Non-steroidal anti-inflammatory drug use is determined by disease activity in axSpA and decreased by biologicals: a longitudinal analysis

• Published in: ARP rheumatology Vol. 2; no. 4; p. 322
• Main Authors: Durak Ediboğlu, Elif, Solmaz, Dilek, Kabadayı, Gökhan, Gücenmez, Sercan, Cinakli, Haluk, Otman Akat, Eda, Özmen, Mustafa, Akar, Servet
• Format: Journal Article
• Language: English
• Published: Portugal 01.10.2023
• ISSN: 2795-4552

To evaluate non-steroidal anti-inflammatory drug (NSAID) use and Assessment in Spondyloarthritis International Society (ASAS)-NSAID scores in patients with axial spondyloarhritis (axSpA) in a longitudinal study. In total, 429 patients with axSpA (59% male; 63.6% with AS) were included in this study. Data about disease activity, C-reactive protein (CRP) levels, and NSAID use and dosage were collected at 0, 12, 24, and 52 weeks retrospectively. The relationship with NSAID use /ASAS-NSAID scores and other factors were tested using generalized estimating equations (GEE). At baseline (0 weeks), 92.8% of patients in biologic disease-modifying anti-rheumatic drugs (bDMARDs) group and 82.1% of patients in conventional treatment group were treated with NSAIDs. At baseline, the proportion (p=0.03) and the median (IQR) ASAS-NSAID scores were higher in bDMARDs group [100 (50) vs 50 (83.4); p<0.001]. During follow-up, NSAID use and ASAS-NSAID scores decreased significantly in patients treated with bDMARDs (p<0.001) and the reduction remained stable throughout the follow-up However, neither NSAID use (p=0.06) nor ASAS-NSAID scores changed in conventional treatment group (p=0.15). In bDMARD-treated patients, ASDAS-CRP and BASFI scores were independent determinants for NSAID use, and BASDAI and PGA were determinants for NSAID dosage. There was no independent significant predictor for ASAS-NSAID scores; PGA was the only significant predictor for NSAID use in the conventional treatment group. Concurrent biologic treatment was associated with low NSAID intake in patients with axSpA, and NSAID use was determined mainly by disease activity and partly by function during bDMARD treatment.