• Internal medicine · Jul 2022

    Immunogenicity against the BNT162b2 mRNA COVID-19 Vaccine in Rheumatic Disease Patients Receiving Immunosuppressive Therapy.

    • Koichi Sugihara, Risa Wakiya, Hiromi Shimada, Tomohiro Kameda, Shusaku Nakashima, Mikiya Kato, Taichi Miyagi, Mao Mizusaki, Rina Mino, Yumi Nomura, Masayuki Inoo, Norimitsu Kadowaki, and Hiroaki Dobashi.
    • Division of Hematology, Rheumatology and Respiratory Medicine, Department of Internal Medicine, Faculty of Medicine, Kagawa University, Japan.
    • Intern. Med. 2022 Jul 1; 61 (13): 1953-1958.

    AbstractObjective To investigate the serum total antibody (immunoglobulin M and immunoglobulin G) titre against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein receptor-binding domain following BNT162b2 messenger ribonucleic acid (mRNA) coronavirus disease 2019 (COVID-19) vaccination in Japanese rheumatic disease patients undergoing immunosuppressive therapy. Methods The serum antibody titre against SARS-CoV-2 spike protein was analysed in 123 outpatients with rheumatic diseases at Kagawa University Hospital and 43 healthy volunteers who had received 2 doses of the BNT162b2 mRNA vaccine with at least 14 days elapsing since the second dose. Results The antibody titre in rheumatic disease patients was significantly lower than that in healthy subjects (p<0.0001). The antibody titres of the 41 patients who received biologics or Janus kinase inhibitors and the 47 patients who received conventional immunosuppressive agents were significantly lower than those of the 35 patients who did not receive immunosuppressive agents (p<0.0001 and p<0.0001, respectively). In addition, the mean antibody titre of the 43 patients on methotrexate was significantly lower than that of the 80 patients not on methotrexate (p=0.0017). Conclusion Immunogenicity to the BNT162b2 mRNA COVID-19 vaccine in rheumatic disease patients was found to be reduced under immunosuppressive treatment. In particular, methotrexate seems to be associated with a decreased antibody response.

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