AB0541 LUPUS MANIFESTATIONS IN A PATIENT WITH SPONDYLOARTHRITIS TREATED WITH TUMOUR NECROSIS FACTOR-ALPHA ANTAGONIST: SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) OR DRUG-INDUCED LUPUS ERYTHEMATOSUS (DILE)?

Background: Systemic lupus erythematosus (SLE) is a multisystem autoimmune inflammatory disease. Drug-induced lupus erythematosus (DILE) is defined as the development of lupus-like symptoms that is temporarily related to continuous drug exposure which resolves with cessation of the offending drug. It is usually accompanied by serologic findings of a positive antinuclear antibody (ANA) and anti-histone antibodies. Tumour necrosis factor-α (TNFα) antagonist-induced lupus-like syndrome (TAILS) is a well-known side effect of this class of substances. A retrospective study reported twenty two cases whose lupus manifestations abated within a few weeks (median eight weeks) in all patients except one with longer-lasting evolution of six months. Objectives: We reported a case which posed a diagnostic challenge to us, a patient with spondyloarthritis (SpA) who presented with lupus-like features during treatment with Golimumab. Methods: Case report Results: A 36-year-old lady was diagnosed as spondyloarthritis when she presented with peripheral arthritis, plantar fasciitis, right eye anterior uveitis and bilateral chronic sacroiliitis confirmed via sacroiliac magnetic resonance imaging. Investigations revealed raised erythrocyte sedimentation rate (ESR) and negative HLA-B27. She developed allergic reaction to sulfasalazine and non-steroidal anti-inflammatory drugs (NSAIDS), thus intravenous Golimumab was initiated. Although she responded to this therapy and ESR had reduced during assessment at 24 weeks, Golimumab was stopped due to funding issue. It was restarted after six months but had to be discontinued again after four months because she developed recurrent fever and malar rash. During this presentation, investigations revealed leukopenia of 2.46 x109, ESR of 93 mm/hr, low complements and positive direct coombs’ test. ANA, anti-double stranded DNA, anti-histone antibody and anti-smith antibody were all negative. Infective screening was negative. TAILS secondary to Golimumab was diagnosed. Apart from discontinuation of Golimumab, 0.5mg/kg/day of prednisolone was started which resulted in improvement of the malar rash and leukopenia. However, four months after the last dose of Golimumab, recurrent fever and leukopenia recurred when the prednisolone dose was reduced to 5mg on alternate-days. At this time, we considered diagnosis of SLE rather than TAILS because of persistent SLE manifestation despite cessation of Golimumab and improvement with oral corticosteroid. Furthermore, although not pathognomonic, the anti-histone antibody was negative. Conclusion: This case posed a diagnostic challenge as both SLE and DILE can present similarly. The approach to managing this patient with coexisting SpA and SLE is also a challenge since there is a dilemma as to what can be offered after failure of NSAIDs and conventional disease-modifying antirheumatic drugs since anti-TNFα is contraindicated in SLE. References [1] Vasoo S. Drug-induced lupus. Lupus, 2006; 15: 757–761 [2] Brussano AM, Aberer W, Massone C. Subacute lupus erythematosus during treatment with golimumab for seronegative rheumatoid arthritis. Lupus, 2014; 23: 201-3. [3] De Bandt M, Sibilia J, Le Loet X, et al. Systemic lupus erythematosus induced by anti-tumour necrosis factor alpha therapy: A French National survey. Arthritis Res Ther, 2005; 7: R545-51 [4] Oscar M. Perez-Fernandez, et al. Spondyloarthropathies in Autoimmune Diseases and Vice Versa. Autoimmune Diseases, 2011: 2012 Disclosure of Interests: None declared