Rituximab, B-Lymphocyte Depletion, and Preservation of Beta-Cell Function

Publication Description
Background The immunopathogenesis of type 1 diabetes mellitus is associated with T-lymphocyte autoimmunity. However, there is growing evidence that B lymphocytes play a role in many T-lymphocyte–mediated diseases. It is possible to achieve selective depletion of B lymphocytes with rituximab, an anti-CD20 monoclonal antibody. This phase 2 study evaluated the role of B-lymphocyte depletion in patients with type 1 diabetes. Methods We conducted a randomized, double-blind study in which 87 patients between 8 and 40 years of age who had newly diagnosed type 1 diabetes were assigned to receive infusions of rituximab or placebo on days 1, 8, 15, and 22 of the study. The primary outcome, assessed 1 year after the first infusion, was the geometric mean area under the curve (AUC) for the serum C-peptide level during the first 2 hours of a mixed-meal tolerance test. Secondary outcomes included safety and changes in the glycated hemoglobin level and insulin dose. Results At 1 year, the mean AUC for the level of C peptide was significantly higher in the rituximab group than in the placebo group. The rituximab group also had significantly lower levels of glycated hemoglobin and required less insulin. Between 3 months and 12 months, the rate of decline in C-peptide levels in the rituximab group was significantly less than that in the placebo group. CD19+ B lymphocytes were depleted in patients in the rituximab group, but levels increased to 69% of baseline values at 12 months. More patients in the rituximab group than in the placebo group had adverse events, mostly grade 1 or grade 2, after the first infusion. The reactions appeared to be minimal with subsequent infusions. There was no increase in infections or neutropenia with rituximab. Conclusions A four-dose course of rituximab partially preserved beta-cell function over a period of 1 year in patients with type 1 diabetes. The finding that B lymphocytes contribute to the pathogenesis of type 1 diabetes may open a new pathway for exploration in the treatment of patients with this condition. (ClinicalTrials.gov number, NCT00279305 [ClinicalTrials.gov] .)

Primary Author
Pescovitz,Mark D.
Greenbaum,Carla J.
Krause-Steinrauf,Heidi
Becker,Dorothy J.
Gitelman,Stephen E.
Goland,Robin
Gottlieb,Peter A.
Marks,Jennifer B.
McGee,Paula F.
Moran,Antoinette M.
Raskin,Philip
Rodriguez,Henry
Schatz,Desmond A.
Wherrett,Diane
Wilson,Darrell M.
Lachin,John M.
Skyler,Jay S.
Type 1 Diabetes TrialNet Anti-CD20 Study Group

Volume
361

Issue
22

Start Page
2143

Other Pages
2152

Publisher
Mass Med Soc

URL
http://content.nejm.org/cgi/content/abstract/361/22/2143

PMID
19940299

PMCID
PMC6410357



Reference Type
Journal Article

Periodical Full
The New England Journal of Medicine

Publication Year
2009

Publication Date
Nov 26,

Place of Publication
United States

ISSN/ISBN
0028-4793

Document Object Index
10.1056/NEJMoa0904452