Steroid induced myopathy

Myopathy due to steroids can be acute or chronic [3] and in some instances may involve the respiratory muscles [9]. The chronic form occurs after prolonged use with a more insidious onset whereas the acute presentation, if present, may be associated with rhabdomyolysis and abrupt onset [9]. Myopathy secondary to steroid may predispose patients to osteoporosis and sedentary life style which exposes to risks of contractures, deep venous thrombosis (DVT) and pressure sores. Stopping the administration of steroids results in insidious response; however, complete recovery may take weeks to months [11]. The laboratory findings are generally non specific [11, 12]. Creatinine kinase (CK) and lactate dehydrogenase (LDH) levels may be within normal limits; however, before development of myopathy the urinary creatinine excretion may specifically rise [3]. Acute myopathy shows increased CK levels with myoglobinuria which is absent in cases of chronic use of steroids [9]. EMG and NCS remains normal in chronic phases but some case reports of acute onset have indicated abnormal spontaneous activity (positive sharp waves and fibrillation potentials) [9]. There is no definite treatment for reversing steroid-induced myopathy; however, stopping the administration of steroids or, in cases where it is essential to be given, administer low doses on alternate days or offering non-fluorinated forms may minimize the risk with improvement in weeks to months. Our patient sufficently showed improvement on withdrawal of steroids and had been ambulatory in the ward three to four weeks after appropriate dose reduction.

During conventional pharmacologic dose corticosteroid therapy, ACTH production is inhibited with subsequent suppression of cortisol production by the adrenal cortex. Recovery time for normal HPA activity is variable depending upon the dose and duration of treatment. During this time the patient is vulnerable to any stressful situation. Although it has been shown that there is considerably less adrenal suppression following a single morning dose of prednisolone (10 mg) as opposed to a quarter of that dose administered every six hours, there is evidence that some suppressive effect on adrenal activity may be carried over into the following day when pharmacologic doses are used. Further, it has been shown that a single dose of certain corticosteroids will produce adrenal cortical suppression for two or more days. Other corticoids, including methylprednisolone, hydrocortisone, prednisone, and prednisolone, are considered to be short acting (producing adrenal cortical suppression for 1¼ to 1½ days following a single dose) and thus are recommended for alternate day therapy.

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.

Body as a Whole: chest pain; abdominal pain; edema; chills; malaise Cardiovascular: atrial fibrillation; tachycardia; palpitations, and other cardiac arrhythmias; postural hypotension, orthostasis; hypotension; syncope Eye: toxic amblyopia; cystoid macular edema; ophthalmoplegia; eye irritation, blurred vision, progression of cataracts Gastrointestinal: activation of peptic ulcers and peptic ulceration; dyspepsia; vomiting; anorexia; constipation; flatulence, pancreatitis; hepatitis; fatty change in liver; jaundice; and rarely, cirrhosis, fulminant hepatic necrosis, and hepatoma, eructation, fatal and non-fatal hepatic failure Metabolic: gout, decreased glucose tolerance Musculoskeletal: muscle cramps; myopathy; rhabdomyolysis; arthralgia, myalgia Nervous: dizziness; insomnia; dry mouth; paresthesia; anxiety; tremor; vertigo; peripheral neuropathy; psychic disturbances; dysfunction of certain cranial nerves, nervousness, burning sensation/skin burning sensation, peripheral nerve palsy Psychiatric depression Skin: hyper-pigmentation; acanthosis nigricans; urticaria; alopecia; dry

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.

Steroid induced myopathy

steroid induced myopathy

Body as a Whole: chest pain; abdominal pain; edema; chills; malaise Cardiovascular: atrial fibrillation; tachycardia; palpitations, and other cardiac arrhythmias; postural hypotension, orthostasis; hypotension; syncope Eye: toxic amblyopia; cystoid macular edema; ophthalmoplegia; eye irritation, blurred vision, progression of cataracts Gastrointestinal: activation of peptic ulcers and peptic ulceration; dyspepsia; vomiting; anorexia; constipation; flatulence, pancreatitis; hepatitis; fatty change in liver; jaundice; and rarely, cirrhosis, fulminant hepatic necrosis, and hepatoma, eructation, fatal and non-fatal hepatic failure Metabolic: gout, decreased glucose tolerance Musculoskeletal: muscle cramps; myopathy; rhabdomyolysis; arthralgia, myalgia Nervous: dizziness; insomnia; dry mouth; paresthesia; anxiety; tremor; vertigo; peripheral neuropathy; psychic disturbances; dysfunction of certain cranial nerves, nervousness, burning sensation/skin burning sensation, peripheral nerve palsy Psychiatric depression Skin: hyper-pigmentation; acanthosis nigricans; urticaria; alopecia; dry

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