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AB0277 Antinuclear antibodies in patients with tnf- inhibitors
  1. J. Eibl1,
  2. W. Klotz1,
  3. M. Herold1
  1. 1Medical University of Innsbruck, Dept Internal Medicine 6, Innsbruck, Austria

Abstract

Background During treatment of patients with rheumatic disease like rheumatoid arthritis (RA), spondylarthritis (SpA) and psoriatic arthritis (PsA) with anti TNF-α antibodies (TNF-inhibitors) induction of antinuclear antibodies (ANA) may occur.

Objectives This study is a retrospective examination, to evaluate the number of patients treated with TNF-inhibitors and developing ANAs during treatment.

Methods In a retrospective case-control-study 117 patients were selected, all of whom had received anti TNF-α therapy for at least 6 months. ANA titers were measured by indirect immunofluorescence using HEp-2 cells. Patients were included with clinical diagnosis of RA (n=83), PsA (n=8), and SpA (n=26) respectively.

Results 24 patients were found with ANA titers >1:100 before anti-TNF treatment and excluded from further testing. This occurred primarily in patients diagnosed with RA (n=22), and was seen only in one patient with PsA and one with SpA. Among the remaining 93 patients, 31 showed a rise in ANA titer (either from negative to titer >1:100 or at least two titer steps) during anti TNF-α treatment, 19 of them were diagnosed RA (22.9 %), 3 PsA (37.5 %) and 9 SpA (34.6 %). HEp-2 patterns were classified as homogenous (n=20, 64.5 %), mixed homogenous & fine speckled (n=8, 25.8 %), fine speckled (n=2, 6.4 %) and nucleolar (n=1, 3.2 %). Median time between start of treatment and occurrence of ANA titers was 33 weeks, with a minimum of 4 and a maximum of 308 weeks. All TNF-inhibitors available in Austria were used (Adalimumab, n=42; Etanercept, n=29; Inflixmab, n=28; Golimumab, n=8; Certolizumab, n=1). ANA were induced in 15 patients treated with Infliximab (53.6 %), 13 treated with Adalimumab (31.0 %), one with Etanercept (3.4 %), one with Golimumab (12.5%) and in the single patient treated with Certolizumab. 13 patients with positive ANA titers were switched to a biological other than TNF-inhibitor. 10 times of which the patients retained ANA titers. One patient showed decreasing titers after changing the drug, but increased again after some time, and two patients showed decreasing ANA titers.

Conclusions Incidence and increase of ANA titers during anti-TNF-treatment is similar in patients with different diseases (RA, SpA, PsA), but there seems to be a different incidence among TNF-inhibitors.

Disclosure of Interest None Declared

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