Background Giant cell arteritis (GCA) is characterised by inflammation of the medium and large vessels. Two forms of GCA are described, C(cranial)-GCA and LV(large vessel)-GCA, which can be present either separately or co-exist in a patient. Clinical features, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels are used for disease diagnosis and monitoring, but are not disease specific. Relapses are common during and after treatment, therefore new biomarkers are needed for diagnosis and disease course prediction. Objectives As the majority of infiltrating cells in in the vessels of GCA patients are macrophages the aim of this project was to identify and compare levels of macrophage products in the serum of GCA patients as potential biomarkers. Methods Forty-one newly diagnosed GCA patients (temporal artery biopsy proven C-GCA and FDG-PET scan-positive LV-GCA) were recruited before start of glucocorticoids. Disease course was monitored and time to glucocorticoid treatment free remission was documented. Thirty age- and sex matched healthy controls (HCs) and 13 infection controls (bladder or lung infection) were also included. Serum concentrations of interleukin (IL)−6, serum amyloid A (SAA), soluble CD163 (sCD163), calprotectin, YKL-40 (human cartilage glycoprotein-39), vascular endothelial growth factor (VEGF), and angiopoietin-1 and 2 were determined by ELISA or Luminex assay. Results IL-6, SAA, sCD163, calprotectin, YKL-40, VEGF and angiopoietin-2 levels are increased in GCA and infection controls compared to HCs. IL-6 levels correlated strongly with CRP, ESR and SAA, all markers of the Acute Phase Response (APR), in GCA. Interestingly, YKL-40, angiopoietin-2 and calprotectin levels showed only weak or no correlation with APR biomarkers, while they were strongly correlated with the APR in infection controls. Monocytes in peripheral blood correlated with APR biomarkers in GCA, whereas neutrophils correlated with the APR in infection controls. Patients with overlapping C-GCA and LV-GCA displayed a significantly stronger APR than patients with C-GCA or LV-GCA alone. High VEGF and angiopoietin-1, but low angiopoietin-2 levels at baseline predicted a shorter time to treatment free remission. This is in contrast to markers of the APR, which did not significantly predict time to treatment free remission. Conclusions In this study, we show that markers of angiogenesis are better predictors of disease outcome than APR biomarkers. It appears that levels of calprotectin, YKL40 and angiopoietin-2 are increased through other than APR pathways during GCA compared to acute infection. Monocytes rather than neutrophils appear to drive the APR in GCA. This response is stronger in GCA patients with both cranial and systemic symptoms. Disclosure of Interest None declared