Inflammatory Myositis

DIES-associated neuropathy has a variety of chnical presentations, including painful symmetric or asymmetric sensorimotor neuropathy, distal sensory neuropathy, mononeuritis multiplex, and demyelinating polyneuropathy (Gherardi et al. 1998). Cranial neuropathy without evidence of a more generahzed neuropathy may occur, typically as a facial nerve palsy in association with parotidomegaly (Itescu et al. 1990 Brew 2003). The neuropathy develops subacutely over days to weeks. In some cases, muscle weakness may be a result of an inflammatory myositis (Kazi et al. 1996). 

Myositis may also have an infective basis. Viral myositis has been recorded in association with influenza and picomavirus infections, particularly those due to viruses of the Coxsackie group, and HIV infection is an increasingly common cause of myositis seen in routine practice. Fungal, bacterial, and parasitic myositis is seen much more rarely in North America and Europe than in tropical parts of the world, but in these regions these forms of infective myositis constitute a significant problem. In any survey of inflammatory muscle disorders, it is also necessary to consider other inflammatory conditions which affect muscle indirectly, but do not cause myositis in the strict sense of the word. In this group are to be found various forms of arteritis and fascitis and granulomatous conditions such as sarcoidosis. 

The sahcylates are useful in the treatment of minor musculoskeletal disorders such as bursitis, synovitis, tendinitis, myositis, and myalgia. They may also be used to relieve fever and headache. They can be used in the treatment of inflammatory disease, such as acute rheumatic fever, rheumatoid arthritis, osteoarthritis, and certain rheumatoid variants, such as ankylosing spondylitis, Reiter s syndrome, and psoriatic arthritis. However, other NS AIDS are usually favored for the treatment of these chronic conditions because of their lower incidence of GI side effects. Aspirin is used in the treatment and prophylaxis of myocardial infarction and ischemic stroke. 

It is a cyclic polypeptide with 11 amino acids. It selectively inhibits T-lymphocytes proliferation, IL-2 and other cytokine production. It is the most effective drug for prevention and treatment of graft rejection reaction. It is used in cardiac, hepatic, renal, bone marrow transplantation and as second line drug in rheumatoid arthritis, inflammatory bowel disease, dermato-myositis, bronchial asthma and certain other autoimmune diseases. 

Radiation recall consists of inflammatory reactions triggered by cytotoxic drugs in previously irradiated areas most are skin reactions. Gemcitabine has been implicated in several cases. The authors of a literature review discovered 12 cases of radiation recall caused by gemcitabine and reported a case of myositis in the rectus abdominis muscle of a patient with pancreatic adenocarcinoma as an effect of radiation recall (23). Most of the cases had inflammation of internal organs or tissues and 30% had dermatitis or mucositis. This is different from the effect of other agents that commonly cause radiation recall (anthracyclines and taxanes), with which 63% are skin reactions. Compared with anthracyclines and taxanes, the interval from the completion of radiation therapy to the start of chemotherapy is less with gemcitabine (median time 56 days, compared with 218 days for the taxanes and 646 days for doxorubicin). 

Myositis, autoimmune. Rare systemic inflammatory myopathies, including primary polymyositis, primary dermatomyositis, myositis associated with malignancy, childhood dermatomyositis, and myositis with multisystem autoimmune disease (e.g. mixed connective tissue disease, systemic sclerosis). Autoantibodies against aminoacyl-tRNA synthetases (e.g. anti-Jo-1), signal recognition particle (e.g. anti-SRP54), nuclear helicase (anti-Mi-2), tRNA and tRNA-protein complexes (e.g. anti-Mas), and translation factor (anti-KJ) have been described as myositis specific. 

Rider LG, Artlett CM, Foster CB, Ahmed A, Neeman T, Chanock SJ, Jimenez SA, Miller FW, for the Childhood Myositis Heterogeneity Collaborative Study Group (2000) Polymorphisms in the IL-1 receptor antagonist gene VNTR are responsible risk factors for juvenile idiopathic inflammatory myopathies. Clin Exp Immunol, 121 47-52. 

Love LA, Leff RL, Fraser DD, et al. A new approach to the classification of idiopathic inflammatory myopathy myositis-specific autoantibodies define useful homogeneous patient groups. Medicine (Baltimore) 1991 70 360-374. 

Selva-O Callaghan A, Labrador-Honillo M, Solans-Laque R, et al. Myositis-specific and myositis-associated antibodies in a series of eighty-eight Mediterranean patients with idiopathic inflammatory myopathy. Arthritis Rheum 2006 55 791-798. 

PM/DM is an idiopathic inflammatory myopathy however, a number of autoantibody subclassifications correlate with features of clinical disease. When clinical muscle weakness is encountered in the pulmonary clinic, one recent addition to the laboratory armamentarium is the myositis antibody panel. These panels of autoantibody tests can define antibodies to many of the aminoacyl-tRNA synthetases and sometimes help define a CTD when previously not suspected. The most common syndrome is now termed the antisynthetase syndrome when autoantibodies are present in the setting of variable components of fever, myositis, Reynaud s phenomenon, arthritis, mechanic s hands, and ILD (40). Alternative PM/DM diagnostic strategies include targeting muscle weakness with magnetic resonance imaging (MRI) or electromyography (EMG) in preparation for muscle biopsy. It should be noted that some forms of idiopathic myopathy, such as inclusion body myositis, have not been associated with ILD but can present with respiratory impairment due to muscle weakness (41). 

Carpenters, KarpatiG, Heller let al. (1978) Inclusion body myositis a distinct variety of idiopathic inflammatory myopathy. Neurology 28, 8-17. 

Inflammatory and autoimmune features of inclusion-body myositis... 

Sivakumar K, Semino-Mora, Dalakas MC. (1997) An inflammatory, familial, inclusion body myositis with autoimmune features and a phenotype identical to sporadic inclusion body myositis studies in 3 families. Brain 120, 653-661. 

Dalakas MC. (2004) Inflammatory disorders of muscle progress in polymyositis, dermatomyositis and inclusion body myositis. Curr Opin Neurol 17, 561-567. 

Schneider C, Gold R, Dalakas MC et al. (1996) MHC class I mediated cytotoxicity does not induce apoptosis in muscle fibers nor in inflammatory T cells studies in patients with polymyositis, dermatomyositis, and in-clnsion body myositis. J Neuropath Exp Neurol 55, 1205-1209. 

Sporadic inclusion-body myositis the main distinctive points of this condition from the GNE myopathy are the later onset and the presence of diffuse inflammatory infiltrates in the muscle sample. Also, in the sporadic condition the quadriceps is usually the first muscle to be involved. 

Inflammatory myopathies include a heterogeneous group of acquired and potentially treatable disorders caused by an autoimmune process (idiopathic inflammatory myosites) or infectious agents (pyo-myositis). Among ischemic conditions, we focus here mainly on diabetic muscle infarction and rhab-domyolysis. As previously stated, compartment syndromes are addressed in Chapter 15. 

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