Inflammatory myopathy(Polymyositis & Dermatomyositis): Diagnosis & Treatments
Diagnosis
Creatine kinase (CK) is the most sensitive enzyme in the diagnosis of inflammatory myopathy among serum muscle enzymes. If the disease is active, it can increase up to 50 times normal. Generally, CK levels are proportional to disease activity, and SGOT, SGPT, LDH, and adolase are also increased.
In PM, inflammation is the primary factor. T cells mainly infiltrate into the muscle bundles, surrounding normal muscle cells individually, and eventually muscle fiber necrosis and predation. MHC-I molecules are scattered in the sarcolemma, which increases the expression of MHC-I molecules in muscle fibers that are not infiltrated into CD8 + cells. The CD8 / MHC-I molecule lesion is the most essential finding in establishing the diagnosis and is a helpful finding in excluding the secondary non-specific inflammatory muscle disease. If the disease is chronic, connective tissues increase and may react positively to alkaline phosphate
Inflammatory myopathy is characterized by an increase in myogenic potential, such as short duration, low amplitude, polyphasic motor unit action potential, fibrillation, complex repetitive discharge, and positive sharp waves, which are observed when myoclonus contracts sharply. Lt; / RTI & gt;
Treatments
The goal of treatment is to restore the patient's strength, to lower CK levels by considering CK as a secondary treatment value, and to eliminate extramuscular manifestations such as fever, dyspnea, and rash. It is important to observe clinical features that restore muscle strength rather than rely on lowering CK levels.
For the treatment of polymyositis, Predinsone is initially suitable for oral administration. High dose at 1 mg / kg in the early stages of possible disease, and slowly lose weight to 1 mg / kg every other week for 3 to 4 weeks. It is also necessary to assess the degree to which the drug responds to the drug after confirming that muscle strength has recovered since the start of Predisone. The proximal leg strength of the patient is assessed by NHISS lower limb strength index 0-4. Long-term administration of prednisone may cause steroid myopathy. This is a situation where the activity of polymyopathy has been increased or drug resistance has developed. If unclear, try to adjust the dose of prednisone to find the cause of recurrent weakness, which is helpful for subsequent treatment. More than 75% of patients receiving prednisone require additional immunosuppressant therapy. Commonly used immunosuppressants include Azathioprine, Methotrexate, Mycophenolate, and Monoclonal anti-CD20 (Rituximab).
Creatine kinase (CK) is the most sensitive enzyme in the diagnosis of inflammatory myopathy among serum muscle enzymes. If the disease is active, it can increase up to 50 times normal. Generally, CK levels are proportional to disease activity, and SGOT, SGPT, LDH, and adolase are also increased.
In PM, inflammation is the primary factor. T cells mainly infiltrate into the muscle bundles, surrounding normal muscle cells individually, and eventually muscle fiber necrosis and predation. MHC-I molecules are scattered in the sarcolemma, which increases the expression of MHC-I molecules in muscle fibers that are not infiltrated into CD8 + cells. The CD8 / MHC-I molecule lesion is the most essential finding in establishing the diagnosis and is a helpful finding in excluding the secondary non-specific inflammatory muscle disease. If the disease is chronic, connective tissues increase and may react positively to alkaline phosphate
Inflammatory myopathy is characterized by an increase in myogenic potential, such as short duration, low amplitude, polyphasic motor unit action potential, fibrillation, complex repetitive discharge, and positive sharp waves, which are observed when myoclonus contracts sharply. Lt; / RTI & gt;
Treatments
The goal of treatment is to restore the patient's strength, to lower CK levels by considering CK as a secondary treatment value, and to eliminate extramuscular manifestations such as fever, dyspnea, and rash. It is important to observe clinical features that restore muscle strength rather than rely on lowering CK levels.
For the treatment of polymyositis, Predinsone is initially suitable for oral administration. High dose at 1 mg / kg in the early stages of possible disease, and slowly lose weight to 1 mg / kg every other week for 3 to 4 weeks. It is also necessary to assess the degree to which the drug responds to the drug after confirming that muscle strength has recovered since the start of Predisone. The proximal leg strength of the patient is assessed by NHISS lower limb strength index 0-4. Long-term administration of prednisone may cause steroid myopathy. This is a situation where the activity of polymyopathy has been increased or drug resistance has developed. If unclear, try to adjust the dose of prednisone to find the cause of recurrent weakness, which is helpful for subsequent treatment. More than 75% of patients receiving prednisone require additional immunosuppressant therapy. Commonly used immunosuppressants include Azathioprine, Methotrexate, Mycophenolate, and Monoclonal anti-CD20 (Rituximab).
