Steroid myopathy patient information

When the symptoms of the attack subside, an individual with MS is said to be in remission. However, MRI data have shown that this is somewhat misleading because MS lesions continue to appear during these remission periods. Patients do not experience symptoms during remission because the inflammation may not be severe or it may occur in areas of the brain that do not produce obvious symptoms. Research suggests that only about 1 out of every 10 MS lesions is perceived by a person with MS. Therefore, MRI examination plays a very important role in establishing an MS diagnosis, deciding when the disease should be treated, and determining whether treatments work effectively or not. It also has been a valuable tool to test whether an experimental new therapy is effective at reducing exacerbations.

If the neurologic examination is unrevealing, a more general physical examination, searching for extramuscular signs, is warranted ( Table 6 5 , 7 – 15 , 17 , 18 , 21 , 24 – 27 , 34 , 36 , 38 ) . Mental status testing may reveal changes suggestive of a myopathy-inducing electrolyte disorder (calcium or magnesium) or an arrest of mental development as occurs in genetic myopathies. 25 , 29 The cardiovascular assessment may elicit changes consistent with a cardiomyopathy—a nonspecific consequence of many myopathy-inducing disorders—or a pericarditis, as occurs with some of the infectious and rheumatologic causes of muscle weakness. 5 , 7 , 8 , 9 , 18 , 21 , 24 , 25 , 29 , 36 , 38

For patients who present with rhabdomyolysis, treatment is aimed at preventing kidney failure in the acute setting. Vigorous hydration with close monitoring of kidney function and electrolytes are paramount. In patients with an underlying metabolic myopathy, education about following a more moderate exercise program and avoiding intense exercise and fasting is necessary in preventing recurrent episodes. Measures that have been suggested to be helpful include sucrose loading before exercise in some glycogen storage disorders and a low-fat, high-carbohydrate diet in patients with lipid storage disorders.

In six patients with Cushing's syndrome and three with steroid myopathy, the clinical, functional, biochemical and structural characteristics of myopathy are described. Proximal muscle weakness occurred in all the patients, preferentially affected the lower limbs and was accompanied by muscle wasting in all but one patient. Force measurements confirmed quadriceps weakness in every patient. Vastus lateralis muscle biopsies showed light microscopic abnormalities in two of three patients with steroid myopathy and one of five patients with Cushing's syndrome. Type II fibre atrophy was the commonest abnormality. Reduced type II mean fibre areas occurred in all the patients with steroid myopathy and were common in Cushing's syndrome patients. Type I mean fibre areas were also reduced in two of the former group and one of the latter group and two further patients in this group had areas at the lower end of the normal range. Abnormalities in electron microscopy, mitochondrial function tests and chemical content of skeletal muscle were frequent and are described and discussed. A plasma creatine kinase activity (CK) at the lower end of the normal range, a myopathic electromyogram (EMG) and a raised 24-h urinary 3-methylhistidine/creatinine ratio on a creatine free diet were other characteristic findings in both groups of patients.

Steroid myopathy patient information

steroid myopathy patient information

In six patients with Cushing's syndrome and three with steroid myopathy, the clinical, functional, biochemical and structural characteristics of myopathy are described. Proximal muscle weakness occurred in all the patients, preferentially affected the lower limbs and was accompanied by muscle wasting in all but one patient. Force measurements confirmed quadriceps weakness in every patient. Vastus lateralis muscle biopsies showed light microscopic abnormalities in two of three patients with steroid myopathy and one of five patients with Cushing's syndrome. Type II fibre atrophy was the commonest abnormality. Reduced type II mean fibre areas occurred in all the patients with steroid myopathy and were common in Cushing's syndrome patients. Type I mean fibre areas were also reduced in two of the former group and one of the latter group and two further patients in this group had areas at the lower end of the normal range. Abnormalities in electron microscopy, mitochondrial function tests and chemical content of skeletal muscle were frequent and are described and discussed. A plasma creatine kinase activity (CK) at the lower end of the normal range, a myopathic electromyogram (EMG) and a raised 24-h urinary 3-methylhistidine/creatinine ratio on a creatine free diet were other characteristic findings in both groups of patients.

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