[Show abstract][Hide abstract] ABSTRACT: The threshold for disease activity required to start antitumour necrosis factor (TNF) therapy has been arbitrarily set in patients with axial spondyloarthritis (axSpA) at Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) ≥ 4. How this relates to spinal inflammation is unknown.
To systematically compare the clinical, laboratory and imaging data of patients with axSpA with respect to their BASDAI level.
A total of 100 consecutive patients with axSpA who had never been treated with TNF blockers were included. Laboratory parameters, spinal MRI and x-rays were quantified. Data were stratified according to BASDAI ≥ 4.
44 patients were diagnosed as non-radiographic axSpA (nraxSpA) and 56 patients as ankylosing spondylitis (AS): median age 40.3 ± 10.4 years; 57% male, mean disease duration since diagnosis 6.4 ± 8.4 years, 88% HLA-B27+, mean modified Stokes Ankylosing Spondylitis Spinal Score 8.3 ± 16.4. 60% of patients had spinal inflammation by MRI. The stratification based on BASDAI ≥ 4 disclosed significant differences in most clinical parameters but not for inflammation: patients with nraxSpA and BASDAI < 4 versus ≥ 4 had 0.9 ± 1.4 and 0.5 ± 0.6 inflammatory lesions/patient, respectively (p=0.6), while patients with AS had 3.6 ± 3.7 and 2.7 ± 3.0 inflammatory lesions/patient, respectively (p=0.4).
The burden of inflammation is quite comparable in patients with axSpA-regardless of disease activity. These data clearly challenge the concept of the recommended cut-off point of BASDAI ≥ 4.
Annals of the rheumatic diseases 04/2012; 71(7):1207-11. · 8.11 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Patients with axial spondylarthritis (SpA) who have structural changes in the sacroiliac joints and/or the spine have been classified as having ankylosing spondylitis (AS), while those without such changes are now classified as having nonradiographic axial SpA (nr-axSpA). The differentiating features are incompletely understood.
Data from 100 consecutive patients with axial SpA not treated with tumor necrosis factor antagonists were compared clinically and with laboratory parameters, spinal radiographs, and magnetic resonance imaging (MRI) of the spine. Standardized clinical assessment tools were used to assess health status.
AS was diagnosed in 56 patients and nr-axSpA in 44 patients. Signs of inflammation were significantly higher in patients with AS than in patients with nr-axSpA, with a median C-reactive protein level of 8.0 versus 3.8 mg/liter, a median Ankylosing Spondylitis Disease Activity Score of 2.2 versus 2.8, respectively, and a median amount of spinal inflammatory lesions on MRI of 2.0 versus 0.0, respectively. Significant differences between these 2 groups were seen in sex (76.8% male AS patients versus 31.8% male nr-axSpA patients). Clinical variables did not differ between patients with AS and nr-axSpA (Bath Ankylosing Spondylitis Disease Activity Index, Bath Ankylosing Spondylitis Functional Index, Ankylosing Spondylitis Quality of Life questionnaire, Short Form 36 health survey).
Patients with nr-axSpA were characterized by the low proportion of male patients and the low burden of inflammation compared to patients with AS. While both groups did not differ regarding health status, disease activity, and physical function, they did differ in signs of inflammation; all were higher in patients with AS. Since many patients with nr-axSpA had not developed structural changes after years of symptoms, we propose that those patients should not be regarded as having preradiographic AS but rather as having nr-axSpA.
Arthritis care & research. 04/2012; 64(9):1415-22.