| Full text | |
| Author(s): |
Milanez, Fernanda Manente
[1]
;
Saad, Carla G. S.
[1]
;
Viana, Vilma T.
[1]
;
Moraes, Julio C. B.
[1]
;
Perico, Gregory Vinicius
[2]
;
Sampaio-Barros, Percival Degrava
[1]
;
Goncalves, Celio R.
[1]
;
Bonfa, Eloisa
[1]
Total Authors: 8
|
| Affiliation: | [1] Univ Sao Paulo Reumatol, Fac Med, Div Rheumatol, Ave Dr Arnaldo 455, 3 Andar, Sala 3192, BR-05403010 Sao Paulo, SP - Brazil
[2] URC, Rua Antonio de Lucca 139, BR-88811503 Criciuma, SC - Brazil
Total Affiliations: 2
|
| Document type: | Journal article |
| Source: | ARTHRITIS RESEARCH & THERAPY; v. 18, FEB 24 2016. |
| Web of Science Citations: | 9 |
| Abstract | |
Background: Advances in pathophysiology and treatment of ankylosing spondylitis (AS) was recently demonstrated. However, the effect of anti-TNF in the newly described inflammatory pathways involved pathogenesis of this disease remains to be determined. The aim of our study was, therefore, to investigate long-term influence of anti-TNF drugs in IL-23/IL-17 axis of AS patients and their possible correlation with treatment, clinical, laboratory and radiographic parameters. Methods: Eighty-six AS anti-TNF naive patients, 47 referred for anti-TNF therapy (active-AS; BASDAI >= 4) and 39 with BASDAI < 4 (control-AS) were included. The active group was evaluated at baseline, 12-months and 24-months after TNF blockade and compared at baseline to control-AS group and to 47 healthy age-and gender-matched controls. Plasma levels of IL-17A, IL-22, IL-23 and PGE2 were measured. Non-steroidal anti-inflammatory drugs (NSAIDs) intake were recorded every 6 months. Radiographic severity and progression was assessed by mSASSS at baseline and 24 months after therapy. Results: At baseline, active-AS group presented higher IL-23 and PGE2 levels compared to control-AS group (p < 0.001 and p = 0.008) and to healthy controls (p < 0.001 and p = 0.02). After 24-months of TNF blockade, IL-23 and PGE2 remained elevated with higher levels compared with the healthy group (p < 0.001 and p = 0.03) in spite of significant improvements in all clinical/inflammatory parameters (p < 0.001). Further analysis of 27 anti-TNF-treated patients who achieved a good response (ASDAS-CRP < 2.1, with a drop >= 1.1) at 24-months revealed that IL-23 plasma levels remained higher than healthy controls (p < 0.001) and higher than control-AS group with similar disease activity (ASDAS-CRP < 2.1, p = 0.01). In active-AS group (n = 47), there was a strong correlation between IL-23 and IL-17A at baseline, 12-months and 24-months after anti-TNF therapy (p <= 0.001). Conclusion: This study provides novel data demonstrating that the IL-23/IL-17 axis is not influenced by TNF blockade in AS patients despite clinical and inflammation improvements and NSAID intake. (AU) | |