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Abstract Steroid myopathy, characterized by muscle atrophy and weakness, is an adverse effect of high-dose steroid therapy. Weakness of proximal muscle that interferes with activities of daily living is a serious problem for patients with steroid myopathy. Here, we outline the pathogenic mechanism, diagnosis, and treatment of steroid myopathy. Recent studies have shown that steroid-mediated induction of ubiquitin ligases (atrogin-1, muscle RING finger-1) and suppression of mammalian/mechanistic target of rapamycin cause an imbalance between anabolism and catabolism of muscle proteins, resulting in muscle atrophy. Despite the progress in understanding the pathogenic mechanism, the diagnosis and treatment of steroid myopathy has not yet been established. Small changes in muscle enzymes, including CK, LDH, and aldolase, make it difficult to define diagnostic criteria. Furthermore, since there is no drug available for treating the disorder, the patients have no opinion except waiting for spontaneous recovery with steroid tapering and exercising. To address these issues, we introduce novel approaches involving branched-chain amino acids that aim at treatment and assessment of steroid myopathy.
Department of Medicine and Rheumatology, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University.
This article was published in the following journal.
Name: Brain and nerve = Shinkei kenkyÅ« no shinpo
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An inhibitor of the enzyme STEROID 11-BETA-MONOOXYGENASE. It is used as a test of the feedback hypothalamic-pituitary mechanism in the diagnosis of CUSHING SYNDROME.
Proteins found usually in the cytoplasm or nucleus that specifically bind steroid hormones and trigger changes influencing the behavior of cells. The steroid receptor-steroid hormone complex regulates the transcription of specific genes.
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