BACKGROUND Chronic intake of high-dose corticosteroids is associated with multiple adverse clinical effects, including hypertension, insulin resistance, impaired wound healing, immunosuppression, myopathy, and osteoporosis. In cases of autoimmune disease, use of steroid-sparing treatment modalities is preferred over chronic steroid therapy to limit these side effects. Glucocorticoid-induced myopathy is a less common side effect of chronic steroid use in patients treated with <10 mg/day of prednisone. However, doses exceeding 40-60 mg/day can induce clinically significant myopathy and weakness. CASE REPORT A 35-year-old woman with a past medical history of hypothyroidism, systemic lupus erythematosus (SLE), and end-stage renal disease secondary to lupus nephritis, on hemodialysis, presented to the local emergency department with progressive bilateral proximal lower extremity weakness. Three months before admission, when her insurance company prematurely discontinued her monthly cyclophosphamide injections, at which time, she was treated with prednisone 60 mg daily. Two months before hospital admission, she reported increasing fatigue, weight gain, difficulty in standing from a seated position and climbing stairs. CONCLUSIONS Elucidating the etiology of progressive neuromotor deficit in immunosuppressed patients can be difficult. The management of SLE and other autoimmune diseases with chronic high-dose steroids is associated with recognized side effects. Differentiating natural disease progression from iatrogenic etiologies is important in this subset of patients, particularly to reduce prolonged clinical management and hospital admissions.
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http://dx.doi.org/10.12659/ajcr.906377 | DOI Listing |
Tissue Cell
December 2024
Department of Medical Physiology, Faculty of Medicine, Mansoura University, Mansoura 35516, Egypt. Electronic address:
Background: Muscle tissue is essential for overall well-being that declines with age and different illnesses. Glucocorticoids, despite being efficient in treating inflammation, can induce muscle weakness (known as glucocorticoid-induced myopathy) by affecting protein breakdown and synthesis. Glucocorticoids have a negative impact on satellite cells, which play a role in muscle regeneration.
View Article and Find Full Text PDFJCI Insight
November 2024
Department of Physiology and Cell Biology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Despite their beneficial actions as immunosuppressants, glucocorticoids (GC) have devastating effects on the musculoskeletal and cardiac systems, as long-term treated patients exhibit high incidence of falls, bone fractures, and cardiovascular events. Herein, we show that GC upregulate simultaneously in bone, skeletal muscle, and the heart the expression of E3 ubiquitin ligases (atrogenes), known to stimulate the proteasomal degradation of proteins. Activation of vitamin D receptor (VDR) signaling with the VDR ligands calcitriol or eldecalcitol prevented GC-induced atrogene upregulation in vivo and ex vivo in bone/muscle organ cultures and preserved tissue structure/mass and function of the 3 tissues in vivo.
View Article and Find Full Text PDFAm J Physiol Endocrinol Metab
November 2024
Department of Health, Nutrition and Food Sciences, Florida State University, Tallahassee, Florida, United States.
Elevated glucocorticoids alter the skeletal muscle transcriptome to induce a myopathy characterized by muscle atrophy, muscle weakness, and decreased metabolic function. These effects are more likely to occur and be more severe in aged muscles. Resistance exercise can blunt the development of glucocorticoid myopathy in young muscle, but the potential to oppose the signals initiating myopathy in aged muscle is unknown.
View Article and Find Full Text PDFJ Physiol
January 2025
Department of Kinesiology and Health Sciences, University of Waterloo, Waterloo, ON, Canada.
J Physiol
January 2025
Department of Health, Nutrition, and Food Sciences, Florida State University, Tallahassee, Florida, USA.
Older adults are vulnerable to glucocorticoid-induced muscle atrophy and weakness, with sex potentially influencing their susceptibility to those effects. Aerobic exercise can reduce glucocorticoid-induced muscle atrophy in young rodents. However, it is unknown whether aerobic exercise can prevent glucocorticoid myopathy in aged muscle.
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