Exacerbation of ulcerative colitis after rituximab salvage therapy

被引:200
作者
Goetz, Martin
Atreya, Raja
Ghalibafian, Maryam
Galle, Peter R.
Neurath, Markus F.
机构
[1] Johannes Gutenberg Univ Mainz, Med Clin 1, Immunol Lab, D-55131 Mainz, Germany
[2] Johannes Gutenberg Univ Mainz, Dept Pathol, D-6500 Mainz, Germany
关键词
inflammatory bowel disease; ulcerative colitis; therapy; rituximab; CD20; interleukin-10;
D O I
10.1002/ibd.20215
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: B-cells are considered to play a pathogenic role in human ulcerative colitis (UC) by producing autoantibodies that cause epithelial cell damage. Here we report on a patient with intractable UC who suffered from a severe exacerbation of UC after salvage therapy with rituximab, a B-cell-depleting anti-CD20-antibody. Methods: A 58-year-old patient with active long-standing UC and unresponsiveness or adverse events to mesalamine, corticosteroids, azathioprine, methotrexate, infliximab, leukapheresis, mycophenolate mofetil, and adalimumab received 375 Mg/m(2) rituximab. Results: A severe exacerbation of UC activity was noted upon therapy that required hospitalization. Subsequent studies showed a complete depletion of CD20-positive mucosal B-cells associated with a suppression of local IL-10 production. Conclusions: In contrast to rheumatoid arthritis patients, rituximab had deleterious effects in our UC patient by blocking IL-10 producing B-cells. Our data suggest an important anti- rather than proinflammatory role of B-cells in UC.
引用
收藏
页码:1365 / 1368
页数:4
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