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so that ber loss, brosis, and residual thin and large bers in haphazard arrangement may eventually impart a dystrophic aspect to the lesions For all these reasons the pathologic picture can be correctly interpreted only in relation to the clinical and other laboratory data Guidelines for the interpretation of the muscle biopsy re ecting these comments, a critical step in correct diagnosis of the in ammatory myopathies, are given in the review by Dalakas and Hohlfeld In DM, there are several additional and distinctive histopathologic changes In contrast to the evident necrosis of single- bers of PM, DM is characterized instead by perifascicular muscle ber atrophy (referring to changes at the periphery of a fascicle, for reasons noted below) Moreover, the in ammatory in ltrates in DM predominate in the perimysial connective tissue, whereas in PM they are scattered throughout the muscle and are most prominent in relation to the muscle ber membrane and the endomysium The muscle lesions in dermatomyositis of childhood are similar to those of the adult form, only greatly accentuated In a biopsy sample, the diagnosis can be inferred from the perifascicular degeneration and atrophy of muscle bers Even more distinctive in DM are changes of a vasculitic nature in the small intramuscular blood vessels Endothelial alterations (tubular aggregates in the endothelial cytoplasm) and occlusion of vessels by brin thrombi are the main abnormalities Occlusion of small vessels also involves the intrafascicular nerves, so that the affected muscle may show both zones of infarction and denervation atrophy The same vascular changes underlie the lesions in the connective tissue of skin, subcutaneous tissue, and gastrointestinal tract This small vessel vasculitis is not seen in PM The perifascicular muscle ber atrophy is probably a result of an ischemic process set up by capillary occlusion Etiology and Pathogenesis The cause of idiopathic PM and DM, as the term indicates, is unknown All attempts to isolate an infective agent have been unsuccessful Several electron microscopists have observed virus-like particles in muscle bers, but their causative role has not been proved A polymyositic illness has not been induced in animals by injections of affected muscle Nevertheless, the notion that an autoimmune mechanism is operative in PM and DM is supported by the association of these disorders with a number of the more clearly established autoimmune diseases (myasthenia gravis, Hashimoto thyroiditis, scleroderma, Sjogren disease, rheumatoid ar thritis, Waldenstrom macroglobulinemia, agammaglobulinemia, and the other connective tissue diseases mentioned earlier) Further evidence of an autoimmune nature is the presence of speci c autoantibodies in nearly half of cases as described earlier Immunopathologic studies have partially substantiated an autoimmune mechanisms and suggested, in addition, that PM and DM can be distinguished from one another on the basis of their immunopathologic characteristics In DM, immune complexes, IgG, IgM, complement (C3), and membrane-attack complexes are deposited in the walls of venules and arterioles, indicating that the immune response is directed primarily against intramuscular blood vessels (Whitaker and Engel; Kissel et al) Such a response is entirely lacking in PM (and in IBM, discussed further on) Engel and Arahata have demonstrated a difference between the two disorders on the basis of the subsets and locations of lymphocytes that make up the intramuscular in ammatory aggregates In PM, there are a large number of activated T cells, mainly of the CD8 class, whereas B cells are sparse Moreover, T cells, accompanied by macrophages enclose and invade nonnecrotic muscle bers In DM, very few
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bers are affected in this manner, and the percentage of B cells at all sites is signi cantly higher than it is in PM Engel and Arahata interpreted these differences as indicating that the effector response in DM is predominantly humoral, whereas in PM the response is composed of cytotoxic T cells, clones of which have been sensitized to a yet unde ned surface antigen on the muscle ber Diagnosis This is secure if there is a subacutely evolving proximal weakness, typical changes in the muscle biopsy, EMG abnormalities of myopathic type with scattered brillation potentials, and elevated serum levels of CK For DM, the nding of one of the typical dermatic features is of great value However, all these criteria have been satis ed in only half of our cases, even in those who are later shown to be responsive to corticosteroids (see later) One must, therefore, often accept the diagnosis when most of the criteria are met Fever, pain beyond that attributable to arthritic involvement, or a greatly elevated sedimentation rate ( 100 mm/ h) suggest an alternative diagnosis The distinction from IBM, discussed further on, can be dif cult and depends to a large degree on the muscle biopsy As mentioned earlier, there has been considerable discussion regarding the diagnostic criteria for the in ammatory myopathies; some of these issues and reservations about the frequency with which the diagnoisis is made are articulated by Amato and Griggs The main point of controversy has been the proposal that true PM is rare and greatly overdiagnosed (see van der Muelen et al), a notion with which we do not fully agree In contrast, in ammatory myopathy coexists with numerous systemic diseases as discussed, and some authors consider it to be a syndrome rather than a disease The problem of determining which patients should have an extensive evaluation for a systemic malignancy and for connective tissue disease is a dif cult one Opinions vary on this point but we have adopted the practice of careful inspection of the chest x-ray on all patients and of undertaking a more extensive evaluation in patients over age 55 or in smokers of any age The evaluation in the latter group includes chest and abdominal computed tomography scans, stool guaiac CA-125, CEA, etc In patients with recent weight loss, anorexia, or other symptoms suggestive of malignancy we have included upper and lower endoscopy and even occasionally resorted to a body positron emission tomography scan The anti-Jo1 antibody test can be obtained in patients with interstitial lung disease or rheumatoid arthritis (it is not referable to an underlying cancer) A routine evaluation for the conventional connective tissue diseases is only necessary if there is clinical evidence to support such a diagnosis In addition to these issues we call attention to the following problems that have arisen repeatedly in connection with the diagnosis of PM: The patient with proximal muscle weakness incorrectly diagnosed as having progressive muscular dystrophy Points in favor of PM are (a) lack of family history; (b) older age at onset; (c) more rapid evolution of weakness; (d) evidence, past or present, of other connective tissue diseases; (e) high serum CK and aldolase values; ( f) many brillation potentials on EMG; (g) marked degeneration and regeneration in muscle biopsy; and nally, if there is still doubt, (h) unmistakable improvement with corticosteroid therapy 2 The patient with a connective tissue disease (rheumatoid arthritis, scleroderma, lupus erythematosus, Sjogren syndrome) suspected of having PM in addition Pain in these conditions 1
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