Background Increasing use of TNF-α inhibitors (TNFi) has revealed that some patients develop antibodies towards TNFi (anti-TNFi) and that some of these antibodies neutralize the effect of the TNFi and thereby impair efficacy of the medication. A relationship has been established between high levels of anti-TNFi and/or low levels of TNFi and impaired clinical response1-3. Knowledge regarding anti-TNFi may aid in determining which patients will not benefit from continued TNFi treatment.
Objectives To investigate the presence of neutralizing anti-TNFi towards adalimumab and infliximab and the serum-concentration of the prescribed TNFi, in patients with rheumatoid arthritis (RA) in clinical remission.
Methods Patients with RA from six out-patient clinics in Denmark, treated with adalimumab or infliximab, and in clinical remission (DAS28CRP<2.6) were included and concentrations of anti-TNFi and TNFi were determined.
Results Among the 93 patients included, 13 tested positive for anti-TNFi. Of these, 4% (2/49) treated with adalimumab and 25% (11/44) treated with infliximab tested positive for anti-TNFi. Median concentrations of TNFi were 9.68 microg/mL (<0.65 – 30.71) for adalimumab and a median of 3.93 microg/mL (0.67 – >31) for infliximab.
Conclusions In the present study, 14% of patients in remission had developed anti-TNFi whilst undergoing treatment with adalimumab or infliximab. Future research may reveal, if presence of anti-TNFi and concentration of TNFi is a predictor of continued remission in case of termination of TNFi treatment.
Bendtzen K, Geborek P, Svenson M, Larsson L, Kapetanovic M C, Saxne T. Individualized monitoring of drug bioavailability and immunogenicity in rheumatoid arthritis patients treated with the tumor necrosis factor alpha inhibitor infliximab. Arthritis Rheum 2006;54:3782-3789.
Radstake T R, Svenson M, Eijsbouts A M, van den Hoogen F H, Enevold C, van Riel P L et al. Formation of antibodies against infliximab and adalimumab strongly correlates with functional drug levels and clinical responses in rheumatoid arthritis. Ann Rheum Dis 2009;68:1739-1745.
Bartelds G M, Krieckaert C L, Nurmohamed M T, van Schouwenburg P A, Lems W F, Twisk J W et al. Development of antidrug antibodies against adalimumab and association with disease activity and treatment failure during long-term follow-up. JAMA 2011;305:1460-1468.
Acknowledgements We would like to thank the Danish Rheumatism Association, the Oak Foundation and Region Zealand for grant support. We are grateful to Klaus Bendtzen, Michael Stoltenberg and Marcin Szkudlarek for their insight and advise.
Disclosure of Interest None Declared
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