Inflammatory myopathies

Patient–physician discordance in idiopathic inflammatory myopathies: a longitudinal analysis of links to disease activity and damage

Rheumatology (Oxford)Published Prospective cohort study

Authors' conclusion

Patient-physician discordance in IIM is an active, upstream driver of future functional loss, mediated significantly by pain, rather than a mere reflection of existing objective damage.

Study context

Population
Patients with idiopathic inflammatory myopathies (IIM) (DM, PM, overlap myositis, anti-synthetase syndrome) in the MyoCite IIM cohort128 followed longitudinally
Participants
244 patients
Outcome
Prevalence of patient–physician discordance (PGA vs PhGA difference ≥ ±1 cm on 0-10 cm scale)
Follow-up
Baseline
Methodological detailslongitudinal, linear mixed-effects models, bidirectional mediation models
  • Longitudinal
  • Linear mixed-effects models
  • Bidirectional mediation models

Main finding

As reported in the abstract

Clinically significant baseline discordance

Clinically significant baseline discordance

19.3%

Positive discordance (PGA > PhGA)

16.8%

Observational data: associations, not effects.

Further findings

Discordance over 24 months

Persistent discordance subset, with high subjective pain despite normalized muscle enzymes
25%
Discordance narrowed with treatment

Baseline positive discordance predicting poorer functional capacity (HAQ) · 1 year

Strongly predicted poorer HAQ
P = 0.034

Objective muscle weakness (MMT-8) as driver of discordance

MMT-8 β
−0.013 (95% CI −0.022 to −0.004)
Standardized β (P = 0.006)
−0.155
  • Fluctuations had minimal absolute impact
  • n = 191 in linear mixed-effects models

Mediation of future functional disability by unmanaged pain

Proportion mediated (P < 0.001)
32.1%
Reverse mediation (HAQ driving discordance via pain) not statistically significant

Original publication

Patient–physician discordance in idiopathic inflammatory myopathies: a longitudinal analysis of links to disease activity and damage. Rheumatology (Oxford). Published 9 June 2026. doi:10.1093/rheumatology/keag298

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