Steroid induced myopathy treatment

The most commonly used AAS in medicine are testosterone and its various esters (but most commonly testosterone undecanoate , testosterone enanthate , testosterone cypionate , and testosterone propionate ), [53] nandrolone esters (most commonly nandrolone decanoate and nandrolone phenylpropionate ), stanozolol , and metandienone (methandrostenolone). [1] Others also available and used commonly but to a lesser extent include methyltestosterone , oxandrolone , mesterolone , and oxymetholone , as well as drostanolone propionate , metenolone (methylandrostenolone), and fluoxymesterone . [1] Dihydrotestosterone (DHT; androstanolone, stanolone) and its esters are also notable, although they are not widely used in medicine. [54] Boldenone undecylenate and trenbolone acetate are used in veterinary medicine . [1]

When administered to juvenile rats (postnatal days [PND] 4 through 80 at 5 to 45 mg/kg/day), no drug related changes were observed at 5 mg/kg/day. At 15 and 45 mg/kg/day, altered body-weight gain was observed during the dosing and 52-day recovery periods as well as slight thinning of the corpus callosum at the end of the recovery period. This finding was not evident in rats examined at the completion of the dosing period and was not associated with any inflammatory or degenerative changes in the brain. The biological relevance of the corpus callosum finding is uncertain due to the absence of any other microscopic changes in the brain or peripheral nervous tissue and because it occurred at the end of the recovery period. Neurobehavioral changes (enhanced acoustic startle responses and increased errors in water-maze learning) combined with evidence of generalized toxicity were noted at 45 mg/kg/day during the later part of the recovery period. Serum Pravastatin levels at 15 mg/kg/day are approximately ≥ 1 times (AUC) the maximum pediatric dose of 40 mg. No thinning of the corpus callosum was observed in rats dosed with Pravastatin (≥ 250 mg/kg/day) beginning PND 35 for 3 months suggesting increased sensitivity in younger rats. PND 35 in a rat is approximately equivalent to an 8- to 12-year-old human child. Juvenile male rats given 90 times (AUC) the 40 mg dose had decreased fertility (20%) with sperm abnormalities compared to controls.

Acute gout attacks can be managed with nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids (intra-articular injection or systemic). All three agents are appropriate first-line therapy for acute gout. Therapy should be initiated within 24 hours of onset. The drug selection is dictated by the patient's tolerance of those medications and the presence of any comorbid diseases that contraindicates the use of a specific drug. For patients with severe or refractory gout attacks, practitioners can try combining agents. If all of these medications are contraindicated in a patient, narcotics may be used short term to relieve pain until the acute attack has resolved. Long-term use of narcotics should be avoided.

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

Steroid induced myopathy treatment

steroid induced myopathy treatment

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

Media:

steroid induced myopathy treatmentsteroid induced myopathy treatmentsteroid induced myopathy treatmentsteroid induced myopathy treatmentsteroid induced myopathy treatment