Response to Rituximab and Timeframe to Relapse in Rheumatoid Arthritis Patients

Pyrpasopoulou, Athina; Δούμα, Στέλλα; Triantafyllou, Αreti; Simoulidou, Elisavet; Samara, Magda; Parapanisiou, Efthymia; Aslanidis, Spyros

doi:10.1007/bf03256352

Cited by 13 publications

(7 citation statements)

References 21 publications

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“…This observation is consistent with recently reported findings regarding the association between a positive response to RTX and RF and/or a-CCP positivity [50][51][52]. It can be assumed that RA patients characterized by greater autoantibody production respond better to therapies directed against B lymphocytes.…”

Section: Discussionsupporting

confidence: 92%

“…Several authors have shown that the presence of RF, which is associated with more severe disease and a reduced therapeutic response in general, is a marker of a higher degree of response to RTX [50][51][52]. However, changes in RF serum levels in the follow-up after RTX treatment is not predictive of response, as we also found in this study, even focusing on IgA-specific RF.…”

Section: Discussioncontrasting

confidence: 55%

“…The choice of treatment and monitoring of treatment of RA with biological agents is currently a field of major interest, but strong data on biological markers still remain undefined [49][50][51]. Several authors have shown that the presence of RF, which is associated with more severe disease and a reduced therapeutic response in general, is a marker of a higher degree of response to RTX [50][51][52].…”

Section: Discussionmentioning

confidence: 99%

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Serum levels of anti-CCP antibodies, anti-MCV antibodies and RF IgA in the follow-up of patients with rheumatoid arthritis treated with rituximab

Fabris¹,

Vita

Blasone³

et al. 2010

Autoimmun Highlights

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at least 6 months of therapy with disease-modifying antirheumatic drugs (DMARDs; methotrexate, leflunomide, cyclosporine, chloroquine) and/or at least 6 months of therapy with anti-TNF biologics. The evaluation of response to RTX was made at month +6 using the EULAR criteria (DAS28). a-CCP, a-MCV, total RF and RF IgA were determined at baseline (before the first infusion of RTX) and after 1, 3 and 6 months. In serum samples obtained before treatment two cytokines essential for Blymphocyte proliferation, interleukin 6 (IL-6) and B-lymphocyte stimulator (BLyS) were also determined. In all patients a significant and consistent reduction in all the tested antibodies was found during follow-up, with no differences in respect of the degree of response to RTX. Of note, at baseline, generally a higher titre of all autoantibodies was seen in patients who then showed a better response to RTX. Finally, there were no differences in serum concentrations of IL-6 and BLyS in patients in relation to the presence or absence of the autoantibodies investigated, nor was there any significant correlation between the serum concentrations of the cytokines and the titres of the autoantibodies. Thus, neither a-MCV compared to a-CCP, nor RF IgA compared to routine total RF, provided any additional predictive information in the follow-up of patients with RA treated with RTX.

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Section: Discussionsupporting

confidence: 92%

Section: Discussioncontrasting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

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Serum levels of anti-CCP antibodies, anti-MCV antibodies and RF IgA in the follow-up of patients with rheumatoid arthritis treated with rituximab

Fabris¹,

Vita

Blasone³

et al. 2010

Autoimmun Highlights

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“…In addition, the present study compared seropositive (RF‐positive and/or anti‐CCP–positive) RA patients (n = 229), who are widely recognized as the best responders to RTX (2–5), to seronegative RA patients (n = 40). Although the number of seronegative patients was limited, our findings suggest a different role of BLyS genetics as a biomarker in either seropositive or seronegative RA, similar to other genetic biomarkers (31–33, 35–38).…”

Section: Discussionmentioning

confidence: 99%

The TTTT B lymphocyte stimulator promoter haplotype is associated with good response to rituximab therapy in seropositive rheumatoid arthritis resistant to tumor necrosis factor blockers

Fabris¹,

Quartuccio²,

Vital³

et al. 2012

Arthritis & Rheumatism

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Objective. To investigate the polymorphisms in the promoter region of the B lymphocyte stimulator (BLyS) gene as markers of response to rituximab (RTX) in rheumatoid arthritis (RA).Methods. The study was first conducted in 152 Italian RA patients and then replicated in an additional 117 RA patients (73 Italian, 44 British). The European League Against Rheumatism response criteria were used to evaluate the response rate at months 4 and 6 after the first cycle of RTX, by means of the Disease Activity Score in 28 joints using the erythrocyte sedimentation rate; patients were classified according to the best response shown between months 4 and 6. BLyS promoter polymorphisms were analyzed by polymerase chain reaction followed by the analysis of the restriction fragments, BLyS promoter haplotypes were analyzed using the expectation-maximization algorithm, and BLyS serum levels were analyzed using enzyme-linked immunosorbent assay. Odds ratios (ORs) were calculated with 95% confidence intervals (95% CIs).Results. The TTTT BLyS promoter haplotype appeared to be significantly associated with response to RTX only in the subset of seropositive patients (those positive for rheumatoid factor and/or anti-cyclic citrullinated peptide). The replication study confirmed that this association was limited to seropositive RA patients in whom treatment with anti-tumor necrosis factor Supported by Regione Friuli-Venezia Giulia, Italy (grant LR26.05.07/art.23).

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“…The effect of rituximab on different CD20+ B cell subpopulations has been assessed in analogous clinical studies. Within the context of specific clinical syndromes, for example, rheumatoid arthritis, rituximab has been shown to be more efficient in subcategories of patients, regarding the specific disease, in seropositive patients [17]. To investigate the immunological imprint of this clinical observation, investigators compared the effects of rituximab on B cells from RF+ and RF− RA patients.…”

Section: Effect Of Rituximab On B Cell Populations: Applications Imentioning

confidence: 99%

CD20+ B Cell Depletion in Systemic Autoimmune Diseases: Common Mechanism of Inhibition or Disease-Specific Effect on Humoral Immunity?

Pateinakis

Pyrpasopoulou

2014

BioMed Research International

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Autoimmunity remains a complex physiologic deviation, enabled and perpetuated by a variety of interplayers and pathways. Simplistic approaches, targeting either isolated end-effectors of more centrally placed interactors of these mechanisms, are continuously tried in an effort to comprehend and halt cascades with potential disabling and deleterious effects in the affected individuals. This review focuses on theoretical and clinically proved effects of rituximab-induced CD20+ B cell depletion on different systemic autoimmune diseases and extrapolates on pathogenetic mechanisms that may account for different interindividual or interdisease responses.

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Response to Rituximab and Timeframe to Relapse in Rheumatoid Arthritis Patients

Cited by 13 publications

References 21 publications

Serum levels of anti-CCP antibodies, anti-MCV antibodies and RF IgA in the follow-up of patients with rheumatoid arthritis treated with rituximab

Serum levels of anti-CCP antibodies, anti-MCV antibodies and RF IgA in the follow-up of patients with rheumatoid arthritis treated with rituximab

The TTTT B lymphocyte stimulator promoter haplotype is associated with good response to rituximab therapy in seropositive rheumatoid arthritis resistant to tumor necrosis factor blockers

CD20+ B Cell Depletion in Systemic Autoimmune Diseases: Common Mechanism of Inhibition or Disease-Specific Effect on Humoral Immunity?

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