Background Patients with Large Vessel Vasculitis (LVV) may experience severe consequences of the disease, caused by underlying vasculitis and prolonged treatment. A validate damage tool specific to LVV is lacking. Moreover, despite new evidence, the overall assessment of the activity is still an unmet need.

Objectives The aim of the present study is to evaluate the efficacy of different regimens in achieving clinical, laboratory and imaging disease remission and in preventing the progression of disease-related damage and treatment-related damage, especially glucocorticoids induced, in Giant Cell Arteritis (GCA).

Methods Consecutive inpatients and outpatients, classified as GCA with LVV involvement, were prospectively enrolled. We included all patients with new diagnosis or relapsing disease who underwent to at least 2 consecutive 18F-FDG PET-CT or MR scan between March 2011 and September 2022.

Before every PET scan demographic, clinical data and disease activity were assessed. Remission was defined as absence of signs and symptoms attributable to GCA and normalization of acute phase reactants (ESR <30 mm/H and CRP <1 mg/dL) [1].

For each PET scan the vessel’s metabolic activity was evaluated using the Meller’s grading and the PETVAS score [2].

The damage was evaluated using the Large-Vessel Vasculitis Index of Damage (LLVDI) and the Composite Glucocorticoid Toxicity Index (GTI), distinct in Cumulative Worsening Score (GTI-CWS) and Aggregate Improvement Score (GTI-AIS) [3,4].

GCA patients were compared according to current treatment regimen: glucocorticoid (GC) monotherapy versus conventional disease modifying anti-rheumatic drug (cDMARDs), and tocilizumab (TCZ).

Results The study included 49 LV-GCA patients (age 28 [21-48], 71.4% female) exposed to a total of 76 treatment regimens (n = 39 GC monotherapy, n = 21 cDMARDs, n = 16 TCZ).

All the treatment led to significant reduction of acute phase reactants (GC-treated: ESR p < 0.001, CRP p < 0.001; cDMARDs - treated: ESR p = 0.033, CRP p = 0.01, and TCZ-treated: ESR p = 0.006, CRP p = 0.003).

Significant improvement in PETVAS was observed in all patients: GC treated 12 4-21 vs 7 2-14 (p=0.033), cDMARDs treated 16 5-20 vs 4 3-10.5 (p = 0.039), and TCZ - treated 12 9-20.2 vs 3 1-9 (p < 0.001).

Daily prednisone dose at last examination was 5 [0-7.25] mg/d in the cDMARDs group vs 0 [0-5] mg/d in the TCZ group (p = 0.148). GC withdrawal was observed in 82% of TCZ-treated patients, while 58% in the GC group (p=0.112).

At last evaluation LLVDI was similar in the three groups (2 [1-6] vs 2 [1-3] vs 3 [2.25-5], p = 0.073).

Baseline GTI resulted higher in the TCZ group, when compared to DMARDs and GC (75 [48- 101] vs 49 [35-64] vs 32 [10-74], respectively, p = 0.008). At the last follow-up TCZ-treated patients showed higher GTI-CWS (97 [77-127] vs 72 [48-81] vs 65 [48-103], p = 0.025) than those treated with DMARDs and GC, while no differences were observed in GTI-AIS (0 [- 19 to 33] vs 0 [77.5 to 127] vs 0 [-16 to 18.7], p = 0.154). When considering only those patients who received TCZ as a first line treatment (n=4), GTI-AIS at last follow-up resulted significantly lower compared to DMARDs and GC treated individuals (-30 [-71 to-5.5] vs 0 [77.5 to 127] vs 0 [-16 to 18.7], p = 0.0249).

Conclusion Tocilizumab treatment significantly reduce vessel’s metabolic activity over time, when compared to conventional treatment. None of the three different treatment regimen reduce the progression of the damage caused by both the vasculitis and the glucocorticoid treatment. TCZ as a first line treatment reduced significantly the GTI-AIS at the last follow up, when compared to the other treatment.

References [1]Stone J, et al. Trial of tocilizumab in giant-cell arteritis. NEJM 2017; 377:317–328.

[2]Meller J, et al. Value of F-18 FDG hybrid camera PET and MRI in early takayasu aortitis. Eur Radiol. 2003 Feb;13(2):400-5

[3]Miloslavsky EM, et al. Development of a Glucocorticoid Toxicity Index (GTI) using multicriteria decision analysis. Ann Rheum Dis 2017;76:543

Acknowledgements: NIL.

Disclosure of Interests None Declared.