The commonest error in managing inflammatory myopathy is escalating immunosuppression against weakness that is no longer inflammatory. Muscle that has been replaced by fat and fibrosis is weak, and it stays weak whatever you add; the patient gets no better and acquires the toxicity anyway.
The distinction is rarely made by one test. A creatine kinase that has normalised while weakness persists points towards damage, but a normal CK does not exclude activity, particularly in dermatomyositis and in the anti-synthetase syndromes, where lung and skin can be active while muscle enzymes sit still. MRI with STIR distinguishes oedema from fatty replacement better than any blood test and is the single most useful investigation at this decision point. Function matters too: weakness that has been stable for months, without new symptoms, is more likely damage than smouldering disease.
The practical discipline is to write down which of the two you believe you are treating, and what would change your mind, before you escalate. If the answer is damage, the intervention is rehabilitation and a conversation about function, not another agent — and if the answer is uncertain, MRI before escalation is cheaper than six months of an added drug.
- Use MRI with STIR to separate active oedema from fatty replacement before escalating.
- Do not treat a rising CK without corresponding clinical or imaging activity, or a flat CK as proof of remission.
- Assess skin, lung and swallow separately from muscle — they do not move together.
- Record a functional measure at every visit so stability is demonstrable, not remembered.
- Refer for structured rehabilitation when the picture is damage; it is the effective treatment there.
Why it matters
Escalating against damage buys the patient toxicity and no benefit, and it is the commonest way myositis treatment goes wrong.
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