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Q: Doc, doc, have a patient with subacute weakness and suspected myositis. Why in the world are we considering these humongous panels of autoantibodies? Can’t we just do a muscle biopsy?
A: Just 2 reasons - diagnosis and prognosis. We send myositis specific antibodies (MSA) and myositis associated antibodies (MAA). MSA are antibodies specifically associated with inflammatory myopathies.
MSA also help to split the different phenotypes of individual inflammatory myopathy syndromes. You don’t have to send them all, but it would be good to understand why we send some or all.
A: Dermatomyositis can be associated w antibodies against Mi2 (skin manifestations, good response to therapy), TIF1 (cancer), NXP2 (cancer, calcinosis), MDA5 (vasculitic skin lesions, ILD, poor prognosis), SAE (ILD). 70% of dermatomyositis is a/w with 1 of these autoantibodies.
A: Inclusion body myositis is associated with NT51a antibodies. 70 percent of cases are associated with this antibody.
A: Necrotizing autoimmune myopathy is associated with antibodies against HMGCR (40 percent of cases) and SRP (12 percent of cases, worse response to immunotherapy).
A: Antisynthethase syndrome is associated with antibodies against Jo1 (fever, arthritis, mechanics hands, 50 percent ILD) and other anti-synthethase antibodies like PL7, PL12 (90 percent ILD). Development of ILD means worse prognosis.
A: What this means is that in the correct clinical context, MSA can help with diagnosis of inflammatory myopathy, not necessarily with the need for muscle biopsy. MSA can predict prognosis - and which patients need closer malignancy and closer ILD screening.
A: MAA are associated with diseases that can cause muscle inflammation - like Sjogren’s, lupus, systemic sclerosis. They may suggest disease phenotype - for example anti-Ro with anti-Jo1 is associated with worse arthritis and myositis.
A: Or possible complications - antibodies against pml-scl, RNA polymerase 3, topoisomerase, centromere suggest systemic sclerosis which can cause renal crisis with high dose steroids which are typically used in inflammatory myopathies.
A: Most importantly of course, you need to know common clinical presentations of each of these inflammatory myopathies - some have skin changes, some have involvement of other organs and some only muscle - these autoantibodies are helpful only in the correct clinical context.
A: Remember that muscle is forgiving - it regenerates, there’s leeway for titering immunotherapy - but lung is a far less forgiving organ. Death in anti-synthethase syndrome is usually caused by ILD. Screen early for ILD and treat early and aggressively.
A: By the same token, screen for malignancy in high risk patients - patients with dermatomyositis and polymyositis. Remember the autoantibodies associated with increased cancer risk.
A: Now you know how to split and lump the auto-antibodies and use some or all of them for diagnosis and prognosis of inflammatory myopathies. Neuromuscular, out.
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