Background Measures for disease activity (BASDAI, ASDAS) are routinely used in patients (pts) with axial spondyloarthritis (axSpA). The ASDAS, a composite score that includes clinical measures and CRP, has high discriminatory capacity for assessment of disease activity. Clinical trial data showed that the ASDAS has a better sensitivity to change than the BASDAI in pts treated with TNF-blockers. However, there are no data on the comparison of ASDAS and BASDAI in axSpA pts treated with NSAIDs, which are recommended as first choice prior to a possible initiation of TNF-blockers.
Objectives We compared the performance of BASDAI and ASDAS in assessing and predicting clinical response to intensive NSAID treatment in axSpA pts with high disease activity.
Methods Consecutive pts with nr-axSpA and AS (n=50 each group) were included in a prospective study if their BASDAI level was ≥4, if they had not yet received the maximally approved dose of NSAIDs and if they had not been treated with anti-TNF agents to date. After inclusion the maximal dose of NSAIDs was administered over one week (wk) and the dose was then reduced in case of BASDAI <4 or, in case of BASDAI ≥4, the NSAID was changed and pts were treated for another 3 wks at maximal doses. Clinical and laboratory parameters were assessed and the dosage of NSAIDs was quantified by using the ASAS-index. Data were collected before (BL) and after 1 and 4 wks of NSAID treatment.
Results Baseline characteristics of AS and nr-axSpA patients were similar. Prior to treatment, an ASDAS >2.1 was found in 74% and 76% of pts with AS and nr-axSpA, respectively. There was a significant decrease in both, ASDAS (BL: 2.5±0.6, 1wk: 1.9±0.8, 4wk: 1.6±0.8) and BASDAI (BL: 5.8±1.3 1wk: 4.1±2.1 4wk: 2.1±3.1). At wks 1 and 4, a BASDAI <3 was achieved by 20% and 22% of AS and 15% and 18% of nr-axSpA pts, respectively. An ASDAS <2.1 was reached by 29% and 34% of AS and 34% and 33% of nr-axSpA pts, respectively. An ASDAS <1.3 indicative of inactive disease was found in 13% and 16% of AS and 15% and 18% of nr-axSpA pts, respectively. However, at wk 4 a BASDAI ≥4 was still present in 34% axSpA pts, but only 15% of these had an ASDAS <2.1. Another 33% of pts had an ASDAS <2.1 but only 4% of those had a BASDAI <4. This difference was much more prominent in nr-axSpA patients (Table). In the univariate logistic regression analysis both, ASDAS (OR: 3.6, p=0.002) and BASDAI (OR: 1.8, p=0.001) predicted the eligibility for anti-TNF therapy after 4wk of NSAIDs at BL, ASDAS performed superior to BASDAI.
Conclusions BASDAI and ASDAS showed a similar magnitude of response on NSAID treatment in both AS and nr-axSpA. Of interest, the discriminative power of the ASDAS was much clearer in patients classified as nr-axSpA and especially in those who could be considered as candidates for anti-TNF treatment. These data challenge the concept of only using the BASDAI cut-off ≥4 for such treatment decisions.
Disclosure of Interest : None declared