Rituximab-induced Crohn’s disease
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Abstract:
The use of rituximab has significantly improved outcomes in patients with haematological malignancies and autoimmune disease. There are reports of rituximab-associated ulcerative colitis; however, we report for the first time, two cases of rituximab-induced Crohn's disease in elderly patients treated for lymphoma. Both patients had evidence of inflammation, ulceration, and granulomas consistent with Crohn's disease, and responded well to immunosuppression. The association of rituximab and ileocolitis suggests a protective effect of CD20 + lymphocytes in the gut, and implicates their depletion to the development and exacerbation of inflammatory bowel disease.Keywords:
Immunosuppression
The aim of this study was to investigate the incidence of antibodies to rituximab, a chimeric monoclonal antibody targeted against the pan-B-cell marker CD20, in patients with chronic lymphocytic leukemia. Serum concentrations of anti-rituximab antibodies were determined in patients with B-chronic lymphocytic leukemia (newly diagnosed and resistant / recurrent forms, previously treated by rituximab) and healthy controls. Results: none of the patients with newly diagnosed disease have antibodies to rituximab. Positive results were recorded in 8 (33%) patients who received rituximab earlier.
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Recent evidence has provided renewed insight into the role of B cells in the pathophysiology of rheumatoid arthritis (RA). The B cell surface antigen CD20 has been identified as an appropriate therapeutic target in the treatment of a number of immune-mediated conditions, including RA. Binding to CD20 results in depletion of B cells, with an associated improvement in symptoms, while leaving stem and plasma cells - which are devoid of this marker - unaffected. In a randomized double-blind controlled trial in patients with severe active RA who had had an inadequate response to disease modifying antirheumatic drugs (DMARD), a single short course of rituximab, an anti-CD20 chimeric monoclonal antibody, resulted in profound, long-lasting selective peripheral depletion of CD20+ B cells without compromising immunoglobulin levels, as well as significant and clinically meaningful improvements in symptoms of RA for up to 48 weeks without further treatment with rituximab. Rituximab added to existing methotrexate treatment was particularly effective and well tolerated, and provided the basis for further exploration of this promising alternative treatment approach in RA.
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CD59
Complement-dependent cytotoxicity
Follicular lymphoma
B-cell lymphoma
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Rituximab is a chimeric human-mouse monoclonal antibody, which binds to the CD20 antigen on B lymphocytes and causes depletion of CD20+ cells. Rituximab is currently registered for the treatment of non-Hodgkin's lymphoma, chronic lymphocytic leukemia and rheumatoid arthritis. Rituximab also demonstrated efficacy in a number of other autoimmune diseases, including systemic lupus erythematosus. Data available from over published 200 cases may indicate that 50-75% of patients with lupus achieve at least partial remission after rituximab therapy. This effect was not confirmed in a randomized, double-blind phase II/III clinical trial. However methodological inaccuracies which might have led to incorrect conclusions in this trial were pointed out. Further studies are needed to evaluate efficacy of rituximab in different clinical and immunological subtypes of systemic lupus erythematosus.
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Monoclonal antibody therapy
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Abstract: The response rate at relapse to rituximab in prior responders B‐cell non‐Hodgkin's lymphoma (NHL) patients is below 50%. Loss of CD20 expression after rituximab therapy may explain this secondary resistance. However, the frequency of CD20 negative relapses cannot be assessed since most patients that relapsed after rituximab therapy have not been re‐biopsied. Here, we present two patients with CD20 positive low grade B‐cell NHL that lost the cell surface and cytoplasmic expression at relapse after rituximab therapy. Our findings suggest that confirmation of CD20 expression on the malignant B cells is required whenever rituximab therapy is considered.
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The combination of cyclophosphamide and glucocorticoids leads to remission in most patients with antineutrophil cytoplasm antibody (ANCA)–associated vasculitides. However, even when patients receive maintenance treatment with azathioprine or methotrexate, the relapse rate remains high. Rituximab may help to maintain remission.
Maintenance therapy
ANCA-Associated Vasculitis
Microscopic polyangiitis
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Rituximab is a chimeric monoclonal antibody that recognizes the CD20 antigen and is used to treat B-cell non-Hodgkin lymphoma (B-NHL). Few studies have been published examining the use of antibody panels to evaluate B-NHL treated with rituximab. The authors performed a retrospective analysis of immunophenotypic changes and clinical outcome in 18 patients with B-NHL following rituximab therapy. The intensity of CD20 expression was evaluated by flow cytometry and/or immunohistochemistry, before and after rituximab therapy; the latter samples were taken 5 to 12 months after initiating rituximab therapy (median 7 months). Nine of the 18 patients (50%) achieved complete or partial clinical remission and did not have morphologic evidence of lymphoma in the post-therapy samples. The other nine patients (50%) had persistent disease. Two patterns of CD20 expression were noted in the post-therapy samples: unchanged expression of CD20 in neoplastic cells (4/9 cases) and loss of or a significant decrease in detected CD20 expression in neoplastic cells (5/9 cases). These results show that in many cases of B-NHL persisting after rituximab therapy, CD20 expression decreases or is lost, raising the possibility of deletion or expression modulation of the CD20 gene in neoplastic cells. This study also underscores the importance of using a panel of antibodies to evaluate rituximab-treated B-NHL.
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