Background AIDAI is a novel validated tool for assessment of disease activity in autoinflammatory diseases.1 CLUSTER study (NCT02059291) demonstrated that canakinumab (CAN; an anti- IL-1β antibody) is efficacious in resolving active flare and in preventing new flare in patients (pts) with colchicine resistant familial Mediterranean fever (crFMF), hyper-IgD syndrome/mevalonate kinase deficiency (HIDS/MKD) and TNF receptor-associated periodic syndrome (TRAPS).2
Objectives To assess AIDAI score and evaluate correlation between AIDAI and disease/response characteristics over 16 weeks (wks) of CAN treatment in CLUSTER.
Methods CLUSTER study design and results have been presented.2 AIDAI was calculated as the sum of 12 items1 for 30 consecutive days. AIDAI score was calculated if the first score was recorded ≥29 days before baseline (BL). Missing items were imputed beyond last evaluable measurement by LOCF. Proportion of pts with inactive disease (ID; AIDAI score <9) was calculated at Wk 16. Correlation analysis of AIDAI with C-reactive protein (CRP), serum amyloid A (SAA), physician global assessment (PGA) and sheehan disability score (SDS), and child health questionnaire–psychological/physical (CHQ–PsCS/PCS) and short form 12–physical/mental (SF12–PCS/MCS) component summaries were performed at BL and Wk 16, with significance set at p<0.05.
Results Median AIDAI scores decreased over time (Fig 1). Proportion of pts with ID at Wk 16 was 52% in crFMF, 40% in HIDS/MKD and 46% in TRAPS cohorts. AIDAI at Wk 16 correlated significantly with: SDS in all 3 cohorts; PGA in HIDS/MKD and TRAPS; SF12–MCS in crFMF and HIDS/MKD (Table 1). CRP and SAA did not correlate with AIDAI.
Conclusions CAN demonstrated rapid and sustained disease control assessed with AIDAI over 16 wks. Approximately half of crFMF and TRAPS pts, and 40% of HIDS/MKD patients had inactive disease after 16 wks of treatment. AIDAI improvements at Wk 16 correlated with patient and physician driven evaluations (PGA, SF12–MCS and SDS). CRP and SAA are indicators of response to treatment, rather than a disease activity parameter.
Piram M, et al. Ann Rheum Dis. 2014;73: 2168–73.
De Benedetti F, et al. Ann Rheum Dis. 2016;75:615–6.
Disclosure of Interest I. Kone-Paut Grant/research support from: Novartis, SOBI and Roche, Consultant for: Novartis, SOBI, Pfizer, AbbVie and Roche, M. Piram Consultant for: Novartis, Pfizer, AbbVie, Speakers bureau: Novartis, S. Benseler Consultant for: Novartis, SOBI and AbbVie, M. Hofer Consultant for: Novartis and AbbVie, H. Lachmann Consultant for: Novartis, SOBI, Takeda and GSK, Speakers bureau: Novartis and SOBI, H. Hoffman Consultant for: Novartis, Speakers bureau: Novartis, M. Gattorno Grant/research support from: Novartis and SOBI, Consultant for: Novartis and SOBI, J. Frenkel Grant/research support from: Novartis and SOBI, J. Kuemmerle-Deschner Grant/research support from: Novartis, Consultant for: Novartis, SOBI and Baxalta, S. Ozen Speakers bureau: Novartis and SOBI, J. Levy Paid instructor for: Novartis, C. Karyekar Employee of: Novartis, F. De Benedetti Grant/research support from: Pfizer, AbbVie, Roche, Novartis, Novimmune and BMS