Steroid myopathy is usually an insidious disease process that causes weakness mainly to the proximal muscles of the upper and lower limbs and to the neck flexors. Cushing originally described it in 1932, and Muller and Kugelberg first studied it systemically in 1959. An excess of either endogenous or exogenous corticosteroids is believed to cause the condition. Excess endogenous corticosteroid production can arise from adrenal tumors. An excess of exogenous corticosteroid can result from steroid treatment for asthma, chronic obstructive pulmonary disease, and inflammatory processes, such as polymyositis, connective tissue disorders, and rheumatoid arthritis. [1, 2, 3]
Steroid myopathy may be more frequent with the use of fluorinated steroids, such as dexamethasone  or triamcinolone, than with nonfluorinated ones, such as prednisone or hydrocortisone. [5, 6] Although the exact mechanism of the muscle pathology is unclear, it may be related to decreased protein synthesis, increased protein degradation, alterations in carbohydrate metabolism, mitochondrial alterations, electrolyte disturbances, and/or decreased sarcolemmal excitability. Sedentary lifestyle may increase the risk of muscle weakness in a patient taking corticosteroids, since corticosteroids seem to affect less active muscles preferentially. Two distinct types of steroid myopathy exist, acute and chronic. The chronic (or classic) form occurs after prolonged use of corticosteroids and has a more insidious course. The acute form is less common, is associated with rhabdomyolysis, and occurs abruptly while the patient is receiving high-dose corticosteroids.
One study used skeletal muscle biopsy of the vastus lateralis and realtime polymerase chain reaction (PCR) to investigate the effects of dexamethasone on skeletal muscle. Twenty-four subjects were studied before and after the administration of dexamethasone 4 mg by mouth daily for 4 days. Following dexamethasone, all subjects (12 female and 12 male) demonstrated similar decreases in serum testosterone and transcription factor 4 (TCF4), an androgen-responsive transcription factor. Additionally, a significant decrease in skeletal muscle androgen receptor mRNA levels occurred following dexamethasone administration. Furthermore, plasma insulinlike growth factor-1 (IGF-1), produced by the liver, increased significantly following dexamethasone administration, whereas skeletal muscle IGF-1 mRNA levels decreased. Further studies are needed to investigate the significance of these findings. 
In a study performed by Levin et al, 60% of participants who used inhaled corticosteroids daily for a year or greater reported muscle weakness and 20% of that group showed objective signs of weakness. These researchers measured inhaled steroid–induced myopathy using a peripheral motor deficits scale, stepper test, ankle/wrist index, neuropathy disability score, and statistical analysis. Peripheral motor deficits scale was formulated to determine early stages of myopathy with physician's rating of the participant's weakness while (1) walking up and down stairs and (2) with difficulty in buttoning/unbuttoning, sewing, or picking up coins. Muscle atrophy measurements were made using an ankle/wrist index, in which the smallest circumference of the dominant leg above the ankle and that of the forearm above the wrist were compared. Neuropathy disability score was determined by evaluation of sensory functions and reflexes. 
A study by Minetto et al found that short-term glucocorticoid administration in healthy subjects produced the sorts of changes in muscle fibers that arise prior to the clinical appearance of myopathy in patients treated with glucocorticoids. In the study, in which dexamethasone was administered to five healthy males for 7 days, type 1 and type 2A muscle fibers demonstrated a reduction in cross-sectional area, myosin, and specific force. 
The exact incidence of steroid myopathy is unknown; sensitivity to particular medications varies among patients.
The weakness seen with steroid myopathy typically resolves after the corticosteroid dose is reduced or discontinued, although recovery can take weeks or months. Case studies have reported a lack of full recovery, as well as difficulty weaning patients off of mechanical ventilation. Osteoporosis, which can occur as a comorbidity with steroid myopathy, can result from the corticosteroid or from decreased mobility and respiratory impairment.  Other comorbidities include joint contractures, pressure ulcers, and deep vein thrombi, although these can occur in any condition causing weakness and immobility. Mortality has not been described. Some case studies have reported patient mortalities, but they provided no indication that steroid myopathy was the cause.
For a given dose of steroid, women appear to be twice as likely as men to develop muscle weakness, although the reason is unclear.
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