The diagnosis of the exact subtype of inflammatory myopathy is based on the combination of clinical history, tempo of disease progression, pattern of muscle involvement, muscle enzyme levels, electromyographic findings, muscle-biopsy analysis, and for some conditions, the presence of certain autoantibodies.
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Initially used for the treatment of immunodeficiencies, intravenous immunoglobulins (IVIg) have increasingly been used as immunomodulatory agent in autoimmune and inflammatory disorders. The mode of action of IVIg is enigmatic, probably involving Fc-dependent and/or F(ab’)2-dependent non-exclusive mechanisms of action. IVIg broadly interacts with the different components of the immune system: cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also has an impact on effector functions of immune cells. These mechanisms of action of IVIg reflect the importance of natural antibodies in the maintenance of immune homeostasis.
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Classic chronic inflammatory demyelinating polyneuropathy (CIDP) is characterized by the occurrence of symmetrical weakness in both proximal and distal muscles that progressively increases for more than two months (setting this condition apart from the Guillain–Barré syndrome, which is self-limited). The condition is associated with impaired sensation, absent or diminished tendon reflexes, an elevated cerebrospinal fluid protein level, demyelinating nerve-conduction studies, and signs of demyelination in nerve-biopsy specimens. The course can be relapsing or chronic and progressive, the former being much more common in young adults.
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These criteria are applied by testing the median, ulnar (stimulated below the elbow), peroneal (stimulated below the fibular head), and tibial nerves on one side of the body. During testing, limb temperature should be no less than 33°C at the palm and no less than 30°C at the external malleolus.
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