The following is a summary of “Analyses of plasma inflammatory proteins reveal biomarkers predictive of subsequent development of giant cell arteritis: a prospective study,” published in the June 2023 issue of Rheumatology by Wadström, et al.
For a study, researchers sought to investigate the association between biomarkers of inflammation and the subsequent development of giant cell arteritis (GCA).
Participants from the population-based Malmö Diet Cancer Study (MDCS; N = 30 ,447) who later received a GCA diagnosis underwent a retrospective study. From the study cohort, GCA-free controls who were matched for sex, birth year, and screening year were chosen. The OLINK proteomics inflammation panel, which assesses 92 inflammatory proteins, was used to examine baseline plasma samples. The analyses were divided into hypothesis-driven and hypothesis-generating categories. In the hypothesis-generating analyses, they used principal component analysis to identify protein groups explaining the proteome variance. Within these components, they investigated proteins with a factor loading of >0.50.
They identified 94 confirmed incident GCA cases (median 11.9 years after inclusion). Among the biomarkers with a priori hypotheses, IFN-γ showed a positive association with GCA (odds ratio [OR] per standard deviation [S.D.] = 1.52; 95% CI 1.00, 2.30). In the hypothesis-generating analyses, eight biomarkers were significantly associated with the development of GCA. Notably, elevated levels of IFN-γ (OR = 2.37; 95% CI 1.14, 4.92) and monocyte chemotactic protein 3 (MCP3) (OR = 4.27; 95% CI 1.26, 14.53) were particularly associated with an increased risk of GCA in the subset sampled less than 8.5 years before diagnosis. Several other proteins important for T cell function, including CXCL9, IL-2, CD40, and CCL25, were also associated with GCA in these analyses.
The findings suggested that elevated IFN-γ levels precede the clinical onset of GCA, indicating that T cell activation may play a role in the development of the disease. The study provided valuable insights into the potential role of inflammation in the pathogenesis of GCA.
Source: academic.oup.com/rheumatology/article/62/6/2304/6762858