Session Information
Session Type: Late-Breaking Abstracts
Background/Purpose: The differences between RA and AS have been recently highlighted (1). There is evidence that there are major clinical, pathophysiological and genetic differences. In addition, the majority of patients with RA are well known to have autoantibodies such as rheumatoid factor and anti-CCP as well as anti-nuclear antibodies and others, autoantibodies in patients with AS have only recently been described which recognise CD74. Although it is well known that ADA develop in response to anti-TNF agents, especially INF and adalimumab, it is unknown whether the degree of ADA development is different between the two diseases. Here we analysed the difference between RA and AS in mounting ADA by taking advantage of the data obtained in two recent trials performed to show biosimilarity between INF and CT-P13 (2,3).
Methods: The determination of ADA was performed by an electrochemiluminescent immunoassay using Meso Scale Discovery technology. Tests were performed by ICON Laboratory, Manchester, UK. Because of the bivalent characteristics of the antibody, only the samples containing antibody bound to both the biotinylated anti-CT-P13/INF and the sulfo-tagged anti-CT-P13/INF, generate an electroche-miluminescent signal that is proportional to the amount of antibody present.
Results: The demographics of both patient groups have been described in detail in the original papers (2,3). Despite of concomitant therapy with methotrexate patients with RA clearly had a higher inciden-ce of ADA to both, INF and CT-P13 in comparison to patients with AS. The observed data are depic-ted in Tables 1a and 1b. There was no difference in ADA development between INF and CT-P13.
Conclusion:
This is the first study to describe a striking discrepancy in ADA development between patients with RA and AS despite methotrexate therapy in the former. Of course, patients with RA and AS differ in age, gender, genetic background and other factors but the reason for the observed difference is not clear. Further research is necessary to clarify its pathophysiologic basis. There seems to be potential to learn about the nature of the disease and the mechanisms of ADA development.
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1a: Comparison of ADA development in patients treated with CT-P13 |
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1b: Comparison of ADA development in patients treated with INF |
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Disclosure:
J. Braun,
None;
X. Baraliakos,
None;
A. Kudrin,
None;
H. Kim,
Celltrion,
3;
S. J. Lee,
CELLTRION, Inc.,
3.
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ACR Meeting Abstracts - https://acrabstracts.org/abstract/striking-discrepancy-in-the-development-of-anti-drug-antibodies-ada-in-patients-with-rheumatoid-arthritis-ra-and-ankylosing-spondylitis-as-in-response-to-infliximab-inf-and-its-biosimilar-ct-p/