La myopathie cortisonique : physiopathologie, stratégie diagnostique et prise en charge

Abstract

Glucocorticoid-induced myopathy is a frequent and potentially disabling complication of prolonged glucocorticoid therapy. This article provides an in-depth exploration of the historical context, epidemiology, pathophysiology, clinical manifestations, diagnostic challenges, and therapeutic strategies associated with this condition. While glucocorticoids are essential in treating numerous inflammatory and autoimmune diseases, they can induce progressive muscle weakness and atrophy, particularly affecting type II muscle fibers. The pathophysiological mechanisms involve inhibition of muscle protein synthesis (via the mTOR/IGF-1 pathway) and activation of protein degradation systems (ubiquitin-proteasome and autophagy-lysosome pathways), triggered by the activation of FOXO transcription factors and the upregulation of atrogenes (MuRF-1 and Atrogin-1). Diagnosis relies on a comprehensive clinical assessment (proximal muscle weakness without pain, selective atrophy of the lower limbs), laboratory investigations (serum creatine kinase levels typically normal or mildly elevated; metabolic panel), electrophysiological study (electroneuromyography), and, in cases of uncertain diagnostic, histological analysis (muscle biopsy revealing preferential atrophy of type II fibers, without inflammatory infiltration). Management strategies include gradual reduction or discontinuation of glucocorticoids, physical rehabilitation (resistance and endurance exercises), and targeted pharmacological therapies. Further research is essential to refine diagnostic tools (e.g., blood or ultrasound biomarkers) and develop personalized therapeutic approaches, incorporating genetic (e.g., ABCB1 and PAI-1 polymorphisms) and metabolic patient profiles.