LAUSR

Low disease activity state has been defined using SLEDAI and used as treatment target in SLE. However, there has not been any such definition using BILAG-2004 index (BILAG-2004).This study was to determine if low disease activity state according to BILAG-2004 is valid for use as treatment target in SLE. We also assessed disease activity longitudinally using BILAG-2004 systems tally (BST). BST is an alternative way of representing BILAG-2004 scores that combines the flexibility and simplification of numerical scoring of BILAG-2004 with the clinical intuitiveness of BILAG-2004 structure.This was a prospective multi-centre longitudinal study in the UK of an inception cohort of SLE patients (recruited within 12 months of achieving 1997 ACR revised criteria for SLE). Data were collected on disease activity (BILAG-2004 and BILAG2004-Pregnancy Index during pregnancy), SLICC/ACR DI (SDI), cumulative drug exposure and death at every visit. This study ran from 1st January 2005 to 31st December 2017. Four low disease activity states (LDA) were defined using BILAG-2004: 1) BILAG-2004 LDA when all 9 systems had scores of C, D or E on assessment (no Grade A or B), 2) BST LDA when there was persistent score of C, D or E in all 9 systems between 2 consecutive visits (equivalent to 2 consecutive visits with BILAG-2004 LDA), 3) BILAG-2004 Remission when all 9 systems had scores of D or E on assessment and 4) Persistent Remission when there was persistent score of D or E in all 9 systems between 2 consecutive visits. Longitudinal analysis using Poisson regression with random effects model was used with development of new damage as the outcome of interest. Gender, cardiovascular risk factors, antiphospholipid syndrome status and most drugs (except hydroxychloroquine, glucocorticoids, mycophenolate and cyclophosphamide) were excluded from the model as they were not associated with development of damage in univariate analysis.273 patients were recruited (91.2% female, 59.3% Caucasian, 17.2% African/Caribbean, 17.2% South Asian) with mean age at recruitment of 38.5 years (SD 14.8). 97.8% had no damage at recruitment (2.2% had SDI score of 1). Median follow-up was 73.4 months (range: 1.8, 153.8) with total follow-up of 1767 patient-years. There were 13 deaths and 114 new damage items occurred during follow-up. There were 6674 assessments with disease activity score: 319 assessments with Grade A activity in 95 patients (84.6% had only 1 system with grade A, range: 1 - 4) and 1704 assessments with Grade A or B activity in 239 patients (78.7% had only 1 system with Grade A or B, range: 1 - 5).BILAG-2004 LDA was achieved in 74.5% of assessments (from 271 patients). BILAG-2004 Remission occurred in 28.2% of assessments (from 234 patients).6401 observations with BST were available (1 observation derived from change in activity between 2 consecutive assessments) and 63.7% were in BST LDA. There was no observation with Persistent Remission between consecutive visits.Table 1 summarises multivariate analysis which showed BILAG-2004 LDA to be inversely associated with damage. Similar results were obtained with BILAG-2004 Remission (RR 0.60 with 95% CI 0.38, 0.96) and BST LDA (RR 0.65 with 95% CI 0.43, 0.99). Cumulative drug exposure since recruitment for mycophenolate was protective against new damage (RR 0.99 with 95% CI 0.99, 0.99).Table 1.VariableRelative Risk (95% CI) for New DamageEthnicityAfro-Caribbean1.22 (0.68, 2.18)South Asian1.81 (0.97, 3.38)Others2.22 (0.63, 7.85)Age at diagnosis1.06 (1.04, 1.08)Prior SDI score0.68 (0.43, 1.06)BILAG-2004 LDA0.60 (0.39, 0.94)Hydroxychloroquine since last visit (per g)0.99 (0.98, 0.99)Steroids since last visit (per 100mg)1.02 (1.01, 1.03)Cyclophosphamide since last visit (per g)1.67 (1.15, 2.41)BILAG-2004 LDA and BST LDA are valid treatment targets in SLE. BILAG-2004 Remission and Persistent Remission are uncommon, which make them unrealistic as a treatment target.[1]Yee C. S., et al. The BILAG-2004 systems tally – a novel way of representing the BILAG-2004 index scores longitudinally. Rheumatology (Oxford) 2012; 51[11]: 2099-2105.Versus Arthritis, Vifor PharmaChee-Seng Yee Consultant of: Bristol Myers Squibb, ImmuPharma, Grant/research support from: Vifor Pharma, Caroline Gordon Speakers bureau: UCB, Consultant of: Center for Disease Control, Astra-Zeneca, MGP, Sanofi and UCB, Mohammed Akil: None declared, Peter Lanyon: None declared, Christopher John Edwards Consultant of: Glaxo Smith Kline, Roche, Grant/research support from: Glaxo Smith Kline, Roche, David Isenberg: None declared, Anisur Rahman: None declared, Lee-Suan Teh: None declared, Sofia Tosounidou: None declared, Robert Stevens: None declared, Ahtiveer Prabu: None declared, Bridget Griffiths: None declared, Neil McHugh: None declared, Ian N. Bruce: None declared, Yasmeen Ahmad: None declared, Munther Khamashta: None declared, Vernon Farewell: None declared