Steroid myopathy emg

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.

It is interesting that the authors of “ Musculoskeletal Complications of Fluoroquinolones: Guidelines and Precautions for Usage in the Athletic Population ” attribute myalgia and rhabdomyolysis to the fluorine atom that is added to quinolones to form fluoroquinolones. The toxicity of fluorine is often overlooked by researchers and “floxies” alike, in part because of the politics associated with assertions that fluorine and fluoride are toxic (they are). As the first sentence in the quote (“Although the etiology of fluoroquinolone-associated muscle disorders has yet to be fully elucidated”) notes though, the exact mechanism through which fluoroquinolones, statins, and fluoroquinolones and statins together, cause adverse reactions is not fully known.

The MAA are found in the sera of 20-50% of patients and are commonly encountered in other connective tissue diseases. The most important antigenic targets of the MAA are the PM/Scl nucleolar antigen, the nuclear Ku antigen, the small nuclear ribonucleoproteins (snRNP), and the cytoplasmic ribonucleoproteins (RoRNP). The anti-PM/Scl autoantibodies are generally found in patients affected by polymyositis overlapping with scleroderma. Anti-Ku antibodies are found in patients with myositis overlapping with other connective tissue diseases.

Steroid myopathy emg

steroid myopathy emg

The MAA are found in the sera of 20-50% of patients and are commonly encountered in other connective tissue diseases. The most important antigenic targets of the MAA are the PM/Scl nucleolar antigen, the nuclear Ku antigen, the small nuclear ribonucleoproteins (snRNP), and the cytoplasmic ribonucleoproteins (RoRNP). The anti-PM/Scl autoantibodies are generally found in patients affected by polymyositis overlapping with scleroderma. Anti-Ku antibodies are found in patients with myositis overlapping with other connective tissue diseases.

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