Refractory Takayasu arteritis successfully treated with rituximab: case-based review
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Rheumatology International https://doi.org/10.1007/s00296-019-04390-w
INTERNATIONAL
CASE BASED REVIEW
Refractory Takayasu arteritis successfully treated with rituximab: case‑based review Tomoyuki Mutoh1 · Tomonori Ishii1 · Tsuyoshi Shirai1 · Kanae Akita1 · Yukiko Kamogawa1 · Yoko Fujita1 · Hiroko Sato1 · Yuko Shirota2 · Hiroshi Fujii1 · Hideo Harigae1 Received: 14 March 2019 / Accepted: 21 July 2019 © Springer-Verlag GmbH Germany, part of Springer Nature 2019
Abstract Takayasu arteritis (TAK) is a subtype of the large-vessel vasculitis, affecting the aorta and its major branches. Although T cell-mediated autoimmunity is mainly involved in vascular inflammation, in recent years, accumulating evidence suggests the important role of B cells in the pathogenesis and effectiveness of B-cell-targeted therapy with rituximab (RTX), a chimeric anti-CD20 monoclonal antibody in refractory TAK. Herein, we report for the first time a case involving a 34-year-old man with TAK who was refractory to four different biologic agents, such as one selective T-cell co-stimulation modulator (abatacept), one anti-interleukin-6 receptor monoclonal antibody (tocilizumab), and two tumor necrosis factor-α inhibitors (infliximab and etanercept), but eventually achieved remission with RTX. He received a total of six courses of RTX, and doses of prednisolone and methotrexate were tapered without relapse. The current case provided further evidence to the potential role of RTX therapy in patients with refractory TAK, and its efficacy needs to be validated in a controlled trial. Keywords Takayasu arteritis · Large-vessel vasculitis · Rituximab · B cells
Introduction Takayasu arteritis (TAK) is a subtype of the large-vessel vasculitis, affecting the aorta and its major branches [1]. Although T-cell-mediated autoimmunity is mainly involved in the pathogenesis of TAK, B cells are also considered to contribute to the development of vascular inflammation [2]. In fact, increased B-cell subsets in the peripheral blood of active TAK patients and the infiltration of B cells into inflamed aortic walls are reported [3, 4]. In addition, serum levels of B-cell-activating factor of the tumor necrosis factor (TNF) family, essential for survival, differentiation, and isotype switching of B cells [5], are significantly higher in patients with active TAK compared with healthy controls [6], and anti-endothelial cell antibodies have been more frequently found in active compared with inactive TAK [7]. * Tomonori Ishii [email protected] 1
Department of Hematology and Rheumatology, Tohoku University Graduate School of Medicine, 1‑1 Seiryo‑machi, Aoba‑ku, Sendai, Miyagi 980‑8574, Japan
Department of Hematology and Rheumatology, Tohoku Medical and Pharmaceutical University, Sendai, Japan
2
More recently, serum IgG from TAK patients has been found to activate mammalian target of rapamycin pathway, leading to endothelial cell proliferation [8]. To support the pathogenic role of B cells, B-cell-targeted therapy with rituximab (RTX), a chimeric anti-CD20
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