Corticosteroid myopathy emg

Geriatric Use : Clinical studies of prednisolone sodium phosphate , USP, oral solution did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience with prednisolone sodium phosphate has not identified differences in responses between the elderly and younger patients. However, the incidence of corticosteroid-induced side effects may be increased in geriatric patients and appear to be dose-related. Osteoporosis is the most frequently encountered complication , which occurs at a higher incidence rate in corticosteroid-treated geriatric patients as compared to younger populations and in age-matched controls. Losses of bone mineral density appear to be greatest early on in the course of treatment and may recover over time after steroid withdrawal or use of lower doses (., ≤5 mg/day). Prednisolone doses of mg/day or higher have been associated with an increased relative risk of both vertebral and nonvertebral fractures, even in the presence of higher bone density compared to patients with involutional osteoporosis.

The National Heart, Lung, and Blood Institute (NHLBI) recommended dosing for systemic prednisone, prednisolone, or methylprednisolone in pediatric patients whose asthma is uncontrolled by inhaled corticosteroids and long-acting bronchodilators is 1–2 mg/kg/day in single or divided doses. It is further recommended that short course, or "burst" therapy, be continued until the patient achieves a peak expiratory flow rate of 80% of his or her personal best or until symptoms resolve. This usually requires 3 to 10 days of treatment, although it can take longer. There is no evidence that tapering the dose after improvement will prevent a relapse.

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 ].

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.

Corticosteroid myopathy emg

corticosteroid myopathy emg

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.

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