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Abstract Number: 1668

Does Fibrinogen Have a Role In The Assessment Of Patients With Giant Cell Arteritis?

Lorraine O' Neill1, Eoghan M. McCarthy2, Anne M. Madigan3, Geraldine M. McCarthy4, Eamonn S. Molloy5, Ursula Fearon6, Douglas J. Veale5 and Conor Murphy7, 1Rheumatology, Dublin Academic Medical Centre, St. Vincent's University Hospital, Dublin, Ireland, 2Rheumatology, Beaumont Hospital, Dublin, Ireland, 3Rheumatology, Mater Misericordiae University Hospital, Dublin 7, Ireland, 4Medicine/Rheumatology, Mater Misericordiae University Hospital, Dublin 7, Ireland, 5Rheumatology, St. Vincent's University Hospital, Dublin 4, Ireland, 6Dublin Academic Medical Centre, Translational Rheumatology Research Group, Dublin, Ireland, 7Department of Ophthalmology, Royal Victoria Eye and Ear Hospital, Dublin, Ireland

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: biomarkers and giant cell arteritis

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Session Information

Title: Vasculitis II

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Giant cell arteritis (GCA) in the most common systemic vasculitis in patients over 50 years of age. Considerable difficulties exist in the evaluation of patients with GCA. Accurate clinical assessment can be challenging due to the wide spectrum of clinical presentations.  Temporal artery biopsy is negative in a substantial minority of patients.

The traditional biomarkers ESR and CRP are non-specific and can be negative.

Therefore development of better disease biomarkers is needed for diagnosis in GCA.

Plasma Fibrinogen has already been demonstrated in Polymyalgia Rheumatica to accurately identify those patients with quiescent disease, to be at least as useful as CRP and ESR for diagnosis of active disease and more specific for confirmation of response to treatment than either ESR or CRP.

Aim:

The aim of this study was to evaluate the utility of plasma Fibrinogen in the assessment of patients with GCA.

Methods:

Patients presenting with suspected new-onset GCA were prospectively enrolled. Plasma fibrinogen, ESR and CRP were assayed at baseline and 3 months following initiation of steroid therapy.

Biomarkers were also assayed in 25 age and sex matched controls attending with osteoarthritis (OA).

Demographic data and categorical variables were assessed using Fischers Exact Test. Receiver operator curves (ROC), predictive values, and likelihood ratios were calculated for all biomarkers measured. Spearman rank correlation coefficient was used to directly compare Fibrinogen, ESR and CRP

Results:

68 patients with suspected GCA were recruited. 30 patients had positive temporal artery biopsies and of the 38 with negative biopsies, 25 met ACR criteria for GCA and were included in the ananlysis. 

Plasma Fibrinogen levels were significantly elevated in patients with GCA when compared with OA controls. (Mean 4.9 g/L vs. 3.05 g/L, p = 0.0017).  Fibrinogen levels were also significantly elevated in patients with GCA who were biopsy positive when compared to those patients fulfilling ACR criteria for GCA but who were biopsy negative (Mean 6.05 g/L vs 3.75 g/L, p = < 0.01) No correlation was observed between Fibrinogen and any clinical variable observed. .

Fibrinogen levels also demonstrated a response to therapy. (Mean of 4.9 g /L at baseline vs. 3.5 g / L at 3 months, p = 0.04)  Baseline Fibrinogen levels correlated with baseline ESR (r = 0.6946, p < 0.0001) and CRP (r= 0.6951, p < 0.0001.  ROC analysis revealed Fibrinogen to be a less sensitive but more specific marker of GCA than CRP  (Sensitivity of 67% vs. 82% and Specificity of 100% vs. 80% respectively) with comparable specificity to ESR above a cut off for ESR  >30 mm/hr.

Values above the upper limit of normal for Fibrinogen (4 g/L) were associated with a positive likelihood ratio of 15.18 for GCA.

Conclusion:

Plasma fibrinogen levels are elevated in patients with GCA, respond to glucocorticoid therapy and correlate with serum ESR and CRP levels. This data suggests that fibrinogen may be a more specific marker for GCA than CRP. Further research is required to define the utility of fibrinogen in assessment of disease activity in patients with GCA.


Disclosure:

L. O’ Neill,
None;

E. M. McCarthy,
None;

A. M. Madigan,
None;

G. M. McCarthy,
None;

E. S. Molloy,
None;

U. Fearon,
None;

D. J. Veale,
None;

C. Murphy,
None.

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