Polymyositis vs Dermatomyositis and inclusion body myositis
How to tell Polymyositis and Dermatomyositis and inclusion body myositis apart when a board question makes them look alike.
Polymyositis is proximal weakness without rash; dermatomyositis is proximal weakness plus rash and malignancy risk; inclusion body myositis is older, distal/asymmetric, and rimmed-vacuole disease.
Side by side
Polymyositis causes symmetric proximal muscle weakness without rash, elevated CK, endomysial CD8 T-cell inflammation, and difficulty rising from chairs or climbing stairs.
Dermatomyositis adds heliotrope rash, Gottron papules, perifascicular atrophy, and malignancy risk; inclusion body myositis is older-age distal/asymmetric weakness with rimmed vacuoles.
Cell-mediated immune injury targets skeletal muscle fibers, producing inflammatory myopathy and muscle enzyme leakage.
Dermatomyositis is complement-mediated microangiopathy, while inclusion body myositis has degenerative inflammatory vacuoles and poor steroid response.
High CK, proximal weakness, EMG myopathy, and endomysial inflammation support polymyositis.
Heliotrope rash and perifascicular atrophy support dermatomyositis; finger flexor/quadriceps weakness with rimmed vacuoles supports inclusion body myositis.
The trap
All cause muscle weakness and high CK, so rash, age, distribution, histology, and treatment response separate them.
The repair move
For inflammatory myopathy, check rash, age, weakness distribution, biopsy pattern, and malignancy association.
Try a free question
CoreA 38-year-old woman has 5 months of progressive symmetric proximal muscle weakness, difficulty climbing stairs and rising from a chair. There is no rash. Labs: CK 4,800 U/L, aldolase elevated, ESR 38 mm/hr. EMG shows myopathic motor unit potentials. Muscle biopsy shows endomysial CD8 T-cell infiltrate around non-necrotic fibers. Which diagnosis is most likely?
Show answer and explanation
Answer: A. Polymyositis. Polymyositis is symmetric proximal muscle weakness WITHOUT rash, with markedly elevated CK and endomysial CD8 T-cell infiltrate; treatment is high-dose corticosteroids with steroid-sparing agents.
Why the other choices are tempting
- B. Dermatomyositis adds heliotrope rash, Gottron papules, and perifascicular atrophy with increased malignancy risk.
- C. Inclusion body myositis affects older men with distal finger flexor and quadriceps weakness, rimmed vacuoles, and slow progression.
- D. Statin-induced myopathy presents with myalgia and modest CK elevation, often resolving with discontinuation.
- E. Hypothyroid myopathy has muscle cramps, slow reflexes, and elevated TSH.
Flashcards
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What rash supports dermatomyositis?
Heliotrope rash or Gottron papules support dermatomyositis.
What biopsy pattern supports inclusion body myositis?
Rimmed vacuoles support inclusion body myositis.
Quick answers
What is the fastest way to tell Polymyositis from Dermatomyositis and inclusion body myositis?
Polymyositis is proximal weakness without rash; dermatomyositis is proximal weakness plus rash and malignancy risk; inclusion body myositis is older, distal/asymmetric, and rimmed-vacuole disease.
What is the key clue for Polymyositis?
Polymyositis causes symmetric proximal muscle weakness without rash, elevated CK, endomysial CD8 T-cell inflammation, and difficulty rising from chairs or climbing stairs.
What is the key clue for Dermatomyositis and inclusion body myositis?
Dermatomyositis adds heliotrope rash, Gottron papules, perifascicular atrophy, and malignancy risk; inclusion body myositis is older-age distal/asymmetric weakness with rimmed vacuoles.
What is the common trap with Polymyositis vs Dermatomyositis and inclusion body myositis?
All cause muscle weakness and high CK, so rash, age, distribution, histology, and treatment response separate them.