Background Biological DMARDs (bDMARD) have been associated with the development of autoantibody induction, with in some instances, development of lupus/vasculitis (Williams EL , Bingham SJ , Jarrett SJ , et al). Routine monitoring is often undertaken to detect such changes.
Objectives We evaluated a single-centre bDMARD cohort to determine (i) the incidence of ANA/dsDNA antibodies in different disease groups (ii) whether differences exist between the different bDMARDs and (iii) whether routine ANA testing predicts the development of lupus/vasculitis. This preliminary report includes the analysis for the rheumatoid arthritis (RA) cohort treated with anti-TNF agents only.
Methods Patients with RA who received anti-TNF therapy as their first biologic agent since 2005 were included. Their serial autoantibody profiles, treatment sequences, with seroconversion and adverse events were collected and evaluated.
Results A total of 635 patients (RA, n=454; PsA, n=100; SpA, n=33; JIA and Still’s, n=28; Other, n=20) were identified and for this study, 454 RA patients included for analysis.
Infliximab was associated with higher ANA seroconversion rates (31.2%) compared with etanercept (11.8%) and adalimumab (16.1%) (p<0.001). Median (range) duration of therapy prior to ANA seroconversion was 10.9 (1.3-80.0) months. Positive anti-dsDNA titres with a median (range) of 77 IU/mL (65-109) were noted in n=6 (0.9%), within a median of 2.0 years (range 0.8-4.2). Only one patient experienced drug-induced lupus. In this patient, positive ANA results were present 2.6 years before the diagnosis and anti-dsDNA antibodies were detected 0.9 months before the diagnosis.
Another 2 cases of drug-induced lupus were recorded in this study. One patient had positive ANA result prior to initial anti-TNF therapy. This patient developed lupus-like symptoms with dsDNA seroconversion (interval between positive test and symptoms was 9.0 months). The second patient developed drug-induced lupus on a subsequent (2nd) anti-TNF agent with ANA/dsDNA seroconversion (interval between positive test and symptoms was 0.5 months).
All drug-induced lupus symptoms improved with subsequent rituximab treatment.
Conclusions As has been previously shown, our preliminary analysis illustrated ANA induction with anti-TNF therapies in RA patients; although this was associated with a disease change to lupus in only a minority of patients and was successfully managed with rituximab therapy. Initial review of monitoring time points did not reveal an obvious pattern to predict the clinical phenotype change. Further, complete analysis will be able to inform whether ANA monitoring should be undertaken routinely, and if so, how this should be undertaken to best predict the development of lupus/vasculitis.
Williams EL et al., Anti-TNF-induced lupus. Rheumatology. 2009;48:716-20.
Bingham SJ et al., Induction of antinuclear antibodies in patients with rheumatoid arthritis treated with infliximab and leflunomide. Arthritis Rheum. 2004;50:4072-3.
Jarrett SJ et al., Anti-tumor necrosis factor-alpha therapy-induced vasculitis: case series. J Rheumatol. 2003;30:2287-91.
Disclosure of Interest None Declared