Steroid induced myopathy pdf

IT SHOULD BE EMPHASIZED THAT DOSAGE REQUIREMENTS ARE VARIABLE AND MUST BE INDIVIDUALIZED ON THE BASIS OF THE DISEASE UNDER TREATMENT AND THE RESPONSE OF THE PATIENT. After a favorable response is noted, the proper maintenance dosage should be determined by decreasing the initial drug dosage in small decrements at appropriate time intervals until the lowest dosage which will maintain an adequate clinical response is reached. Situations which may make dosage adjustments necessary are changes in clinical status secondary to remissions or exacerbations in the disease process, the patient’s individual drug responsiveness, and the effect of patient exposure to stressful situations not directly related to the disease entity under treatment. In this latter situation it may be necessary to increase the dosage of the corticosteroid for a period of time consistent with the patient’s condition. If after long-term therapy the drug is to be stopped, it is recommended that it be withdrawn gradually rather than abruptly.

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.

Neuroactive steroids are also called as neurosteroids . They are endogenous steroids that rapidly alter neuronal excitability through interaction with ligand-gated ion channels and other cell surface receptors. Neuroactive steroid refers to steroids that are synthesized by an endocrine gland that reach the brain through the bloodstream and have effects on brain function. Neurosteroids have a wide range of potential clinical applications from sedation to treatment of epilepsy and traumatic brain injury. Ganaxolone is a synthetic analog of the endogenous neurosteroid. Allopregnanolone is under investigation for the treatment of epilepsy.

An intracellular signaling molecule with protein kinase activity known as Akt1 (a major isoform of Akt) [ 6 ] may play a central role in the atrophic and hypertrophic responses of muscle to glucocorticoids and IGF-I, respectively [ 7,8 ]. Glucocorticoid-induced suppression of Akt1 ultimately results in increased amounts of the ubiquitin-ligase atrogin-1 (MAFbx) that targets muscle proteins for degradation [ 7,9 ]. Conversely, IGF-I signaling leads to enhanced activity of Akt1 that suppresses muscle atrophy and that induces muscle hypertrophy [ 8 ].

Steroid induced myopathy pdf

steroid induced myopathy pdf

An intracellular signaling molecule with protein kinase activity known as Akt1 (a major isoform of Akt) [ 6 ] may play a central role in the atrophic and hypertrophic responses of muscle to glucocorticoids and IGF-I, respectively [ 7,8 ]. Glucocorticoid-induced suppression of Akt1 ultimately results in increased amounts of the ubiquitin-ligase atrogin-1 (MAFbx) that targets muscle proteins for degradation [ 7,9 ]. Conversely, IGF-I signaling leads to enhanced activity of Akt1 that suppresses muscle atrophy and that induces muscle hypertrophy [ 8 ].

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