nach oben

Erschienen in:

10.03.2022 | Original Article

Differential efficacy of TNF inhibitors with or without the immunoglobulin fragment crystallizable (Fc) portion in rheumatoid arthritis: the ANSWER cohort study

verfasst von: Yoichi Nakayama, Ryu Watanabe, Kosaku Murakami, Koichi Murata, Masao Tanaka, Hiromu Ito, Wataru Yamamoto, Kosuke Ebina, Kenichiro Hata, Yuri Hiramatsu, Masaki Katayama, Yonsu Son, Hideki Amuro, Kengo Akashi, Akira Onishi, Ryota Hara, Keiichi Yamamoto, Koichiro Ohmura, Shuichi Matsuda, Akio Morinobu, Motomu Hashimoto

Erschienen in: Rheumatology International | Ausgabe 7/2022

Einloggen, um Zugang zu erhalten

Abstract

Rheumatoid factor (RF) binds to the fragment crystallizable (Fc) portion of immunoglobulin. It could bind to the Fc portion of anti-TNF inhibitors (TNFi) and attenuate the clinical efficacy. We tried to determine whether the therapeutic efficacy of TNFi with Fc might be lower than that of TNFi without Fc in rheumatoid arthritis (RA) patients with high titres of RF. The Kansai Consortium for Well-being of Rheumatic Disease Patients (ANSWER) cohort is an observational multi-center registry of patients with RA in the Kansai district of Japan. RA patients treated with TNFi were included and divided into two groups based on the structural characteristics between TNFi with Fc (infliximab, adalimumab, golimumab, and etanercept) and TNFi without Fc (certolizumab pegol). Patients were classified into 4 groups according to RF titre quartiles. The sequential disease activity score in 28 joints using erythrocyte sedimentation rate (DAS28-ESR) was compared by Mann–Whitney U test between TNFi with and without Fc in each RF titre group. Multiple linear regression analysis was used to analyze the effect of TNFi without Fc for the change of DAS28-ESR adjusted after potential confounders. A total of 705 RA patients were classified into four groups (RF¹; RF 0–15.0 IU/mL, RF²; 15.0–55.0, RF³; 55.0–166, RF⁴; 166–7555). In RF⁴, RA patients treated with TNFi without Fc had a significantly lower DAS28-ESR than those treated with TNFi with Fc [3.2 (2.3–4.2) vs. 2.7 (2.0–3.0)] after 12 months. This effect of TNFi without Fc for the change of DAS28-ESR after 12 months treatment retained in multivariate analysis in RF⁴. TNFi without Fc may be more efficacious than TNFi with Fc in RA patients with high RF titres.

Nur mit Berechtigung zugänglich

Bourne T, Fossati G, Nesbitt A (2008) A PEGylated Fab’ fragment against tumor necrosis factor for the treatment of Crohn disease: exploring a new mechanism of action. BioDrugs 22:331–337. https://doi.org/10.2165/00063030-200822050-00005CrossRefPubMed

Rivkin A (2009) Certolizumab pegol for the management of Crohn’s disease in adults. Clin Ther 31:1158–1176. https://doi.org/10.1016/j.clinthera.2009.06.015CrossRefPubMed

Ingegnoli F, Castelli R, Gualtierotti R (2013) Rheumatoid factors: clinical applications. Dis Markers 35:727–734. https://doi.org/10.1155/2013/726598CrossRefPubMedPubMedCentral

Smolen JS, Landewé RBM, Bijlsma JWJ, Burmester GR, Dougados M, Kerschbaumer A et al (2019) EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2019 update. Ann Rheum Dis 79:685–699. https://doi.org/10.1136/annrheumdis-2019-216655CrossRef

Ebina K, Hashimoto M, Yamamoto W, Hirano T, Hara R, Katayama M et al (2019) Drug tolerability and reasons for discontinuation of seven biologics in 4466 treatment courses of rheumatoid arthritis-the ANSWER cohort study. Arthritis Res Ther 21:91. https://doi.org/10.1186/s13075-019-1880-4CrossRefPubMedPubMedCentral

Hashimoto M, Furu M, Yamamoto W, Fujimura T, Hara R, Katayama M et al (2018) Factors associated with the achievement of biological disease-modifying antirheumatic drug-free remission in rheumatoid arthritis: the ANSWER cohort study. Arthritis Res Ther 20:165. https://doi.org/10.1186/s13075-018-1673-1CrossRefPubMedPubMedCentral

Maeda Y, Hirano T, Ebina K, Hara R, Hashimoto M, Yamamoto W et al (2021) Comparison of efficacy between anti-IL-6 receptor antibody and other biological disease-modifying antirheumatic drugs in the patients with rheumatoid arthritis who have knee joint involvement: the ANSWER cohort, retrospective study. Rheumatol Int 41:1233–1241. https://doi.org/10.1007/s00296-021-04862-yCrossRefPubMed

Jinno S, Onishi A, Dubreuil M, Hashimoto M, Yamamoto W, Murata K et al (2021) Comparison of the drug retention and reasons for discontinuation of tumor necrosis factor inhibitors and interleukin-6 inhibitors in Japanese patients with elderly-onset rheumatoid arthritis-the ANSWER cohort study. Arthritis Res Ther 23:116. https://doi.org/10.1186/s13075-021-02496-wCrossRefPubMedPubMedCentral

Aletaha D, Neogi T, Silman AJ, Funovits J, Felson DT, Bingham CO 3rd et al (2010) 2010 Rheumatoid arthritis classification criteria: an American college of rheumatology/European league against rheumatism collaborative initiative. Arthritis Rheum 62:2569–2581. https://doi.org/10.1002/art.27584CrossRefPubMed

10.

van Gestel AM, Prevoo ML, van’t Hof MA, van Rijswijk MH, van de Putte LB, van Riel PL (1996) Development and validation of the European league against rheumatism response criteria for rheumatoid arthritis. Comparison with the preliminary American college of rheumatology and the World Health Organization/International league against rheumatism criteria. Arthritis Rheum 39:34–40. https://doi.org/10.1002/art.1780390105CrossRefPubMed

11.

Fries JF, Spitz P, Kraines RG, Holman HR (1980) Measurement of patient outcome in arthritis. Arthritis Rheum 23:137–145. https://doi.org/10.1002/art.1780230202CrossRefPubMed

12.

Laurent L, Anquetil F, Clavel C, Ndongo-Thiam N, Offer G, Miossec P et al (2015) IgM rheumatoid factor amplifies the inflammatory response of macrophages induced by the rheumatoid arthritis-specific immune complexes containing anticitrullinated protein antibodies. Ann Rheum Dis 74:1425–1431. https://doi.org/10.1136/annrheumdis-2013-204543CrossRefPubMed

13.

Takeuchi T, Miyasaka N, Inui T, Yano T, Yoshinari T, Abe T et al (2017) High titers of both rheumatoid factor and anti-CCP antibodies at baseline in patients with rheumatoid arthritis are associated with increased circulating baseline TNF level, low drug levels, and reduced clinical responses: a post hoc analysis of the RISING study. Arthritis Res Ther 19:194. https://doi.org/10.1186/s13075-017-1401-2CrossRefPubMedPubMedCentral

14.

Takeuchi T, Miyasaka N, Tatsuki Y, Yano T, Yoshinari T, Abe T et al (2011) Baseline tumour necrosis factor alpha levels predict the necessity for dose escalation of infliximab therapy in patients with rheumatoid arthritis. Ann Rheum Dis 70:1208–1215. https://doi.org/10.1136/ard.2011.153023CrossRefPubMed

15.

Azuma Y, Kaji K, Katogi R, Takeshita S, Kudo A (2000) Tumor necrosis factor-alpha induces differentiation of and bone resorption by osteoclasts. J Biol Chem 275:4858–4864. https://doi.org/10.1074/jbc.275.7.4858CrossRefPubMed

16.

Salgado E, Maneiro JR, Carmona L, Gómez-Reino J (2014) Rheumatoid factor and response to TNF antagonists in rheumatoid arthritis: systematic review and meta-analysis of observational studies. Jt Bone Spine 81:41–50. https://doi.org/10.1016/j.jbspin.2013.04.004CrossRef

17.

Potter C, Hyrich KL, Tracey A, Lunt M, Plant D, Symmons DPM et al (2009) Association of rheumatoid factor and anti-cyclic citrullinated peptide positivity, but not carriage of shared epitope or PTPN22 susceptibility variants, with anti-tumour necrosis factor response in rheumatoid arthritis. Ann Rheum Dis 68:69–74. https://doi.org/10.1136/ard.2007.084715CrossRefPubMed

18.

Bobbio-Pallavicini F, Caporali R, Alpini C, Avalle S, Epis OM, Klersy C et al (2007) High IgA rheumatoid factor levels are associated with poor clinical response to tumour necrosis factor alpha inhibitors in rheumatoid arthritis. Ann Rheum Dis 66:302–307. https://doi.org/10.1136/ard.2006.060608CrossRefPubMed

19.

Santos-Moreno P, Sánchez G, Castro C (2019) Rheumatoid factor as predictor of response to treatment with anti-TNF alpha drugs in patients with rheumatoid arthritis: results of a cohort study. Medicine 98:e14181. https://doi.org/10.1097/MD.0000000000014181CrossRefPubMedPubMedCentral

20.

Julià A, López-Lasanta M, Blanco F, Gómez A, Haro I, Mas AJ et al (2021) Interactions between rheumatoid arthritis antibodies are associated with the response to anti-tumor necrosis factor therapy. BMC Musculoskelet Disord 22:372. https://doi.org/10.1186/s12891-021-04248-yCrossRefPubMedPubMedCentral

21.

Lequerré T, Jouen F, Brazier M, Clayssens S, Klemmer N, Ménard J-F et al (2007) Autoantibodies, metalloproteinases and bone markers in rheumatoid arthritis patients are unable to predict their responses to infliximab. Rheumatology 46:446–453. https://doi.org/10.1093/rheumatology/kel262CrossRefPubMed

22.

Onishi S, Yoshio T, Nagashima T, Minota S (2010) Decrease in the levels of anti-cyclic citrullinated peptide antibody in Japanese patients with rheumatoid arthritis who responded to anti-tumor necrosis factor-α. Mod Rheumatol 20:528–530. https://doi.org/10.1007/s10165-010-0305-7CrossRefPubMed

23.

Lv Q, Yin Y, Li X, Shan G, Wu X, Liang D et al (2014) The status of rheumatoid factor and anti-cyclic citrullinated peptide antibody are not associated with the effect of anti-TNFα agent treatment in patients with rheumatoid arthritis: a meta-analysis. PLoS ONE 9:e89442. https://doi.org/10.1371/journal.pone.0089442CrossRefPubMedPubMedCentral

24.

Klaasen R, Cantaert T, Wijbrandts CA, Teitsma C, Gerlag DM, Out TA et al (2011) The value of rheumatoid factor and anti-citrullinated protein antibodies as predictors of response to infliximab in rheumatoid arthritis: an exploratory study. Rheumatology 50:1487–1493. https://doi.org/10.1093/rheumatology/ker010CrossRefPubMed

25.

Hirosaki H, Maeda Y, Shimojima M, Maeda K, Iwata H, Takeyoshi M (2019) Effects of soluble tumor necrosis factor (TNF) on antibody-dependent cellular cytotoxicity of therapeutic anti-TNF-α antibody. Immunol Invest 48:441–450. https://doi.org/10.1080/08820139.2018.1549067CrossRefPubMed

26.

Jones JD, Shyu I, Newkirk MM, Rigby WFC (2013) A rheumatoid factor paradox: inhibition of rituximab effector function. Arthritis Res Ther 15:R20. https://doi.org/10.1186/ar4152CrossRefPubMedPubMedCentral

27.

Liu L (2018) Pharmacokinetics of monoclonal antibodies and Fc-fusion proteins. Protein Cell 9:15–32. https://doi.org/10.1007/s13238-017-0408-4CrossRefPubMed

28.

Ward ES, Ober RJ (2018) Targeting FcRn to generate antibody-based therapeutics. Trends Pharmacol Sci 39:892–904. https://doi.org/10.1016/j.tips.2018.07.007CrossRefPubMedPubMedCentral

29.

Ternant D, Arnoult C, Pugnière M, Dhommée C, Drocourt D, Perouzel E et al (2016) IgG1 allotypes influence the pharmacokinetics of therapeutic monoclonal antibodies through FcRn binding. J Immunol 196:607–613. https://doi.org/10.4049/jimmunol.1501780CrossRefPubMed

30.

Artandi SE, Calame KL, Morrison SL, Bonagura VR (1992) Monoclonal IgM rheumatoid factors bind IgG at a discontinuous epitope comprised of amino acid loops from heavy-chain constant-region domains 2 and 3. Proc Natl Acad Sci U S A 89:94–98. https://doi.org/10.1073/pnas.89.1.94CrossRefPubMedPubMedCentral

31.

Roopenian DC, Akilesh S (2007) FcRn: the neonatal Fc receptor comes of age. Nat Rev Immunol 7:715–725. https://doi.org/10.1038/nri2155CrossRefPubMed

32.

Porter C, Armstrong-Fisher S, Kopotsha T, Smith B, Baker T, Kevorkian L et al (2016) Certolizumab pegol does not bind the neonatal Fc receptor (FcRn): consequences for FcRn-mediated in vitro transcytosis and ex vivo human placental transfer. J Reprod Immunol 116:7–12. https://doi.org/10.1016/j.jri.2016.04.284CrossRefPubMed

33.

Newkirk MM (2002) Rheumatoid factors: host resistance or autoimmunity? Clin Immunol 104:1–13. https://doi.org/10.1006/clim.2002.5210CrossRefPubMed

34.

Harrold LR, Shan Y, Rebello S, Kramer N, Connolly SE, Alemao E et al (2020) Disease activity and patient-reported outcomes in patients with rheumatoid arthritis and Sjögren’s syndrome enrolled in a large observational US registry. Rheumatol Int 40:1239–1248. https://doi.org/10.1007/s00296-020-04602-8CrossRefPubMedPubMedCentral

Titel: Differential efficacy of TNF inhibitors with or without the immunoglobulin fragment crystallizable (Fc) portion in rheumatoid arthritis: the ANSWER cohort study
verfasst von: Yoichi Nakayama
Ryu Watanabe
Kosaku Murakami
Koichi Murata
Masao Tanaka
Hiromu Ito
Wataru Yamamoto
Kosuke Ebina
Kenichiro Hata
Yuri Hiramatsu
Masaki Katayama
Yonsu Son
Hideki Amuro
Kengo Akashi
Akira Onishi
Ryota Hara
Keiichi Yamamoto
Koichiro Ohmura
Shuichi Matsuda
Akio Morinobu
Motomu Hashimoto
Publikationsdatum: 10.03.2022
Verlag: Springer Berlin Heidelberg
Erschienen in: Rheumatology International / Ausgabe 7/2022
Print ISSN: 0172-8172
Elektronische ISSN: 1437-160X
DOI: https://doi.org/10.1007/s00296-021-05086-w

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

^{Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag}

Kostenlos registrieren

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen

Live-Webinar "Urologie und Sexualmedizin in der Praxis"

Springer Medizin

Differential efficacy of TNF inhibitors with or without the immunoglobulin fragment crystallizable (Fc) portion in rheumatoid arthritis: the ANSWER cohort study

Abstract

Leitlinien kompakt für die Innere Medizin

Neu im Fachgebiet Innere Medizin

Ist Fasten vor Koronarinterventionen wirklich nötig?

Typ-2-Diabetes: Ernährungsunsicherheit vervierfacht Risiko für schwere Hypoglykämien

Mehr Brustkrebs, aber weniger andere gynäkologische Tumoren mit Levonorgestrel-IUS

GLP-1-Agonist Semaglutid wirkt kardio- und nephroprotektiv

Update Innere Medizin

Live-Webinar "Urologie und Sexualmedizin in der Praxis"

Springer Medizin

Abstract

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 7/2022

Association of various myositis-specific autoantibodies with dermatomyositis and polymyositis triggered by pregnancy

IgG4-related disease in pediatric patients: a single-center experience

Probiotic use in the prophylaxis of periodic fever, aphthous stomatitis, pharyngitis, and adenitis (PFAPA) syndrome: a retrospective cohort study

Hypercalcemia in IgG4-related disease: coincidental or associated? Case based review

Hepatitis B vaccination response of treatment-naive patients with juvenile idiopathic arthritis

The prevalence and clinical characteristics of anti-HMGCR (anti-3-hydroxy-3-methyl-glutaryl-coenzyme A reductase) antibodies in idiopathic inflammatory myopathy: an analysis from the MyoCite registry

Leitlinien kompakt für die Innere Medizin

Neu im Fachgebiet Innere Medizin

Ist Fasten vor Koronarinterventionen wirklich nötig?

Typ-2-Diabetes: Ernährungsunsicherheit vervierfacht Risiko für schwere Hypoglykämien

Mehr Brustkrebs, aber weniger andere gynäkologische Tumoren mit Levonorgestrel-IUS

GLP-1-Agonist Semaglutid wirkt kardio- und nephroprotektiv

Update Innere Medizin