Rituximab Therapy In Patients Research Articles

Опыт применения биоаналога генно-инженерного биологического препарата у больных ревматоидным артритом в реальной клинической практике

The article presents the data of the Moscow Unified Arthritis Register (MUAR) and the results of rituximab therapy in patients with rheumatoid arthritis (RA).Aim: to evaluate the efficacy and safety of switching from the original rituximab (MabThera®) to its biosimilar (Acellbia®) in patients with RA in real clinical practice.Patients and Methods: patients with RA, included in MUAR register, were evaluated with an assessment of therapy efficacy and safety with the original rituximab (MabThera®), as well as after switching to the rituximab biosimilar (Acellbia®). A standard examination was performed to determine the number of swollen and tender joints, erythrocyte sedimentation rate, and C-reactive protein. Treatment efficacy was assessed using the DAS28 composite index, HAQ-DI (Health Assessment Questionnaire Disability Index) and RAPID-3 (Routine Assessment of Patient Index Data 3). In terms of safety, adverse events were recorded based on patient reports.Results: switching therapy regimen of 46 patients with RA from the original rituximab to the biosimilar was not accompanied by a decrease in the treatment efficacy. There was statistically significant increase in the proportion of the patients with low disease activity (DAS28<3.2) from 39.1% to 52.2% and remission (DAS28<2.6) from 17.4% to 23.9%, respectively. Further positive dynamics of HAQ-DI and RAPID-3 indices were noted. According to the authors, the increase in the frequency of a positive response to the treatment was associated with the duration of rituximab use in general. The frequency of adverse events during therapy with the original rituximab and its biosimilar was comparable: 9.22 and 10.9 per 100 patient years respectively.Conclusion: there were no significant differences between the original rituximab and its biosimilar. The results of switching therapy regimen of patients with RA from the original rituximab (MabThera®) to its biosimilar (Acellbia®), observed in real clinical practice, confirm their therapeutic equivalence.KEYWORDS: rheumatoid arthritis, rituximab, biosimilar, real clinical practice.FOR CITATION: Zhilyaev E.V., Koltsova E.N., Shmidt E.I. et al. Experience of using a genetically engineered biological drug biosimilar in patients with rheumatoid arthritis in real clinical practice. Russian Medical Inquiry. 2020;4(8):492–497. DOI: 10.32364/2587-6821-2020-4-8-492-497.

Hepatitis C virus-associated cryoglobulinemic vasculitis: A 20-year experience with treatment

To summarize the experience of a multidisciplinary therapy hospital in treating patients with hepatitis C virus (HCV)-associated cryoglobulinemic vasculitis (CV). Seventy-two patients (mean age, 49.4±10.3 years) with HCV-associated CV were examined and followed up for an average period of 2.8±3.6 years. The efficiency of traditional (corticosteroids ± cyclophosphamide) and selective (rituximab) immunosuppressive therapy (IST) was estimated in 31 and 15 observations, respectively, and that of antiviral therapy (AVT) in 25. Vasculitis activity was assessed using the Birmingham vasculitis activity score (BVAS). The patients' survival was studied; multivariate logistic regression analysis was carried out. 24 (33.4%) of the 72 patients had a stage of liver cirrhosis (LC). The pretreatment mean BVAS was 11.9±7.2 (range 2 to 36). Severe CV (BVAS ≥15) was present in 30.6% of the patients. AVT was accompanied by achievement of sustained virologic response in 48% of the patients, clinical remission in 68% and had an advantage over IST in relation to long-term treatment results. Rituximab was significantly more effective than traditional immunosuppressants (remission rates of 73 and 13%, respectively). Combined therapy (rituximab and AVT) was most effective in patients with severe forms of vasculitis. Sixteen patients died from complications of vasculitis (37.5%), infection (37.5%), and LC (25%). The factors adversely affecting prognosis were age >55 years (odds ratio (OR), 4.49), the presence of LC (OR, 3.68), renal failure (OR, 4.66) and the use of glucocorticosteroids (OR, 3.91). HCV-associated CV can determine the prognosis of chronic HСV infection. AVT is the treatment of choice in all patients with HСV-associated CV. AVT must be combined with rituximab therapy in patients with severe forms of vasculitis.

Late-onset neutropenia after rituximab therapy in patients with autoimmune thrombotic and hemostatic disorders: a single center analysis.

Autoimmune thrombotic and hemostatic disorders, caused by autoantibodies against various factors regulating thrombosis and hemostasis, are rare. Rituximab (RTX) is on occasion used for treating these disorders. Late-onset neutropenia (LON) has been described as a side effect of RTX treatment for patients with hemato-oncological and/or rheumatological diseases but not for those with autoimmune thrombotic and hemostatic disorders. Eleven patients with autoimmune thrombotic and hemostatic disorders received RTX in our institution. Four of these 11 cases (36.4%) developed LON after a median 72.6 days of RTX administration (range 43-122). Three cases required G-CSF, but no severe infections developed.

Efficacy and safety of rituximab therapy in patients with pemphigus vulgaris: first report from Turkey.

Pemphigus vulgaris (PV) is a severe, chronic, and potentially life-threatening autoimmune blistering disease that affects the skin and mucous membranes. Rituximab is a monoclonal anti-CD20 antibody which has been used increasingly in the therapy of PV. The present study sought to test the efficacy and safety of rituximab as an adjuvant therapy by retrospective analysis of clinical and immunological data for 29 patients with PV who were treated with rituximab between 2010 and 2015. Response to therapy, duration of clinical remission, serology of the response, and adverse effects of rituximab were evaluated. The mean ± standard deviation (SD) follow-up time was 17.48 ± 13.18 months. In all patients, findings showed either a decrease in antibody titers or that antibodies were completely undetectable after therapy. Rituximab use resulted in a significant reduction in steroid dosage during follow-up. At the end of the follow-up period, 26 patients (96.2%) had achieved complete remission with or without therapy (one patient had no follow-up and one patient had died, most probably as the result of a thromboembolic event). In 44.4% of patients, a clinical relapse occurred after a mean ± SD period of 13.1 ± 4.7 months after the initiation of rituximab therapy. Relapses were managed with additional infusions of rituximab. Rituximab is a beneficial and relatively safe adjuvant treatment for PV that facilitates prolonged clinical remission and has a significant steroid-sparing effect.

Current Treatment of Cryoglobulinemic Vasculitis

For patients with cryoglobulinemic vasculitis, we consider treatment of the underlying disorder (if present) to be first-line therapy. For hepatitis C virus (HCV)-associated cryoglobulinemic vasculitis, antiviral therapy directed at HCV should be considered first-line treatment for patients who are candidates. Interferon-free direct acting antiviral regimens have been shown to be very effective in the treatment of chronic HCV infection and preliminary results of the use of these regimens are promising for the treatment of HCV-associated cryoglobulinemic vasculitis. Close collaboration with a gastroenterologist or hepatologist is needed, given the complexity in choosing from the various treatment options. Patients with severe life- or organ-threatening manifestations of cryoglobulinemic vasculitis may benefit by treatment with rituximab in addition and potentially prior to the initiation of antiviral therapy. We also recommend treatment with rituximab in patients who have a contraindication to or who have failed antivirals. Plasmapheresis, in conjunction with immunosuppression, can be used as adjunctive therapy to antiviral and/or rituximab therapy for patients with severe organ- or life-threatening disease. Cyclophosphamide use is best reserved for patients with severe disease who are unable to be treated with antiviral or rituximab therapy. The role of glucocorticoid use remains poorly defined, with some studies supporting moderate or high-dose prednisone use to treat active disease.

Efficacy and Safety of Rituximab in Systemic Lupus Erythematosus and Sjögren Syndrome Patients With Refractory Thrombocytopenia: A Retrospective Study of 21 Cases.

Recent studies suggested a potential of rituximab (RTX) in treating autoimmune thrombocytopenia (AITP) secondary to autoimmune diseases. In this study, we retrospectively evaluated the efficacy and safety of RTX therapy in patients with refractory AITP secondary to systemic lupus erythematosus (SLE) and Sjögren syndrome (SS). Twenty-one SLE and/or SS patients with treatment-resistant AITP were treated once or repeatedly with RTX at the Rheumatology Clinic Renji Hospital, during the period March 2012 to June 2014. Clinical and laboratory variables recorded at every follow-up visit were analyzed. The median age of all patients was 37.05 ± 3.15 years (range, 13-67 years; 20 female and 1 male). The median AITP duration before RTX treatment was 5.46 years. Previous treatments of 21 patients included immunosuppressive agents such as corticosteroids (n = 19), cyclosporine (n = 9), mycophenolate mofetil (n = 2), methotrexate (n = 3), cyclophosphamide (n = 2), vincristine (n = 3), and hydroxychloroquine (n = 15), and 7 patients received concomitantly intravenous immunoglobulin therapy. Two patients had undergone splenectomy without improvement. Seventeen patients (80.95%) were treated repeatedly with RTX during the follow-up period. The overall response rate to RTX treatment (including complete response, 52.38%; partial response, 28.57%) was 80.95%. A significant increase (P < 0.05) of platelet counts was seen after 1 month (median, 32.24 × 10/mL vs 66.53 × 10/mL). Relapses occurred mostly during the first 9 months, and maintaining duration of response was 10.27 months (range, 2-17 months) on average after the first RTX infusion. Antiplatelet antibodies, especially IgG isotype, decreased significantly (P < 0.05) after RTX treatment. No adverse effects were observed among 15 patients (71.4%); however, 2 cases died of severe pneumonia, and another developed lymphoma. Rituximab is an additional potent therapeutic treatment option for SLE and SS patients with AITP refractory to conventional immunosuppressive treatments. For most patients, RTX was safe and well tolerated.

Phase II clinical trail of patients with relapsed follicular lymphoma treated with a humanized antiprogrammed death-1 monoclonal antibody combined with rituximabrreport in the 54th ASH annual meeting

Objective A phase Ⅱ trial of anti-programmed death-1 (PD-1) monoclonal antibody CT-011,an anti PD-1 humanized monoclonal antibody combined with rituximab therapy in patients with relapsed follicular lymphoma (FL) were conducted.Methods In order to evaluate the safety and efficacy of CT-011,the impacts of CT-011 on immune cells both from the peripheral blood (PB) samples and tumor microenvironment were examined.PB and core needle biopsies from involved lymph nodes were collected prior to and on day 14 after the first infusion of CT-011.PB mononuclear cells (PBMC) were analyzed by multiparametric flow cytometry to determine various immune cell subsets.Whole genome gene expression profiling (GEP) was performed on core needle biopsies.Results A significant increase in the absolute number of PB immune cells were observed in day 14 samples compared with baseline including total lymphocyte count (P ＜ 0.01),CD+3 T cells (P =0.01),CD+4 T cells (P ＜ 0.01).Comparison of GEP from core needle biopsies obtained pretreatment and day 14 (n =8 pairs) showed up regulation of several genes associated with T cell activation.Conclusion Administration of CT-011 was associated with increase in the numbers of CD+4 T cells and resulted in activation of T cells in the PB and the tumor microenvironment in FL.These results provide insight into the mechanism of action of CT-011 and offer a predictive biomarker for selection of patients for future clinical trials with this class of agents in FL. Key words: Programmed death-1; Immunotherapy; T-lymphocytes; Lymphoma, follicular; ASH annual meeting

Effect of rituximab on B cell phenotype and serum B cell-activating factor levels in patients with thrombotic thrombocytopenic purpura.

Autoantibodies inhibiting the activity of the metalloproteinase, ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13), underlie the pathogenesis of thrombotic thrombocytopenic purpura (TTP). Rituximab (RTX) combined with plasma-exchange (PEX) is an effective treatment in TTP. Patients can remain in remission for extended periods following PEX/RTX, and this is associated with continuing reduction in antibodies to ADAMTS13. Factors controlling B cell differentiation to autoantibody production, including stimulation through the B cell receptor and interactions with the B cell-activating factor (BAFF), may thus impact length of remission. In this cross-sectional study, we measured naive and memory B cell phenotypes [using CD19/immunoglobulin (Ig)D/CD27] following PEX/RTX treatment in TTP patients at B cell return (n=6) and in 12 patients in remission 10-68 months post-RTX. We also investigated relationships among serum BAFF, soluble CD23 (sCD23(-) a surrogate measure of acquiring B memory (CD27(+) ) phenotype) and BAFF receptor (BAFF-R) expression. At B cell return after PEX/RTX, naive B cells predominated and BAFF-R expression was reduced compared to healthy controls (P<0.001). In the remission group, despite numbers of CD19(+) B cells within normal limits in most patients, the percentage and absolute numbers of pre-switch and memory B cells remained low, with sCD23 levels at the lower end of the normal range. BAFF levels were correlated inversely with BAFF-R expression and time after therapy. In conclusion, the long-term effects of RTX therapy in patients with TTP included slow regeneration of memory B cell subsets and persistently reduced BAFF-R expression across all B cell subpopulations. This may reflect the delay in selection and differentiation of potentially autoreactive (ADAMTS13-specific) B cells, resulting in relatively long periods of low disease activity after therapy.

Regulation of serum matrix metalloproteinases and tissue inhibitor of metalloproteinases-1 following rituximab therapy in patients with rheumatoid arthritis refractory to anti-tumor necrosis factor blockers.

In our article, we evaluated the regulatory effects of the infusions of rituximab, a monoclonal antibody directed against CD20+ B cells, on the serum matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases-1 (TIMP-1) levels in patients with active rheumatoid arthritis (RA) not responding to anti-tumor necrosis factor (anti-TNF) therapy. Twelve RA patients were planned to receive four infusions of 1,000 mg of rituximab at weeks 0, 2, 24 and 26. The therapy was combined with methotrexate (MTX) (20–30 mg/week). Seven patients were refractory to previously received infliximab, and five to etanercept. Serum concentrations of interstitial collagenase (MMP-1), stromelysin-1 (MMP-3), gelatinase B (MMP-9) and TIMP-1 were measured by ELISA on weeks 0, 2, 12, 24, 36 and 52. Initial infusion of rituximab downregulated serum MMP-1 (p < 0.01), MMP-3 (p < 0.001), MMP-9 (p < 0.001) and TIMP-1 (p < 0.05) levels. Second drug administration caused even more remarkable reduction of measured MMPs (p < 0.001 in all cases) and TIMP-1 level (p < 0.01). These findings were accompanied by significantly decreased ratios of measured MMPs to TIMP-1. Next rituximab infusions on weeks 24 and 26 sustained the suppression of serum MMPs levels. Prior to the initial rituximab infusion, serum concentrations of studied MMPs and TIMP-1 significantly correlated with markers of RA activity such as disease activity score (DAS28) and CRP levels. Rituximab therapy, beside a rapid clinical improvement, reduced serum MMPs concentrations in RA patients refractory to anti-TNF treatment. Repeated infusions of rituximab maintained initial serum MMPs suppression.Electronic supplementary materialThe online version of this article (doi:10.1007/s00296-014-3112-1) contains supplementary material, which is available to authorized users.

Longterm followup of rituximab therapy in patients with rheumatoid arthritis: results from the Belgian MabThera in Rheumatoid Arthritis registry.

Our study reports the results of the MIRA (MabThera In Rheumatoid Arthritis) registry, set up to collect data about clinical usage, patient profile, and retention of rituximab (RTX) treatment in daily clinical practice in Belgium. Patients with active rheumatoid arthritis (RA) who failed at least 1 anti-tumor necrosis factor (anti-TNF) treatment were included in our study between November 2006 and October 2011. At baseline, demographics, medication, disease history, disease activity, rheumatoid factor (RF), and anticyclic citrullinated peptide antibodies (anti-CCP) status were recorded. Evolution of the 28-joint Disease Activity Score (DAS28)-erythrocyte sedimentation rate, retreatments, and reasons for therapy stop were followed prospectively. The MIRA registry included 649 patients, with mean disease duration of 12.8 ± 0.4 years and DAS28 values at inclusion of 5.85 ± 0.48. Patients received on average 2.82 ± 0.07 (range 1-9) RTX treatments, over a mean followup period of 93.1 ± 2.6 weeks. At database lock, 433 patients (66.7%) were still under RTX treatment, 182 (28.0%) had stopped treatment, and 34 (5.2%) were lost to followup. Ineffectiveness (n = 108, 59%) and safety concerns (n = 39, 22%) were the most frequent reasons for discontinuing RTX therapy. From 2006 to 2011, RTX practice patterns clearly evolved toward RTX being started in patients with a lower number of previously failed anti-TNF drugs and lower baseline DAS28 values. A lower number of previous anti-TNF drugs, and positivity for RF and anti-CCP, predicted more successful longterm treatment. RTX treatment provided adequate longterm disease control. In our daily practice study, RTX provided good longterm disease control and treatment retention in refractory patients with RA. Over the years, rheumatologists tended to start this treatment in patients with fewer previous anti-TNF treatments and lower disease activity.

Use of whole-blood transcriptomic profiling to highlight several pathophysiologic pathways associated with response to rituximab in patients with rheumatoid arthritis: data from a randomized, controlled, open-label trial.

To identify a molecular signature that could be predictive of the clinical response to rituximab (RTX) and elucidate the transcriptomic changes after RTX therapy in patients with rheumatoid arthritis (RA), with the use of whole-blood transcriptomic profiling. A microarray assay of the whole human genome was performed using RNA from peripheral blood samples obtained before the first cycle of RTX from 68 patients with RA in the SMART study. The transcriptomic profile was also assessed 24 weeks after the first administration of RTX (among 24 nonresponders and 44 responders, according to the European League Against Rheumatism response criteria at week 24). Ingenuity Interactive Pathways Analysis was used to identify molecular pathways that were modified by RTX therapy according to the clinical response. Quantitative polymerase chain reaction was performed to confirm the microarray results. In total, 198 genes showed significant baseline differential expression between patient groups according to their subsequent response to RTX (good or moderate responder versus nonresponder). This molecular signature could be reduced to 143 genes, which allowed for correctly classifying 89% of the patients by their EULAR response status at week 24, with 93% identification of responders and 100% identification of nonresponders. The signature for response featured up-regulation of inflammatory genes centered on NF-κB, including IL33 and STAT5A, and down-regulation of the interferon pathway. As expected, at week 24 post-RTX therapy, genes involved in the development and functions of B cells were the genes most strongly down-regulated, without any difference between the 2 groups. Whole-blood transcriptomic analyses may accurately identify patients with RA who will not respond to RTX therapy. These findings could open new perspectives on the clinical management of RA.

AB0447 Regulation of Serum Matrix Metalloproteinases and Tissue Inhibitor of Metalloproteinases-1 following Rituximab Therapy in Patients with Rheumatoid Arthritis Refractory to Anti-Tumor Necrosis Factor Blockers

BackgroundSerum matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) play important role in the pathogenesis of rheumatoid arthritis (RA).ObjectivesIn our article we evaluated the regulatory effects of the infusions...

Rituximab therapy in patients with refractory dermatomyositis or polymyositis: differential effects in a real-life population

While a double-blind trial has not met its endpoint, rituximab (RTX) is still seen as useful in refractory DM and PM. In this study we analysed the charts of all patients receiving RTX for myositis in our institutions for objective outcome parameters. In a retrospective way, the charts of all patients with PM or DM who received RTX were analysed for glucocorticoid dose, creatine phosphokinase (CPK) and lung function tests, as well as for serious adverse events. A total of 19 patients were identified, 1 of whom died from aspiration pneumonia 3 weeks after the first RTX infusion. The charts of 18 patients (13 PM, 5 DM) could be further analysed. In addition to the fatal pneumonia, six more severe infections were seen. One patient developed hypogammaglobulinaemia. Two patients had mild infusion reactions. Under RTX, both CPK and daily prednisolone dose were reduced by week 18. Six of eight patients with alveolitis improved under RTX. Overall, 9 of 13 PM patients responded. Six of the responders and two patients without documented response, all anti-synthetase syndrome patients, were re-treated. In contrast, all five DM patients responded and none required re-treatment. In a real-life population of patients with severe, refractory PM or DM, objective improvement was seen in the majority of patients with regard to CPK and lung function tests, and glucocorticoids could be reduced. In contrast to the subgroup with DM, where one cycle of RTX appeared sufficient, patients with anti-synthetase syndromes commonly experienced flares necessitating RTX re-treatment. Infections are of concern.

AB0337 Blood b cell counts as predictor of early clinical response after rituximab in patients with rheumatoid arthritis

BackgroundB cell depletion with rituximab is effective for reducing the symptoms and inhibiting the progression of joint damage in patients with rheumatoid arthritis (RA). However, the use of peripheral B...

Persistent memory B cell down-regulation after 6-year remission induced by rituximab therapy in patients with systemic lupus erythematosus

Persistent memory B cell down-regulation after 6-year remission induced by rituximab therapy in patients with systemic lupus erythematosus

Factors correlated with improvement of endothelial dysfunction during rituximab therapy in patients with rheumatoid arthritis

Increased cardiovascular mortality has been associated with rheumatoid arthritis (RA). There are reports indicating that tumor necrosis factor (TNF) blockers may exert favorable but transient effects on the lipid profile, flow-mediated vasodilatation (FMD) of the brachial artery, and the common carotid intima–media thickness (ccIMT) in RA. We evaluated 38 RA patients (33 females and five males with a mean age of 66.7 ± 10.2 years) who were unresponsive to TNF blockers. The patients received one or more courses of two rituximab (RTX) 1000 mg infusions. Disease activity was evaluated at each visit. Investigations included erythrocyte sedimentation rate, C-reactive protein (CRP) levels, the 28-joint disease activity score (DAS28), DAS28CRP, the Health Assessment Questionnaire, the FMD percent change from baseline (FMD%), and the postnitroglycerine endothelium-independent vasodilatation. In comparison with the baseline, there was a significant improvement in clinical variables and acute-phase reactants 24 months after the start of RTX therapy. There was also a major improvement in FMD% (from baseline 5.24 ± 1.12 to 5.43 ± 1.16; P = −0.03) and a smaller change in the ccIMT (from baseline 0.69 ± 0.16 to 0.67 ± 0.12 mm P = 0.25). Univariate analysis showed that global health (P < 0.034) was associated with the improvement in FMD%. Multivariate models showed that GH (odds ratio [OR] 0.91; 95% CI: 0.99–0.83; P = 0.032), CD19+ cells (OR 1.024; 95% CI: 1.045–1.003; P = 0.025), IgM (OR 1.025; 95% CI: 1.045–1.004; P = 0.016), and interleukin (IL)-8 (OR 0.487; 95% CI: 0.899–0.264; P = 0.021) were statistically associated with the improvement of FMD%, and that IL-8 (OR 0.717; 95% CI: 0.926–0.555; P = 0.018) was also statistically associated with improvement of ccIMT. The findings of the study confirm that RTX reduces the progression of accelerated atherosclerosis in patients with RA. They also show that improvement in CD19+ cells, IgM and GH after treatment are statistically associated with the improvement of FMD%, and that improvement in IL-8 levels after treatment is statistically associated with improved FMD% and with decrease in the ccIMT.

Evaluation of the clinical efficiency of tocilizumab versus rituximab therapy in patients with rheumatoid arthritis

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The use of rituximab therapy in patients with acquired factor v inhibitors

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Rituximab-induced hepatitis C virus reactivation in rheumatoid arthritis

The B-cell depletion agent rituximab (RTX) is used in lymphoma and rheumatoid arthritis (RA), and there have been several case reports of an RTX-induced reactivation of hepatitis C virus in patients with lymphoma. However, there have been no papers detailing hepatitis C virus reactivation after RTX therapy in a patient with RA. Here we report a case of RTX-induced hepatitis C virus reactivation in a patient with RA. Physicians should be aware that a close follow-up of liver function and viral load is mandatory after RTX therapy in patients with RA and concomitant hepatitis C.

Analysis of hepatitis B surface antibody titers in B cell lymphoma patients after rituximab therapy

Hepatitis B virus (HBV) reactivation is a well-known complication after rituximab therapy in patients with B cell lymphoma. Traditionally, hepatitis B surface antibody (anti-HBs) is a protective antibody, but the effect of rituximab on these antibodies has not been well studied. In 29 B cell lymphoma patients who were positive for anti-HBs before rituximab therapy, anti-HBs serologies before and after rituximab therapy were compared. Anti-HBs titers after rituximab treatment were significantly lower (P < 0.001) than those before treatment. None of the ten cases with pre-treatment anti-HBs titers above 100mIU/mL became negative for anti-HBs after rituximab therapy. In contrast, 8 of the 19 patients with pre-treatment anti-HBs titers below 100mIU/mL lost their anti-HBs (P = 0.027). Of these, one patient developed HBsAg seroreversion and HBV reactivation after rituximab therapy. Regarding patients with loss of anti-HBs or not, there was no significant difference in pre- and post-treatment immunoglobulin G levels between both groups. The rate of anti-HBs loss increased with advanced lymphoma stage and international prognostic index (P = 0.002 and <0.001, respectively). Multiple logistic regression analysis showed that pre-treatment anti-HBs titer is the only independent factor influencing the loss of anti-HBs (per one log mIU/mL, odds ratio, 0.003; 95% confidence interval, 0.000-0.302; P = 0.014). In conclusion, we found that anti-HBs titers decreased significantly (P < 0.001) after rituximab treatment. B cell lymphoma patients with low pre-treatment anti-HBs titers (<100mIU/mL) were more likely to lose anti-HBs antibodies and were at risk of HBV reactivation after rituximab immunochemotherapy.