The Gestalt of Early Arthritis in Europe: Beyond expert opinion alone


Research in rheumatology has successfully focused on early diagnosis and early intervention, resulting in reduced burden of disease. However, the ‘early aggressive’ approach may also have ‘side effects’: overdiagnosis/overtreatment. Disentangling early arthritis (EA) patients with a ‘full blown disease’ prognosis and those who may fare a milder course or even go into spontaneous remission is a real challenge at presentation. Expert-based classification criteria have been revised to capture these early patients better but suffer from circularity. We propose an analytical, non-expert-based, approach that allows us to gain a more unbiased insight into the concept of EA, by investigating EA’s ‘latent constructs’ (latent class analysis) and how these constructs change over time (latent transition analysis).

Facts and Figures

Project Lead
R Landewé
University of Amsterdam
FOREUM research grant: € 226.186

Meet the Team

Project Lead

R Landewé
University of Amsterdam
D van Schaardenburg
University of Amsterdan
A van der Helm-van Mil
UMC Leiden
S Ramiro
Leiden University
S A Bergstra
Leiden University
B Combe
University of Montpellier
A Sepriano
Nova Medical School
M de Wit
E Frazão Mateus
A Kent
B T van Dijk
Leiden University Medical Centre

Final results

We identified five distinctive and recognizable early arthritis (EA) phenotypes using an analytical technique (latent class analysis) which circumvents the experts’ diagnosis. Radiographic progression primarily occurs in EA patients with autoantibodies and acute phase reactants elevation (a phenotype we labelled as autoimmune inflammatory polyarthritis). Phenotypes that deviate from this classical ‘RA-construct’ have negligible structural progression, but remarkably, similar long-term disability, quality of life and work ability. Our study therefore provides evidence that clinicians and researchers should aim at developing treatment strategies beyond those targeting the prevention of irreversible joint damage, in order to further improve the lives of people with EA.

Lay Summary

The clinical presentation of early arthritis (EA) is variable, and patients may evolve differently over time. Some will develop rheumatoid arthritis (RA) or psoriatic arthritis; while others may remain with mild symptoms or even become symptom free. Distinguishing, at disease onset, which patients will evolve to a more severe disease from those who will not, can help clinicians in managing EA in clinical practice. Experienced clinicians will intuitively recognize different forms of disease presentation, but they will often be influenced by preconceived ideas about which characteristics are more important to their concept of RA. Using data from three cohorts with more than 5,000 EA patients followed up to 24 years we evaluated the phenotypes of EA using a data-driven approach and whether these phenotypes have different prognostic implications. We identified five distinctive EA phenotypes. Two with symmetrical polyarthritis emerged; One of these, labelled as autoimmune inflammatory polyarthritis (AIPA), had high likelihood of inflammatory markers (e.g., CRP) and autoantibody-positivity, while the other (mild-inflammatory polyarthritis; MIPA) had not. Another phenotype had less joints involved (oligoarthritis of upper limbs; OAUL) and could be subdivided into autoimmune OAUL and mild-inflammatory OAUL. A fifth phenotype had oligoarthritis of lower limbs. Joint damage was worse in patients with inflammatory markers/autoantibodies (AIPA) than in those without (MIPA). No meaningful differences across phenotypes in disability, quality of live or work ability over time were found. This study demonstrates that clinicians should not only aim at preventing joint damage, but look beyond structural progression in order to further improve the lives of people with EA.


EULAR Abstratcts

  • POS0318  Sepriano A, Van Dijk B, Ramiro S, et al. DISTINCTION AND PROGNOSIS OF EARLY ARTHRITIS PHENOTYPES: AN ANALYSIS IN THREE EUROPEAN COHORTS Annals of the Rheumatic Diseases 2023;82:403-404.

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