LAUSR

Background: : Observational studies have previously found associations between glucocorticoid therapy and irreversible organ damage in SLE. As glucocorticoid use and lupus disease activity are highly concordant, disease activity potentially confounds analysis of the contribution of glucocorticoid use to organ damage. This could be obviated through the study of damage accrual in patients without detectable disease activity. Objectives: We studied whether glucocorticoids contribute to damage accrual in SLE in the absence of disease activity, by analysing the effect of glucocorticoids on SLE damage accrual in patients with no clinical or serological lupus disease activity (SLEDAI-2K=0). Methods: 1707 SLE patients were recruited from 13 centres in 8 countries and followed longitudinally between 2013-2016. As per a standardised protocol, disease activity (SLEDAI-2K) and treatment details were recorded at each visit, and organ damage measured annually (SDI). Cox-proportional hazards analyses were used to examine time-dependent associations of glucocorticoid use with damage accrual. Results: 196/1707 (11.4%) patients had no clinical or serological disease for the entire study period (time adjusted mean (TAM) SLEDAI2K=0). Of these, 95% were female; median (IQR) age at diagnosis 36.5yrs (26.0-46.5) years, median (IQR) baseline SDI 0 (0-1). 68% were exposed to prednisolone, with a median (IQR) TAM-prednisolone dose 2mg/day (0-5). Despite SLEDAI2K=0 throughout, irreversible damage accrual occurred in 13% of the cohort, with 26 damage events captured over median (range) 1.9 years (1.0-2.2) followup. Prednisolone exposure at doses in the upper two quartiles was associated with damage accrual (HR 1.11 (1.02, 1.22), p=0.02). Conclusion: Irreversible damage accrual occurs in patients with no clinical or serological disease activity as captured by SLEDAI-2K, and glucocorticoid use contributes to the risk of organ damage in these patients. Disclosure of Interests: : Diane Apostolopoulos: None declared, Rangi Kandane-Rathnayake: None declared, Worawit Louthrenoo: None declared, Shue Fen Luo: None declared, Yeong-Jian Wu: None declared, Aisha Lateef : None declared, Vera Golder: None declared, Sargunan Sockalingam: None declared, Sandra Navarra: None declared, Leonid Zamora: None declared, Laniyati Hamijoyo: None declared, Yasuhiro Katsumata: None declared, Masayoshi Harigai: None declared, Madelynn Chan: None declared, Sean O’Neill: None declared, Fiona Goldblatt: None declared, Alberta Hoi Grant/research support from: GSK, AstraZeneca, UCB and Merck Serono, Consultant for: Janssen Steering Committee, Speakers bureau: Novartis, Mandana Nikpour: None declared, Eric F. Morand Grant/research support from: AstraZeneca, Bristol Myers Squibb, Janssen, Merck Serono, and UCB, Consultant for: AstraZeneca, Eli Lilly, Janssen, and Merck Serono, Speakers bureau: AstraZeneca