Steroid myopathy

Introduction to steroid myopathy In 1932, Chusing first observed that corticosteroids can cause muscle atrophy and muscle weakness, and proposed the concept of steroid myopathy. This disease is also known as corticosteroid polymyopathy. Steroid myopathy is not uncommon because of the widespread use of steroids in the clinic. Steroid myopathy can be divided into acute and chronic types. Chronic steroid myopathy is more common than acute, and the onset is concealed. The main manifestation is that the pelvic muscles are weak and gradually progress, affecting the scapular muscles and the proximal muscles of the extremities. Subjective muscle weakness symptoms are often heavier than objective muscle strength tests. Myalgia is common. After steroid reduction, myalgia disappears, indicating that myalgia is one of the symptoms of steroid myopathy. basic knowledge Sickness ratio: 0.0012% Susceptible people: no special people Mode of infection: non-infectious Complications: cough

Etiology of steroid myopathy

(1) Causes of the disease

Corticosteroid polymyopathy is a type of muscle lesion caused by the widespread use of corticosteroids, similar to Cushing syndrome with muscle changes.

(two) pathogenesis

The exact pathogenesis is unknown. It may affect the metabolism of proteins, imbalance the synthesis and decomposition of muscle contractile components (such as myosin, contractile protein), leading to clinical weakness and muscle atrophy. Steroids can inhibit RNA synthesis. Reduce protein translation efficiency, thereby blocking protein synthesis. Steroids can also promote the breakdown of muscle contractile proteins through ubiquitin protease system and alkaline myofibrillar protease. The synthesis of myocyte protein is reduced. The direct consequence of decomposition is myofibrillar. The structural changes, functional decline, steroid myopathy, and steroid dose and treatment time are not positively related. If the sudden increase in dose during long-term treatment may lead to steroid myopathy, others think that the longer the dose, the longer the treatment, the more It is prone to steroid myopathy, and fluorosteroid preparations may be more likely to cause steroid myopathy.

Acute steroid myopathy is characterized by a large number of muscle fiber necrosis, regeneration and phagocytosis, and extensive muscle fiber atrophy. Both types of fibers are involved. The main pathological changes of chronic steroid myopathy are selective type II muscle fiber atrophy, muscle necrosis and regeneration. It is not obvious, so some scholars have suggested that "steroidal muscle atrophy" is more accurate than "steroidal myopathy" in such patients. Ultrastructural observation shows a slight increase in glycogen and lipid between submucosal and myofibrils, mitochondria transsexual.

Steroid myopathy prevention

The male anabolic hormone phenylpropionate can partially counteract the pro-protein breakdown of steroids and can be used to prevent the development of steroid myopathy.

Steroid myopathy complications Complications cough

Can be complicated by muscle weakness, clinical manifestations of swallowing, coughing, respiratory distress, difficulty and even stop the serious condition.

Symptoms of steroid myopathy common symptoms dyspnea myasthenia gravis renal failure reflex disappearing sclerosis protein urinary tremor toxemia long-term use of cortic... Inflammatory cell infiltration

1. 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 the same as the degree of muscle weakness There is no obvious correlation. Some people think that fluorine-containing hormone is more likely to cause the disease than other hormones. In fact, all corticosteroids can cause disease. The mechanism of corticosteroid-induced disease is unknown, but amino acid intake and protein synthesis are found in corticosteroid-treated animals. The level has dropped significantly.

Clinical features:

(1) The muscles of the proximal muscles and limbs of the limbs are weak, generally symmetrically distributed, first invading the proximal end of the lower limbs, gradually progressing to the scapular muscles, and finally affecting the distal muscles of the limbs.

(2) Serum CK and aldolase are generally normal, EMG is normal or slightly myogenic damage, no self-generating position, muscle biopsy only found a slight change in muscle fiber size, may be associated with type II fiber atrophy, few muscle fiber necrosis and inflammatory cells Infiltration, electron microscopy revealed mitochondrial accumulation and glycogen, lipid deposition, and mild atrophy of mild muscle fibers. These lesions are exactly the same as the characteristic changes of Cushing disease, which may prompt diagnosis.

2. Acute corticosteroid myopathy is a critical illness myopathy or acute quadric plegic myopathy caused by corticosteroids.

Patients are often treated with high-dose corticosteroids for severe refractory asthma or various systemic diseases, as well as critically ill patients such as sepsis, sometimes with neuromuscular blocking agents such as muscle relaxant Pankuronin. (pancuronium bromide) can promote the onset, and can also be caused by the combination of aminoglycoside antibiotics, often with severe muscle weakness when the systemic disease improves.

Animals with a large amount of corticosteroids after muscle denervation may have a selective myosin deficiency, which is a characteristic manifestation of this disease. Restoration of myosin depends on nerve regeneration instead of stopping steroids, but multiple Patients with sclerosing have not found corticosteroid myopathy with high-dose corticosteroids. Panegyres et al observed a patient with myasthenia gravis who developed severe myosin-deficient myopathy after treatment with high-dose methylprednisolone.

Clinical features:

(1) rapid onset, extensive involvement of limb muscles and respiratory muscles, manifested as severe systemic muscle weakness and dyspnea, sputum reflexes are normal or weakened, or even disappear, do not involve the sensory system, most patients after several weeks of withdrawal Improved, a small number of patients with muscle weakness can last for 1 year.

(2) serum CK is often increased in the early stage of the disease, severe muscle necrosis may be associated with significant increase in CK levels, myoglobinuria and renal failure, EMG can be found in myopathy, common muscle fiber tremor, muscle biopsy shows varying degrees of muscle fiber necrosis and Cavitation degeneration, mainly involving type II fibers, often has significant loss of thick myofilament.

Examination of steroid myopathy

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.

3. EMG examination is non-specific, can be found to have myopathy characteristics, common muscle fiber tremor, chronic steroid myopathy EMG is normal or slightly myogenic damage, no self-generating position, can be neurogenic, myogenic or mixed Acute type can be accompanied by a large number of spontaneous activities.

4. Muscle biopsy chronic type only found a slight change in muscle fiber size, can 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 varying degrees of muscle fiber necrosis and vacuolar degeneration, mainly involving type II fibers, often with significant loss of thick myofilament.

Diagnosis and diagnosis of steroid myopathy

Diagnostic criteria

Chronic steroid myopathy is insidious and easy to miss diagnosis. The clinical diagnosis is mainly based on the following points:

1. After treatment with steroids, muscle weakness and severe Cushing syndrome occurred, and 24h uric acid excretion increased.

2. When steroid treatment of polymyositis, the symptoms of myasthenia were aggravated, but serum CK levels were stable, and muscle weakness was observed after 24 hours of creatinine increase or steroid addition.

3. Muscle biopsy showed selective type II muscle fiber atrophy with increased lipids in type I fibers.

4. For patients suspected of having steroid myopathy, after withdrawal of steroids, muscle weakness can be alleviated and the diagnosis can be confirmed.

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 medical history, combined with CT and MRI examinations, is not difficult to identify.

2. Pay attention to distinguishing from other types of skeletal muscle diseases.

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