Dermatomyositis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Pathophysiology

The diagnosis of dermatomyositis can be confirmed by muscle biopsy, EMG, and blood tests. It should be noted, however, that only muscle biopsy is truly diagnostic (pathognomic); liver enzymes and EMG are relatively non-specific. Liver enzymes, specificly creatine phosphokinase (CPK), are the major tool in assessing the progress of the disease and/or the efficacy of treatment. On the muscle biopsy, there are two classic microscopic findings of dermatomyositis. They are:

  • A mixed B- and T-cell perivascular inflammatory infiltrate
  • Perifascicular muscle fiber atrophy

Dermatomyositis is associated with autoantibodies, especially anti-Jo1 antibody.[1]

Mechanism

The mechanism is conjectured to be complement-mediated damage of microscopic vessels with muscle atrophy and lymphocytic inflammation secondary to tissue ischemia.[2]

References

  1. Ghirardello, A (2006). "Clinical implications of autoantibody screening in patients with autoimmune myositis". Autoimmunity. 39 (3): 217–221. doi:10.1080/08916930600622645. PMID 16769655. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  2. Benveniste, O (2004). "Pathogenesis of primary inflammatory myopathies". Presse Médicale. 33 (20): 1444–1450. doi:10.1016/S0755-4982(04)98952-X. PMID 15611679. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)

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