Background: Patients with chronic back pain (CBP) of less than two-years (2y) duration suspected of axial spondyloarthritis (axSpA) referred to the rheumatologist can be reliably diagnosed.[1] However, the time to diagnosis from symptom onset and its determinants remain poorly studied in patients with recent-onset CBP. Objectives: Investigate the time to diagnosis after symptom onset in patients with CBP suspected of axSpA referred to the rheumatologist and assess the main determinants for an early axSpA diagnosis. Methods: We analysed the 2y-data from SPACE, a multi-centre cohort of patients (<45y) with CBP (≥3 months, ≤2y) of unknown origin. The diagnostic work-up comprised evaluation of clinical SpA features, acute phase reactants, HLA-B27, radiographs and MRI (sacroiliac joints and spine), with repeated assessments. At each visit (baseline, 3-month, 1y and 2y), rheumatologists reported a diagnosis of axSpA or non-axSpA with level of confidence (LoC; 0-not confident at all to 10-very confident). We used survival analysis methodology to compute time to event and its determinants. An event was defined as a diagnosis of axSpA given by the rheumatologist with a LoC≥7 either at 2y (complete follow-up) or last observation (incomplete follow-up) or, if the LoC<7, a diagnosis of axSpA should be present in ≥2 last consecutive visits. The time to event (months) was computed from the start of the axial symptoms until the first visit in which the event occurred. Patients without the event were censored at 2y or at loss to follow-up. SpA features were considered at the time of diagnosis as 'once a feature, always a feature'. Local reports were used with standardization (ASAS definitions2), except for imaging (local assessment: radiographs [mNY criteria]; MRI [presence of inflammatory and/or structural lesions]). Median survival times were computed overall and for each SpA feature (un-/adjusted for covariates). Univariable and multivariable Cox regression models were fitted to identify axSpA diagnosis determinants. From the final multivariable Cox regression model, subgroup comparisons could be performed for the time to event for each SpA feature (ever present vs absent), while adjusting for the effect of the remaining SpA features in the model (adjusted Kaplan-Meier curves, Figure 1). Results: The SPACE cohort included 548 unknown-origin CBP patients with information on diagnosis, LoC and symptom duration. These were included in the survival analysis (mean [standard deviation, SD] age and symptom duration: 31 [8] years and 13 [7] months, 35% male, and 41% HLA-B27 positive). Of these, 215 (39%) received a 2y diagnosis of axSpA. As expected, the axSpA group showed a higher prevalence of SpA features (Table 1). The median time to diagnosis was 35 months. The lowest adjusted median survival times (up to 24 months) were observed for sacroiliitis on radiographs (8 months), sacroiliitis on MRI (12 months), inflammatory bowel disease (12 months), HLA-B27 positivity (18 months) and peripheral arthritis (24 months) (Table 1). Visual representations of the median survival times and probability of axSpA diagnosis are given in Kaplan-Meier curves (Figure 1). A contrasting example of a SpA feature not determining the diagnosis (inflammatory back pain) is also shown. Multivariable Cox regression models emphasized HLA-B27 positivity and sacroiliitis on MRI as the strongest determinants implying a 4.2- and 3.5-times adjusted higher likelihood for the diagnosis of axSpA, respectively (Table 1). Peripheral arthritis, anterior uveitis or psoriasis implied each ~2-times higher risk for the axSpA diagnosis. Good response to NSAIDs, male sex and a younger age increased the probability for the diagnosis of axSpA slightly. Conclusion: Half of the patients with CBP suspected of axSpA referred to the rheumatologist received the diagnosis within the first 35 months after symptom onset. HLA-B27 positivity, sacroiliitis on imaging and peripheral arthritis are the SpA features most contributing to an early (up to 2y after symptom onset) diagnosis of axSpA in these patients. REFERENCES: [1] Marques ML, Ann Rheum Dis. 2024 [epub ahead of print]; ²Sieper J, Ann Rheum Dis. 2009;68 Suppl 2:ii1-44. Acknowledgements: NIL. Disclosure of Interests: Mary Lucy Marques: None declared, Désirée van der Heijde AbbVie, ArgenX, Bayer, BMS, Cyxone, Eisai, Galapagos, Gilead, Glaxo-Smith-Kline, Janssen, Lilly, Novartis, Pfizer, Takeda, UCB Pharma. Director of Imaging Rheumatology bv., Liese J.E. de Bruin: None declared, Miranda van Lunteren: None declared, Robert Landewé AbbVie, Eli-Lilly, Janssen, Galapagos, Gilead, Novartis, Pfizer, UCB. Director of Imaging Rheumatology bv., Karen Minde Fagerli: None declared, Maikel van Oosterhout: None declared, F. A. van Gaalen MSD, AbbVie, Novartis and BMS., Novartis, Sofia Ramiro AbbVie, Eli Lilly, Janssen, MSD, Novartis, Pfizer, Sanofi, UCB., AbbVie, Galapagos, MSD, Novartis, Pfizer, UCB.
No takes yet. Share an insight, caveat, or question.
Marques et al. (2024) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: