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FRI0207 The input of measuring of infliximab and adalimumab levels and levels of antibodies to these drugs in the management of patients with autoimmune diseases treated with anti tnf monoclonal antibodies.
  1. Y. Braun-Moscovici1,2,
  2. S. Ben Horin3,4,
  3. A. Dagan1,
  4. K. Toledano1,2,
  5. D. Markovits1,
  6. A. Saffouri1,
  7. R. Beshara1,
  8. A. Rozin1,2,
  9. M. A. Nahir1,2,
  10. Y. Chowers2,5,
  11. A. Balbir-Gurman1,2
  1. 1B. Shine Rheumatology Unit, Rambam Health Care Campus
  2. 2The Bruce Rappaport Faculty of Medicine, Technion-Institute of Technology, Haifa
  3. 3Department of Gastroenterology, Sheba Medical Center
  4. 4Sackler School of Medicine, Tel-Aviv University, Tel Aviv
  5. 5Gastroenterology Institute, Rambam Health Care Campus, Haifa, Israel


Background In patients (pts) with RA and other autoimmune diseases the immunogenicity during infliximab (INF) or adalimumab (ADA) therapy lead to the r loss of response. Increasing the drug dose or shortening the re-treatment intervals has economical implications. Switching to another biological agent may be suitable. High levels of anti-INF or anti ADA antibodies (Ab) is accompanied by significant reduction in serum drug concentrations.

Objectives To assess the input of measuring serum INF and ADA levels and levels of anti-INF-Ab and anti-ADA-Ab in the management of pts with RA and other autoimmune diseases trated with these drugs.

Methods Trough serum levels of INF and ADA and anti-INF-Ab and anti-ADA-Ab were measured by ELISA. Anti-INF-Ab were identified by anti-human lambda chain Ab in order to minimize the interference of serum INF. Treated pts were classified into responders and non-responders based on disease activity. Statistics: descriptive statistics, T test, Spearman’s correlation and multiple logistic regression analysis.

Results 131 serum tests for INF and 48 - for ADA were performed in 101 pts (mean age 50.2 and disease duration 9.9 years). Among responders 51 pts received INF and 16 pts – ADA. Among non-responders 34 pts had no response and 10 pts losed response ( 24 pts – INF; 20 pts - ADA). Levels (µg/ml, mean, SD) of INF and ADA in responders 4.2(2.3) and 7(5.95) were significantly higher than in non-responders1.09(0.45) and 2.9(0.45) respectively; levels of anti-INF-Ab and anti-ADA-Ab in responders 4.59(1.0) and 0.1(0) were significantly lower than in non-responders 13.13(6.1) and 8.1(1.0). Patients with RA and ankylosing spondylitis had significantly higher Ab levels than pts with psoriatic arthritis: 8.37(3.8), 9.6(0.3) and 3.5(0)µg/ml respectively. High anti-INF-Ab or anti-ADA-Ab levels predicted treatment discontinuation. In all non-responders with low INF/ADA levels and low anti-INF-Ab/anti-ADA-Ab the shortening of re-treatment intervals lead to significant improvement (Table 1).

Conclusions Assessment of immunogenicity of anti-TNF monoclonal antibodies proved useful imformation for guiding the therapy in autoimmune diseases with suboptimal clinical response. Patients with low INF/ADA levels and low levels of corresponding Ab may benefit from increasing the drug dose or decreasing of re-treatment intervals. In pts with negligible serum levels of INF/ADA and high levels of corresponding Ab the therapy should be switched to a different drug.

Disclosure of Interest: None Declared

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