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FRI0464 Arterial wall inflammation is not affected by ANTI-IL17 treatment in patients with peripheral spondyloarthritis
  1. LJJ Van Mens1,
  2. SL Verweij2,
  3. AWR van Kuijk3,
  4. ESG Stroes2,
  5. DL Baeten1,4
  1. 1AMC, Amsterdam Immunology and Rheumatology Center
  2. 2Vascular medicine, Academisch Medisch Centrum
  3. 3Reade, Amsterdam Immunology and Rheumatology Center, Amsterdam, Netherlands
  4. 4UCB, Brussels, Belgium

Abstract

Background Patients with spondyloarthritis (SpA), a chronic inflammatory disease, have an increased cardiovascular risk, which is partly due to increased inflammatory activity in the arterial wall.

IL-17A blockade with secukinumab is an effective treatment for SpA. The role of IL-17A in atherogenesis is controversial, some studies suggest that IL-17A is pro-atherogenic, while others indicate that IL-17A is athero-protective. So, it is not known wat the effect is of treatment with IL-17A blockade on inflammatory activity in the arterial wall.

Objectives To assess the effect of 3 months treatment with secukinumab on arterial wall inflammation in SpA patients with peripheral disease (pSpA).

Methods We included 20 patients with clinical pSpA in a 12 week open-label trial. Treatment consisted of 300 mg secukinumab once a week during the first 4 weeks and then every 4 weeks thereafter. EULAR DAS response was used to define a responder/non responder state. To measure arterial wall inflammation we performed a 18-fluorodeoxyglucose positron emission tomography with computed tomography (18F-FDG PET/CT) imaging in 18 patients at baseline and week 12, which is a validated method to quantify arterial wall inflammation. Arterial wall inflammation is measured in both the ascending aorta and carotids, maximal FDG uptake is shown as the maximal target-to-background ratio (TBRmax).

Results 18 patients with pSpA (age 44±12, 72% male) and without a previous cardiovascular event underwent imaging. Overall, three months treatment with secukinumab resulted in a significant improvement of disease activity with 17/18 patients achieving a EULAR DAS response (9 good and 8 moderate responders). Correspondingly, CRP levels decreased significantly (baseline: 3.2 [1.2–12.40] mg/dl vs. wk 12: 2.0 [1.1–5.8] mg/dl, p=0.011). Importantly, treatment with secukinumab did not affect cholesterol levels (total cholesterol baseline: 5.1±1 mmol/l v.s wk 12: 5.5±1 mmol/l, p=0.167; LDL-c baseline: 3.2±0.8 mmol/l v.s wk 12: 3.5±0.9 mmol/l, p=0.219). Additionally, arterial wall inflammation as measured by PET-CT did not change over the course of the 12 weeks treatment with secukinumab (aorta TBRmax baseline: 3.3±0.9 vs. wk 12: 3.3±0.7, p=0.861; carotid TBRmax baseline: 1.88±0.6 vs. wk 12: 1.76±0.4, p=0.067).

Conclusions This pilot study in 18 patients with pSpA without any preexisting CV events showed that treatment with secukinumab for 3 months has no effect on arterial wall inflammation as measured by PET-CT. Further research in larger patient groups, over a longer period of treatment, and with different measurements remains warranted to fully elucidate the effect of IL-17A blockade on vascular inflammation.

Acknowledgements This study was funded by an unrestricted grant from Novartis.

Disclosure of Interest L. Van Mens: None declared, S. Verweij: None declared, A. van Kuijk Grant/research support from: UCB, Pfizer, MSD, Janssen, Consultant for: Novartis, Celgene, E. Stroes Speakers bureau: Amgen, Sanofi, Merck, D. Baeten Grant/research support from: Pfizer, MSD, AbbVie, Novartis, UCB, Janssen, Boehringer Ingelheim, Consultant for: Pfizer, MSD, AbbVie, Novartis, UCB, Janssen, Boehringer Ingelheim, Eli Lilly, Roche, BMS, Glenmark, Employee of: UCB

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