Clinical implications

• Do not assume muscle symptoms in IBD are polymyositis.
• Classic inflammatory myopathy causes subacute, symmetric proximal weakness: difficulty rising from a chair, climbing stairs, lifting the arms, or swallowing. Pain may occur but true weakness is the leading feature.
• “Polymyositis” is now used cautiously because mimics are common. These include dermatomyositis, immune-mediated necrotizing myopathy, antisynthetase syndrome, inclusion-body myositis, muscular dystrophy, endocrine disease, infection, and medication-related myopathy.

Important differential diagnoses in a patient with IBD

1. Glucocorticoid myopathy
   Painless proximal weakness after sustained corticosteroid exposure. CK is usually normal, helping distinguish it from active inflammatory myositis.
2. Anti-TNF-associated inflammatory myopathy
   Infliximab, adalimumab, and other TNF inhibitors have rarely been associated with new or worsening dermatomyositis/polymyositis-like syndromes. This is based mainly on case reports and small series, so it should prompt specialist review rather than automatic attribution. A review of inflammatory myopathies notes that TNF inhibitors can be ineffective and may trigger or exacerbate disease in some patients.
3. Crohn-related gastrocnemius myalgia syndrome
   This is a rare focal inflammatory syndrome, usually with calf pain and MRI abnormalities, rather than generalized proximal weakness. It is not the same as classic polymyositis.
4. Electrolyte, nutritional, or metabolic myopathy
   Consider hypokalemia, hypophosphatemia, vitamin D deficiency, thyroid disease, malnutrition, and infection, particularly with severe IBD or recent hospitalization.

Suggested evaluation

• CK, aldolase, AST/ALT, LDH
• ESR/CRP, though these may reflect IBD activity
• Thyroid function, electrolytes, vitamin D, medication review
• Myositis antibody panel, including antisynthetase antibodies
• MRI of symptomatic muscle to identify active inflammation and guide biopsy
• EMG when diagnosis remains uncertain
• Muscle biopsy when needed to confirm subtype and exclude mimics
• Dysphagia and pulmonary assessment if there are swallowing symptoms, dyspnea, cough, or suspected interstitial lung disease

Treatment principles

• Active inflammatory myopathy is often initially treated with systemic glucocorticoids, then a steroid-sparing immunosuppressant such as methotrexate, azathioprine, mycophenolate, tacrolimus, IVIG, rituximab, or other targeted therapy depending on phenotype and organ involvement.
• Coordinate therapy with the IBD team, since some agents can address both immune disorders, while others may be appropriate for one but not the other.
• If symptoms begin after anti-TNF exposure, review temporal association, autoantibodies, CK, MRI and biopsy findings before deciding whether to stop or change biologic therapy.
• Screen for infection before escalating immunosuppression, especially if already receiving corticosteroids, thiopurines, biologics, or JAK inhibitors.

Seek urgent assessment if

• dysphagia, choking, nasal regurgitation, or aspiration
• breathlessness, reduced cough strength, or rapidly progressive weakness
• dark urine or marked CK elevation suggesting rhabdomyolysis
• fever or immunosuppression with suspected infection