosteroids in each patient's specific context.
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Endogenous corticosteroid production
Corticosteroid-induced myopathy is a common occurrence, with muscle weakness developing in 47.5% of patients with autoimmune blistering disease (AIBD) treated with glucocorticoids. An excess of endogenous corticosteroids is believed to cause this condition. Excess endogenous corticosteroid production can arise from adrenal tumours.
Endogenous corticosteroids, or glucocorticoids, are steroid hormones produced in the zona fasciculata of the adrenal cortex. They are part of the feedback mechanism in the immune system, reducing certain aspects of immune function, such as inflammation. Glucocorticoids are also distinguished from mineralocorticoids and sex steroids by their specific receptors, target cells, and effects. Cortisol (or hydrocortisone) is the most important human glucocorticoid, regulating and supporting important cardiovascular, metabolic, immunologic, and homeostatic functions.
Glucocorticoids are also produced synthetically for therapeutic use. They are used to treat diseases caused by an overactive immune system, such as allergies, asthma, autoimmune diseases, and sepsis. They are also administered as post-transplantory immunosuppressants to prevent acute transplant rejection and graft-versus-host disease. However, they have many side effects, including muscle weakness.
In patients with adrenal insufficiency, evidence suggests that cortisol synthesis is ongoing at very low levels. This is based on the detection of low concentrations of 11-deoxycortisol, a precursor of cortisol. This finding has interesting implications, as low levels of 11-deoxycortisol may impact quality of life and cognition.
Treatment for corticosteroid-induced myopathy typically involves reducing or discontinuing the use of corticosteroids. Physical therapy, including range-of-motion exercises, stretching, and resistance exercises, can also help prevent and treat muscle weakness.
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Muscle atrophy
Corticosteroids can cause muscle atrophy, or myopathy, through a variety of mechanisms. The exact incidence of steroid myopathy is unknown, but it is believed that an excess of either endogenous or exogenous corticosteroids can cause this condition. Endogenous corticosteroid production can be increased due to adrenal tumors, while exogenous corticosteroid excess can result from steroid treatments for conditions such as asthma, chronic obstructive pulmonary disease, and inflammatory processes like polymyositis, connective tissue disorders, and rheumatoid arthritis.
Myopathy may also be a complication of pituitary and adrenal adenomas, though modern reports of myopathy resulting from Cushing syndrome are rare. In Cushing disease, elevated levels of adrenocorticotropic hormone may directly cause myopathy.
Oral and intravenous formulations of corticosteroids are most associated with myopathy, but there are also reports of myopathy following inhaled, intramuscular, epidural, and intra-articular injections. All synthetic corticosteroid preparations used in clinical practice can produce myopathy, but fluorinated corticosteroids, including triamcinolone, betamethasone, and dexamethasone, are particularly likely to cause it.
The mechanisms through which corticosteroids act on muscles are not fully understood, but several hypotheses have been proposed. One hypothesis is that corticosteroids alter muscle protein synthesis and degradation, leading to a decrease in protein synthesis and an increase in protein catabolism, resulting in muscle atrophy. Corticosteroids may also alter muscle metabolism, reduce sarcolemmal excitability, and induce hypokalemia, which can contribute to muscle weakness.
In terms of treatment, the goal is to lower the corticosteroid dose as much as possible, and physical therapy, including resistance and aerobic exercise, has been shown to help prevent and treat steroid-induced myopathy. In some cases, switching to a different type of steroid or altering the dosage may be recommended.
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Corticosteroid dose and duration
The dose and duration of corticosteroid treatment associated with the development of myopathy vary widely. Most patients have received therapy for at least four weeks, but high-dose corticosteroids can cause weakness within two weeks of starting treatment. The fluorinated corticosteroids, including triamcinolone, betamethasone, and dexamethasone, are particularly likely to cause myopathy.
The risk of developing myopathy is more than twofold greater in persons of older age, of male gender, or with obesity. However, for a given dose of steroid, women appear to be twice as likely as men to develop muscle weakness. In addition, the risk of myopathy appears greater for fluorinated corticosteroids.
The exact incidence of steroid myopathy is unknown. In cases of myopathy caused by long-term corticosteroid use, decreasing the corticosteroid dose to below a 30 mg/d threshold may result in improvement. The goal of treatment is to lower the corticosteroid dose as much as possible. Recovery may take weeks to months but is usually excellent.
Corticosteroid-induced myopathy is almost always reversible, with improvement in myopathy within 3 to 4 weeks of tapering corticosteroids. If stopping the steroid is not possible, changing to a different type of steroid or altering the dosage may help reduce symptoms. For patients unable to taper off steroids, replacement of fluorinated glucocorticoids with non-fluorinated glucocorticoids, such as dexamethasone with prednisone or hydrocortisone, should be considered.
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Treatment options
Steroid Withdrawal or Tapering
The mainstay of treatment is the reduction or discontinuation of corticosteroids, with close monitoring for adrenal insufficiency and exacerbation of the primary illness. Improvement in muscle weakness may be observed within 3 to 4 weeks, but full recovery may take months to a year.
Alternate Day Dosing
Alternate-day dosing of steroids may also be considered to reduce the risk of myopathy.
Switching to Non-fluorinated Glucocorticoids
For patients unable to taper off steroids, switching from fluorinated glucocorticoids to non-fluorinated alternatives, such as prednisone or hydrocortisone, can help manage corticosteroid-induced myopathy.
Physical Therapy
Physical activity, particularly resistance and aerobic exercise, can prevent and treat muscle weakness caused by corticosteroid use. Therefore, patients should be encouraged to engage in physical therapy as a preventive and treatment modality.
Experimental Treatments
Other experimental treatments, such as IGF-I, branched-chain amino acids, creatine, androgens, and glutamine, may also be explored. Additionally, ensuring adequate protein intake can help prevent the rapid worsening of symptoms.
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Frequently asked questions
Treatment for corticosteroid-induced myopathy involves lowering the corticosteroid dose or discontinuing its use altogether. Physical therapy, including resistance and aerobic exercises, can also help prevent and treat the condition.
Risk factors include older age, male gender, and obesity, and having an autoimmune blistering disease. In addition, the use of fluorinated corticosteroids such as triamcinolone, betamethasone, and dexamethasone may increase the risk.
The condition typically causes progressive weakness in the proximal muscles of the upper and lower limbs, as well as the neck flexors. Patients may experience difficulty rising from chairs, climbing stairs, and performing overhead activities.
Symptoms can develop within days or weeks of starting corticosteroid treatment, and they may occur even with low doses. However, the time frame varies, and in some cases, muscle weakness may manifest after long-term use.
Complications can include osteoporosis, joint contractures, pressure ulcers, and deep vein thrombi. In rare cases, high-dose intravenous corticosteroids combined with neuromuscular blocking agents can result in acute quadriplegic state or necrotizing myopathy.




















