Limited utility of novel serological biomarkers in patients newly suspected of having giant cell arteritis

Abstract

Aim Diagnosing and monitoring vascular activity in giant cell arteritis (GCA) is difficult due to the paucity of specific serological biomarkers. We assessed the utility of 8 novel biomarkers in an inception cohort of newly suspected GCA patients. Method Consecutive patients were enrolled between May 2016 and December 2017. Serum was collected within 72 hours of commencing corticosteroids and at 6 months. It was analyzed for levels of intra‐cellular adhesion molecule 1, vascular endothelial growth factor (VEGF), pentraxin 3, von Willebrand factor and procalcitonin (5‐plex R&D Systems multiplex assay) and interleukin (IL)6, IL12 and interferon‐γ (high‐sensitivity 3‐plex ProcartaPlex multiplex assay). A GCA specific positron emission tomography / computed tomography (PET/CT) scan was performed at enrolment with uptake in each vascular territory graded and summed to derive a total vascular score (TVS). Results For the 63 patients enrolled, 12 (19%) had a final diagnosis of biopsy‐positive GCA and a further 9 had a clinical diagnosis of biopsy‐negative GCA. None of the 8 biomarkers was significantly higher in GCA patients compared with those with alternative diagnoses, or demonstrated a positive correlation with the PET/CT TVS. This was in contrast to the C‐reactive protein (CRP) and erythrocyte sedimentation rate (ESR) which were higher in the biopsy‐positive GCA cohort (P < .04) and showed weak positive correlations with the TVS (correlation coefficient 0.34, P < .01). Procalcitonin did not distinguish between GCA and infection. Concentrations of CRP, ESR, VEGF and pentraxin 3 decreased between diagnosis and 6 months in GCA patients. Conclusion This study did not identify new serological biomarkers to assist in diagnosing or assessing the vasculitis burden in GCA.

The Relationship of Carotid Intima-Media Thickness with Cell Adhesion Molecules and Pentraxin-3 in Patients with Psoriatic Arthritis

“…An increase in CIMT was also detected in vasculitides such as giant cell arteritis (GCA) [38]. Systemic inflammatory response markers including IL-6, IL-1, IL-17, IL-23, VEGF, von Willebrand factor, ICAM1, and PTX3 are responsible from chronic inflammation and an increase in CIMT in patients with GCA [39]. Theoretically, secukinumab (IL17 inhibitor), which have been shown to be effective in the treatment of GCA [40] and PsA [41] are likely to prevent the increase in CIMT and thus subclinical atherosclerosis in PsA patients.…”

Cytokine and chemokine multiplex analysis-based exploration for potential treatment and prognostic prediction in large-vessel vasculitis: A preliminary observational study

“…There are proteomic studies for the pathophysiological clustering by serum cytokine/chemokine profiles in the patients with some diseases such as Sjögren's syndrome and psoriatic arthritis (9,10). In LVV, a few proteomic studies analysing serum cytokines/ chemokines were reported, and the analysis results are useful for clarifying pathogenic pathways associated with TAK and evaluating the disease activity of TAK (11)(12)(13). However, there has been no study analysing serum cytokine/chemokine profiles to predict the clinical courses of patients with LVV.…”