Muscle weakness glucocorticoids

An endocrine disorder first described by the British Physician Thomas Addison in the mid 1800 s. The adrenal glands fail to produce sufficient amounts of glucocorticoid hormones (cortisol) and sometime mineralocorticoid (aldosterone). If left untreated it is life-threatening, the patient will show muscle weakness, hyperpigmentation and even depression. Typical treatment is hydrocortisone replacement therapy. 

Glucocorticoids are widely used as drugs to treat arthritis and dermatitis. In pharmacological doses, they are used to suppress various allergic, inflammatory and autoimmune diseases. They are also administered as post-transplant immunosuppressants. Nevertheless, they do not prevent infection and they also inhibit subsequent regenerative processes. Excessive glucocorticoid levels have side effects on many systems, such as the inhibition of bone formation, delayed wound healing, muscle weakness and an increased risk of infection. 

Q6 Brian s muscle weakness, tiredness, weight gain, redistribution of body fat (truncal obesity), limb muscle atrophy, frequent infections, changes in mood and attitude are characteristic of Cushing s disease, which is caused by hypersecretion of glucocorticoids. If his plasma and urinary cortisol is also found to be elevated above the normal value or there is found to be overproduction of ACTH, this confirms the diagnosis. Cushing s syndrome is less common, exhibits more severe symptoms and occurs when there is excessive secretion of cortisol. 

This topic has been re-analysed in a systematic review of published papers, in which relevant information from a total of 34 patients was identified (163). AU but two patients were also taking concomitant drugs known to affect the muscles, among which glucocorticoids, simvastatin, lovastatin, colchicine, and pyrazinamide were the most frequently cited. Ciclosporin is therefore difficult to implicate in most patients, but at least one case with positive ciclosporin re-administration supported a causative role. The clinical picture was non-specific, with myalgia, cramps, and muscle weakness, sometimes associated with raised serum creatine kinase activity, and heterogeneous histopathology. FinaUy, skeletal muscle abnormalities have rarely been described in patients without muscle symptoms. 

Proximal muscle weakness in an elderly patient associated with a normal electromyogram (EMG) can be caused by type-2 muscle fiber atrophy, which is diagnosable only on muscle biopsy. One should seek an identifiable cause, such as cachexia, disuse, glucocorticoid toxicity, a "remote" neoplasm, hyperparathyroidism, subtle denervation, or supra-segmental central nervous system (CNS) abnormality. This mainly-sensory nerve neuropathy can cause slowed sensory nerve conductions, if involving large diameter fiber, small diameter ones. 

Dermatomyositis causes a moderately or rapidly progressive muscle weakness, with or without skin manifestations. Muscle biopsy is nearly always diagnostic. Treatment is typically begun with a glucocorticoid, usually prednisone, and it is often effective in restoring good to excellent strength. 

Over-secretion of the glucocorticoids, particularly cortisol, causes Cushing s disease, with changes in distribution of body fat, muscle wasting and weakness, osteoporosis, immune suppression with frequent infections, poor wound healing and mood changes, which include depression and sometimes paranoia. 

Among reports of myopathy in patients taking glucocorticoids, involvement of the respiratory muscles is often mentioned (235,236), possibly because this is particularly likely to have clinical consequences. Patients on mechanically assisted ventilation may be particularly at risk of myopathy (SEDA-18, 390). However, any muscle can be affected one often sees weakness and atrophy of the hip muscles and (in about half the cases) the shoulder muscles and the proximal muscles of the limbs. 

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