Prednisone induced myopathy

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    Prednisone induced myopathy


    Glucocorticoid-induced myopathy, characterized by muscle weakness without pain, fatigue and atrophy, is an adverse effect of glucocorticoid use and is the most common type of drug-induced myopathy. This muscle disturbance has a frequency of 60%, and it has been most often associated with fluorinated glucocorticoid preparations. Glucocorticoids have a direct catabolic effect on muscle, decreasing protein synthesis and increasing the rate of protein catabolism leading to muscle atrophy. In clinical practice, it is important to differentiate myopathy due to glucocorticoid from muscle inflammatory diseases. The treatment is based on reduction or, if possible, on discontinuation of the steroid. Fluorinated glucocorticoids such as dexamethasone should be replaced with nonfluorinated glucocorticoids such as prednisone. Other experimental treatments may be tried such as IGF-I, branched-chain amino acids, creatine, androgens such as testosterone, nandrolone and dehydroepiandrosterone (DHEA), and glutamine. Corticosteroid myopathy is likely the most common drug-induced myopathy. There are two distinct types of corticosteroid-induced myopathies: acute and chronic. Acute corticosteroid myopathy occurs less often than the chronic variety. The acute variety is usually encountered in the setting of high-dose systemic corticosteroid treatment (e.g. Approximately a week after high doses of corticosteroids have been started, patients often present with generalized proximal and distal weakness, including the respiratory musculature. There is support for a direct correlation between the occurrence of an acute corticosteroid myopathy and the type or total dose of corticosteroids administered. In addition, combining corticosteroids and an aminosteroid-based nondepolarizing neuromuscular blocking agent appears to increase the risk of developing an acute myopathy (see earlier discussion of thick filament myopathy). Examples of these blockers include pancuronium, vecuronium, pipecuronium, and atracurium.

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    Steroid-induced myopathy is frequently related with the use of fluorinated steroids, as compared to nonfluorinated steroids 2. Corticosteroids may cause weakness of both skeletal and respiratory J Clin Endocrinol Metab. 1985 Jul;61183-8. Evidence that prednisone-induced myopathy is reversed by physical training. Horber FF, Scheidegger JR, Grünig. Prednisone has interactions with eleven of my other medications and interacts with three of my medical conditions. During my first year of treatment I was on high dosage of prednisone and liptor which resulted in serious problems with steroid myopathy.was not until I changed doctors and questioned being on Liptor and high dosage prednisone before the myopathy was diagnosis.

    Steroid myopathy is usually an insidious disease process that causes weakness mainly to the proximal muscles of the upper and lower limbs and to the neck flexors. Cushing originally described it in 1932, and Muller and Kugelberg first studied it systemically in 1959. An excess of either endogenous or exogenous corticosteroids is believed to cause the condition. Excess endogenous corticosteroid production can arise from adrenal tumors. An excess of exogenous corticosteroid can result from steroid treatment for asthma, chronic obstructive pulmonary disease, and inflammatory processes, such as polymyositis, connective tissue disorders, and rheumatoid arthritis. Although the exact mechanism of the muscle pathology is unclear, it may be related to decreased protein synthesis, increased protein degradation, alterations in carbohydrate metabolism, mitochondrial alterations, electrolyte disturbances, and/or decreased sarcolemmal excitability. Sedentary lifestyle may increase the risk of muscle weakness in a patient taking corticosteroids, since corticosteroids seem to affect less active muscles preferentially. Patrick M Foye, MD Director of Coccyx Pain Center, Professor of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School; Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, University Hospital Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation Disclosure: Nothing to disclose. Francisco Talavera, Pharm D, Ph D Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Received salary from Medscape for employment. Kat Kolaski, MD Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Physical Medicine and Rehabilitation Disclosure: Nothing to disclose. Stephen Kishner, MD, MHA Professor of Clinical Medicine, Physical Medicine and Rehabilitation Residency Program Director, Louisiana State University School of Medicine in New Orleans Stephen Kishner, MD, MHA is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine Disclosure: Nothing to disclose. Patrick J Potter, MD, FRCSC Associate Professor, Department of Physical Medicine and Rehabilitation, University of Western Ontario School of Medicine; Consulting Staff, Department of Physical Medicine and Rehabilitation, St Joseph's Health Care Centre Patrick J Potter, MD, FRCSC is a member of the following medical societies: Academy of Spinal Cord Injury Professionals, College of Physicians and Surgeons of Ontario, Canadian Association of Physical Medicine and Rehabilitation, Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada Disclosure: Nothing to disclose. Dena Abdelshahed Rutgers New Jersey Medical School Disclosure: Nothing to disclose. Gloria E Hwang, MD, MPA Rutgers New Jersey Medical School Disclosures: Nothing to disclose. Debra Ibrahim New York College of Osteopathic Medicine Disclosure: Nothing to disclose.

    Prednisone induced myopathy

    Corticosteroid-Induced Myopathy Clinical Presentation History, Physical, Evidence that prednisone-induced myopathy is reversed by physical.

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  7. Clinical Presentation History Chronic classic steroid myopathy This form is the classic presentation of steroid myopathy. This condition can develop after prolonged administration of prednisone

    • Steroid Induced Myopathy authorSTREAM.
    • Prednisone and Steroid Myopathy - Reviews - Treato.
    • Steroid myopathy Some unresolved issues SpringerLink.

    Acute steroid myopathy history findings are as follows This form is encountered less frequently than is the chronic type. Acute, generalized weakness, including weakness of the respiratory muscles, typically occurs 5-7 days after the onset of treatment with high-dose corticosteroids. Myopathy has been recognized as a side effect of glucocorticoid corticosteroid therapy since its introduction as a therapeutic agent in the. Glucocorticoid-induced myopathy, characterized by muscle weakness without pain, fatigue and atrophy, is an adverse effect of glucocorticoid use and is the.

     
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