Exacerbation of ulcerative colitis after rituximab salvage therapy.
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.
Goetz
Martin
M
I. Medical Clinic, University of Mainz, Germany.
Atreya
Raja
R
Ghalibafian
Maryam
M
Galle
Peter R
PR
Neurath
Markus F
MF
D000911:Antibodies, Monoclonal / Q000009:adverse effects*; D058846:Antibodies, Monoclonal, Murine-Derived; D001402:B-Lymphocytes / Q000187:drug effects; D003093:Colitis, Ulcerative / Q000139:chemically induced* / Q000473:pathology; D006801:Humans; D016753:Interleukin-10 / Q000172:deficiency; D008875:Middle Aged; D000069283:Rituximab; D016879:Salvage Therapy / Q000009:adverse effects
D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D016753:Interleukin-10; D000069283:Rituximab