IIM–ILD · PNEUMOGENESIS RESEARCH HUB
Phenotype atlas, assay interpretation, clinical practice and trial watch.
An antibody shifts probability; it is not a diagnosis by itself. Read it with age, organ pattern, CK, HRCT, cancer risk, co-antibodies and assay method.
RP-ILD · CADM
Signature: clinically amyopathic/hypomyopathic DM, ulcerative/palmar skin disease, arthritis; strongest MSA association with acute/subacute or rapidly progressive ILD. Think next: Ro52, ferritin/LDH, oxygenation, HRCT burden, infection risk under intensive immunosuppression.
LiteratureCANCER SIGNAL
Signature: adult dermatomyositis with strong malignancy association and characteristic cutaneous phenotype. ILD: comparatively uncommon; do not infer an MDA5-like lung phenotype from TIF1γ positivity.
LiteratureDM · MALIGNANCY / CALCINOSIS CONTEXT
Signature: severe muscle phenotype, dysphagia/edema; calcinosis is particularly relevant in juvenile disease. Adult cancer association varies across cohorts. ILD: not a classic dominant pulmonary serotype.
LiteratureCLASSIC DM
Signature: classic cutaneous DM with prominent muscle involvement and generally favorable treatment response. ILD: usually less prominent than in MDA5 or antisynthetase phenotypes.
LiteratureDM · DYSPHAGIA
Signature: skin disease may precede muscle disease; dysphagia can be prominent. ILD: reported, but pulmonary risk is less consistently defined than MDA5/ARS; commercial assay interpretation deserves care.
LiteratureIMNM · SEVERE MYOPATHY
Signature: severe proximal weakness, marked CK elevation and necrotizing pathology. ILD: can occur, but an independent MDA5-like RP-ILD phenotype is not established. Weak line-blot positivity without a matching phenotype deserves confirmation.
LiteratureIMNM · STATIN CONTEXT
Signature: necrotizing autoimmune myopathy, often but not exclusively associated with statin exposure; persistent weakness/CK despite statin withdrawal is a clue. ILD: not a defining feature; think muscle-first.
LiteratureSUPPORTIVE · NOT SPECIFIC
Signature: supportive marker for inclusion-body myositis when the clinical pattern fits. Caveat: not sufficiently specific to diagnose IBM alone; positivity also occurs in other autoimmune diseases.
LiteratureSEVERITY MODIFIER
Why interesting: a modifier rather than a stand-alone myositis subtype. Particularly informative with MDA5; in ASyS it tracks pulmonary burden/relapse more consistently than universal mortality.
LiteratureSCLEROMYOSITIS OVERLAP
Signature: myositis–systemic-sclerosis overlap, Raynaud, mechanic’s hands, ILD and sometimes calcinosis. Clinical pearl: the overlap phenotype can be more informative than forcing classification into “pure” myositis or SSc.
LiteratureOVERLAP · ASSAY CAUTION
Signature: overlap CTD with myositis and possible ILD; phenotype varies substantially by cohort. Caveat: interpret commercial assay positivity in clinical context.
LiteratureMCTD / OVERLAP
Signature: mixed connective-tissue/overlap phenotype with Raynaud, arthritis, myositis and pulmonary involvement. Think next: ILD and pulmonary hypertension are different pulmonary problems and should not be conflated.
LiteratureCTD CONTEXT
Systemic-sclerosis and overlap-context antibodies, not classic MSAs. Read them with the full CTD phenotype; pulmonary involvement may include ILD or pulmonary vascular disease.
LiteratureEducational and research material, not individual medical advice. Sources and the question bank have a separately recorded review date. Personal authorship or endorsement by Prof. Demosthenes Bouros is not claimed.