Muscle lesions caused by long-term corticosteroid use
Introduction
Introduction Chronic corticosteroid myopathy (chronic corticosteroid myopathy) is a long-term use of corticosteroids caused by muscle lesions. Patients often have a history of high-dose corticosteroids for months or years. The dose is usually not significantly different from the degree of muscle weakness. Some people think that fluoride is more likely to cause the disease than other hormones. In fact, all the cortex Hormones can cause disease.
Cause
Cause
Long-term use or extensive use of glucocorticoids can lead to steroid myopathy. Through glucocorticoid receptor-mediated signal transduction, glucocorticoids can positively or negatively regulate the expression of related genes, resulting in related effects such as accelerated protein degradation and slowed protein synthesis. Experiments in cell models or animal models have shown that glucocorticoids can disrupt the homeostasis of skeletal muscle cells from disturbances in skeletal muscle energy metabolism, amino acid balance, protein metabolism, and myogenesis, which may be glucocorticoid-induced steroids. The mechanism of myopathy. Activation of the MAPKs signaling pathway or G-protein coupled receptor signaling pathway may inhibit glucocorticoid signaling. Unbalanced synthesis and decomposition of muscle contractile components (such as myosin, contractile protein), resulting in clinical muscle weakness and amyotrophic steroids can inhibit RNA synthesis, reduce protein translation efficiency and block protein synthesis.
Steroids can also promote the breakdown of muscle contraction proteins through the ubiquitin protease system and alkaline myofibrils. Protease reduces the degradation of protein synthesis, and the direct consequence of decomposition is the decline of structural changes in myofibrils, the occurrence of steroid myopathy. There is no positive relationship between the dose of steroid and the treatment time. If the sudden increase in dose during long-term treatment may lead to steroid myopathy, it is also believed that the longer the dose, the longer the steroidal myopathy. In addition, fluoride-containing steroid preparations may be more susceptible to steroid myopathy.
Examine
an examination
Related inspection
Urinary creatine electromyography creatinine serum creatinine
Chronic steroid myopathy is insidious, and it is easy to miss clinical diagnosis based on the following points:
1. After treatment with steroids, muscle weakness and severe Cushing syndrome increased 24h uric acid excretion.
2. When steroid treatment of polymyositis, the symptoms of myasthenia were aggravated but the serum CK level was stable. Muscle weakness was observed after 24h creatinine increase or steroid addition.
3. Muscle biopsy showed selective type II muscle fiber atrophy with increased lipids in type I fibers.
4. After withdrawal of steroids from patients suspected of having steroid myopathy, the muscles can be relieved and the diagnosis can be confirmed.
Diagnosis
Differential diagnosis
1. It should be differentiated from signs and symptoms such as muscle weakness and muscle atrophy caused by brain and spinal cord lesions, especially when corticosteroids are used in large amounts after brain disease crisis. Detailed examination of medical history combined with CTMRI examination, etc., identification is not difficult.
2. Pay attention to distinguishing from other types of skeletal muscle diseases.
Laboratory inspection:
1. Serum muscle enzymes Chronic steroid myopathy is mostly normal; serum CK is often increased in the early stage of acute corticosteroid myopathy, and severe muscle necrosis may be associated with a significant increase in CK levels.
2. The excretion of creatinine is significantly increased and can occur early in the disease, and is therefore a sensitive indicator for the diagnosis of steroid myopathy.
Other auxiliary inspections:
1. Electromyography is non-specific and can be found to have myopathy characteristics. Common muscle fiber tremors Chronic steroid myopathy EMG is normal or slightly myogenic damage. Self-generated position can be neurogenic, myogenic or mixed, acute Can be accompanied by a large number of spontaneous activities.
2. Muscle biopsy chronic type only found a slight change in muscle fiber size, may be associated with type II fiber atrophy, few muscle fiber necrosis and inflammatory cell infiltration, electron microscopy found mitochondria accumulation and glycogen, lipid deposition, with mild muscle fiber atrophy These lesions are exactly the same as the characteristic changes in Cushing's disease, suggesting a diagnosis.
Acute type shows different degrees of muscle fiber necrosis and vacuolar degeneration, mainly involving type II fibers, which often have significant loss of thick myofilament.
