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Comparison of two interferon-γ release assays and tuberculin skin test for detecting latent tuberculosis in patients with immune-mediated inflammatory diseases
  1. S Kleinert1,
  2. O Kurzai2,
  3. J Elias2,
  4. K Marten3,
  5. C Engelke3,
  6. M Feuchtenberger1,
  7. J Sandstede4,
  8. M Frosch2,
  9. H-P Tony1,
  10. C Kneitz1
  1. 1Department of Rheumatology and Clinical Immunology, Medizinische Klinik und Poliklinik II, University Hospital of Würzburg, Würzburg, Germany
  2. 2University of Würzburg, Institute of Hygiene and Microbiology, Würzburg, Germany
  3. 3Department of Radiology, Georg August University of Göttingen, Göttingen, Germany
  4. 4Department of Radiology, University Hospital of Würzburg, Würzburg, Germany
  1. Correspondence to S Kleinert, Department of Rheumatology and Clinical Immunology, Medizinische Klinik und Poliklinik II, University Hospital of Würzburg, Würzburg, Germany; kleinert_s{at}klinik.uni-wuerzburg.de

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Biological agents interfering with proinflammatory tumour necrosis factor α (TNFα) signalling have become an established tool in the treatment of rheumatoid arthritis and other chronic inflammatory conditions. Their use is associated with an increased risk for some infections including the reactivation of latent tuberculosis infection (LTBI).1 Consequently, screening for LTBI prior to onset of anti-TNFα therapy is recommended. Interferon γ release assays (IGRAs) are novel diagnostic tools for the diagnosis of LTBI and show a high specificity compared with the tuberculin skin test (TST).2 However, optimal screening procedures are still a matter of debate.1 Furthermore, questions remain with regard to the performance of IGRAs in patients receiving immunosuppressive therapy and the comparative performance of the two commercially available IGRAs.2 To address these questions, 90 successive patients from the outpatient department of rheumatology (representing an LTBI low prevalence patient group) at the University Hospital of Würzburg, Germany were prospectively screened for LTBI using TST, TSPOT.TB (TSPOT; Oxford Immunotec, Abingdon, Oxfordshire, UK) and Quantiferon Gold (QFT; Cellestis Europe, Darmstadt, Germany) before initiation of anti-TNF treatment). Underlying disease entities included ankylosing spondylitis (n=18 patients), rheumatoid arthritis (n=51), psoriatic arthritis (n=10) and other autoimmune diseases (n=11). Nineteen patients were receiving a steroid regimen of ≥7.5 mg prednisone equivalent and …

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