Background High mobility group box 1 (HMGB1) is a non-histone DNA-binding protein. It exists in all types of cells and has complex functions. When secreted extracellularly HMGB1 acts as an alarmin and induces and potentiates NF-κB activity. HMGB1 is raised in patients with active granulomatous vasculitis (1). However, a recent study did not find any association of HMGB1 protein concentration and disease activity in Giant cell arteritis (GCA) (2). Our aim was to investigate whether HMGB1 protein rises during the active phase of giant cell arteritis (GCA) and falls after initiation of treatment.
Objectives Our aim was to investigate whether HMGB1 protein rises during the active phase of giant cell arteritis (GCA) and falls after initiation of treatment.
Methods GCA patients were recruited at the Department of Rheumatology at the Hospital of Southern Norway in Kristiansand between January 2012 and January 2014. The diagnosis was based on positive ultrasonography of temporal arteries and /or large vessels and typical clinical manifestations. All patients fulfilled the ACR classification criteria. Blood samples were drawn at time of diagnosis and before treatment and after clinical remission. HMGB1 levels in serum were measured by ELISA (IBL International GMBH, Hamburg, Germany), using a high sensitive protocol (range 0,313–10 ng/ml).
Results Fifteen GCA patients (mean age 68 years (SD 9.2), 3 males and 12 females), were included during the study period. The median time until remission was 6 months (range 1–6). Eight patients had isolated cranial arteritis while seven patients had in addition large vessel vasculitis (LVV). Mean HMGB1 concentration at diagnosis and in clinical remission were 5.5 ng/ml (SD 5.4) and 3.3 ng/ml (SD 3.0) respectively. The difference was not significant (mean difference 2.2 ng/ml (CI 95% -1.2–5.7, p=0.182), Figure 1. No differences were observed for HMGB1 concentrations at diagnosis nor at remission for cranial (p=0.2) or LVV (p=0.7).
Conclusions In GCA patients, no differences in HMGB1 protein levels were observed at diagnosis compared with remission. In addition, no differences were seen between pure cranial and LVV. Thus, HMGB1 protein seems not to be a useful biomarker for disease activity in GCA.
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Disclosure of Interest None declared