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AB0033 High Mobility Group box 1 Protein Is Not Elevated in Active Phases of Giant Cell Arteritis
  1. A. Diamantopoulos1,2,
  2. G. Myklebust1,
  3. I. Kvivik3,
  4. R. Omdal3
  1. 1Rheumatology, Hospital of Southern Norway Trust, Kristiansand
  2. 2Rheumatology, Hospital for Rheumatic Diseases in Haugesund, Haugesund
  3. 3Clinical Immunology Unit, Stavanger University Hospital, Stavanger, Norway

Abstract

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.

  1. Henes FO, Chen Y, Bley TA, Fabel M, Both M, Herrmann K, et al. Correlation of serum level of high mobility group box 1 with the burden of granulomatous inflammation in granulomatosis with polyangiitis (Wegener's). Ann Rheum Dis. 2011;70(11):1926–9.

  2. de Souza AW, van der Geest KS, Brouwer E, Pinheiro FA, Oliveira AC, Sato EI, et al. High mobility group box 1 levels in large vessel vasculitis are not associated with disease activity but are influenced by age and statins. Arthritis Res Ther. 2015;17:158.

Disclosure of Interest None declared

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