THU0306 NEUTROPHIL ADHESION MOLECULES AND INFLAMMATORY CYTOKINES AS BIOMARKERS FOR MONITORING DISEASE PROGRESSION IN GIANT CELL ARTERITIS
Authors: Tadeja Kuret, Katja Lakota, Gerhard Thallinger, Polona Zigon, Sasa Cucnik, Matija Tomsic, Snežna Sodin-Šemrl, Alojzija Hocevar
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background:</h3> Monitoring giant cell arteritis (GCA) activity with appropriate biomarkers is important, as current evaluation, based mainly on clinical symptoms/signs and traditional markers of inflammation, is not always sufficient and reliable. <h3>Objectives:</h3> Our goal was to identify cellular and molecular biomarkers that could help clinicians to closely monitor GCA progression and/or treatment response. <h3>Methods:</h3> Peripheral blood was obtained from 27 GCA patients at time of diagnosis (before glucocorticoid (GC) treatment), and subsequently at weeks 1, 4, 12, 24 and 48 of follow-up (FU). At diagnosis, all patients received GC in line with EULAR recommendations with a slow GC tapering starting after week 4. At week 12, some of the patients (16/27) received additionally leflunomide (10 mg). Whole blood samples were stained, lysed, fixed and analyzed by flow cytometry. The expression of adhesion molecules (CD62L, CD11b) was determined on neutrophils. Sera levels of serum amyloid A (SAA) and IL-6 were measured by nephelometry and ELISA, respectively. Levels of IL-8, IL-18, IL–23, L-selectin and CHI3L1 were determined by MagPix using human pre-mixed multi-analyte kits. <h3>Results:</h3> At weeks 1 and 4 of FU we detected a decrease in neutrophil expression of CD62L and CD11b, as well as in sera levels of SAA, IL-6, IL-8, IL-18, L-selectin and CHI3L1 in all GCA patients. At week 12 (8 weeks after GC tapering) an elevation of CD11b, SAA, IL-6 and IL-23 as compared to week 4 was observed (Figures 1 and 2). At weeks 24 and 48 of FU we identified four different groups of biomarkers. The first group consisted of neutrophil CD62L (p&lt;0.05) and serum IL-6, that showed a marked increase in patients receiving GC therapy only, while decreasing in patients receiving GC in combination with leflunomide. The second group is represented by neutrophil CD11b and serum IL-8 that were higher at week 24 in the GC-treated group (the first FU after receiving leflunomide), however their levels were equal at week 48 in both groups of GCA patients (Figures 1 and 2). In the third group, the serum levels of SAA, IL-18 and L-selectin decreased at week 24 and remained stable through week 48, regardless of therapy used. The fourth group of biomarkers included serum IL-23 and CHI3L1, levels of which declined at weeks 24 and 48 in patients receiving GC only and substantially increased in patients receiving leflunomide and GC (Figure 2). <h3>Conclusion:</h3> Neutrophil surface markers CD62L and CD11b together with inflammatory parameters (SAA, IL-6, IL-8 and IL-23) could represent informative biomarkers for monitoring disease progression in GCA patients. Important biomarker differences were observed between GC-treated GCA patients, in the presence and absence of leflunomide, serving as a good basis for predicting relapses. <h3>Acknowledgement:</h3> The authors would like to acknowledge funding from the Slovenian Research Agency (ARRS) for the National Research Program P3-0314. <h3>Disclosure of Interests:</h3> None declared