Exacerbation of ulcerative colitis after rituximab salvage therapy

M Goetz, R Atreya, M Ghalibafian… - Inflammatory bowel …, 2007 - academic.oup.com
M Goetz, R Atreya, M Ghalibafian, PR Galle, MF Neurath
Inflammatory bowel diseases, 2007academic.oup.com
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 …
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/m2 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.
Oxford University Press