Acquired Neuromuscular Disorders by Corrado Angelini

Author:Corrado Angelini
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

11.2 Steroid Myopathy

Steroid myopathy may be endogenous or iatrogenic. The onset of weakness is usually insidious, starting in the proximal muscles of the legs and arms. Myalgia may accompany the weakness. The levels of serum lactate dehydrogenase, aspartate aminotransferase, creatine kinase and aldolase are usually normal. Patients suffering from steroid myopathy usually have other clinical signs of glucocorticoid excess. The diagnosis of steroid myopathy is simple when significant muscle weakness occurs in a patient receiving steroids for a condition unrelated to the musculoskeletal system. The differentiation of steroid myopathy from an inflammatory myopathy is more difficult. The following criteria can be used: steroid myopathy takes time to develop and weakness that occurs at the onset of a steroid treatment in polymyositis is probably still related to the inflammatory process. If the relevant serum enzymes are elevated, the weakness is probably not steroid induced. Among patients with steroid myopathy, there is a wide range in dose and duration of steroid treatment received. Patients who have received steroids for less than 4 weeks rarely develop steroid myopathy. Women are twice as likely as men to develop steroid myopathy with the same glucocorticoid dose. Lowering the steroid dose will usually correct the weakness. On EMG needle insertion, activity is normal and the motor unit potentials are of low amplitude and short duration [16]. Although many commonly used steroids can cause myopathy, the fluorinated steroids such as dexamethasone, betamethasone and triamcinolone are more likely to produce muscle weakness [16].

Myopathology

Histological studies in either iatrogenic steroid myopathy or Cushing’s disease [17] show a selective type 2 fibre atrophy. The biopsy shows atrophic type 2 fibres staining darkly for myofibrillar ATPase. Sometimes the atrophy is so intense that it can resemble a neurogenic atrophy, except that other features of neurogenic disorders (‘targets’ or ‘type grouping’) are absent. Lipid droplets are frequently seen in type 1 fibres and electron microscopy shows mitochondrial aggregates and vacuolisation.

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