Reactivation of Hepatitis B Virus (HBV) Associated with Rituximab Use in Lymphoma: Under Reporting and Lack of Data Quality Reported to the FDA.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1370-1370
Author(s):  
Andrew M. Evens ◽  
Bara Fintel ◽  
Brian Chiu ◽  
Leo I. Gordon ◽  
Daniel Ganger ◽  
...  

Abstract Abstract 1370 Poster Board I-392 Background: HBV is a major public health problem with infection that can lead to cirrhosis, liver failure, and death. Immunosuppressive therapy, such as steroids and/or chemotherapy, is known to cause a flare or “reactivation” of HBV (HBV-react). Rituximab was approved in 1997 for the treatment of B-cell lymphoma. In 2004, based on 3 case reports, the FDA warned healthcare professionals of rituximab-associated HBV-react. Since that time, multiple cases and retrospective series of rituximab-induced HBV-react have been reported in the literature. However, the characteristics and scope of this association still remains largely unknown. We evaluated the characteristics of patients with lymphoma who developed HBV-react after exposure to rituximab, and the quality of case reports available in the medical literature and at the FDA. Methods: Data sources included 2 observations at Northwestern Memorial Hospital, 83 reports from the medical literature, and 10 reports obtained from the FDA MedWatch database (n=97). Two reports of rituximab-related HBV-react not associated with lymphoma (vasculitis and gloumerulonephritis) were excluded. HBV-react was defined as ≥ 2-fold increase in serum HBV DNA with an increase in serum ALT compared with baseline. A completeness analysis was performed comparing cases submitted to the FDA MedWatch database vs. the medical literature and active surveillance. Results: Of 83 unique cases of HBV-react associated with rituximab reported in the literature, 28 were published as case reports, while 55 were included in case series. Of these 83 cases, 46 occurred in patients (pts) with anti-HBV core antibody (HBcAb+) in the absence of HBV surface antigen (HBsAg-), while 37 cases involved pts with chronic HBV hepatitis (i.e, HBsAg+). Among the 28 case reports and 2 Northwestern cases (n=30; HBcAb+ n=16, HBsAg+ n=14), the median age at HBV-react was 55 years (23M/9F). Histology of these cases were diffuse large B-cell lymphoma (n=19), indolent lymphoma (n=8), CLL (n=2), and mantle-cell lymphoma (n=1). In terms of concomitant treatment at time of HBV-react, 25 pts were receiving concurrent immunosuppressive therapy (chemotherapy +/- steroids n=22 and steroids n=3), while only 5 cases involved single-agent rituximab treatment. Each of these 5 latter pts had received chemotherapy prior to rituximab treatment (2, 3, 12, 24, and 34 months). The median number of rituximab doses received prior to HBV-react was 6 (range 3-10). The median time from last rituximab dose to HBV-react was 5 months (0-21 months); of note, 30% of cases occurred >6 months from last rituximab dose. In terms of outcome, 60% of pts experienced fulminant liver failure, while the remaining had HBV-related hepatitis. Furthermore, 40% (12/30) of pts died due to HBV-react. Quality comparison of source data of the literature and surveillance reports vs. the FDA is contained in Table 1. Overall completeness ratio for literature and observed reports vs. the FDA was 2.18. Of rituximab-related HBV-react occurrences (n=55) reported in 8 case series, five studies included a control group; there was a suggestion of increased risk of HBV-react with rituximab-based therapy, especially with concurrent steroids, although the absolute risk was not consistent (e.g., among HBcAb+ cases, reported rate of HBV-react: 2.7% to 23.8%). Conclusions: We have found 95 total cases of rituximab-associated HBV-react. A paucity of safety reports regarding rituximab-associated HBV-react have been reported to the FDA MedWatch. Furthermore, published cases in the medical literature and through active surveillance were superior in data quality compared with FDA reports. However, the absolute risks of rituximab-related HBV-react in HBsAg+ or HBcAb+ pts are still not known. Further examination of the relationship of HBV-react with single-agent rituximab and rituximab combined with immunosuppressive therapy, with and without steroids, using an active surveillance strategy is warranted. Disclosures: No relevant conflicts of interest to declare.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 370-370
Author(s):  
Kenneth R. Carson ◽  
Andrew M. Evens ◽  
Steven T. Rosen ◽  
Jane N. Winter ◽  
Leo I. Gordon ◽  
...  

Abstract Background- Progressive multifocal leukoencephalopathy (PML) is a demyelinating disorder of the brain caused by the reactivation of latent JC polyoma virus. Rituximab (Rituxan, Mabthera) is a B-cell depleting, monoclonal antibody which has been linked to reactivation of the hepatitis B virus. HIV infection, purine analog therapy, hematopoietic transplant and lymphoma have previously been associated with PML. We evaluated the characteristics of patients with B-cell lymphoproliferative disorders who developed PML after exposure to rituximab, and the quality of case reports available in the medical literature and at the FDA. Methods- Data sources included 1 observation at Northwestern Memorial Hospital, 14 reports obtained from the FDA MedWatch database, 9 case reports from the medical literature, and 21 reports from the manufacturer, Genentech, that were submitted to the FDA. Reports that did not confirm the diagnosis of PML, were associated with HIV infection, or rituximab use for a rheumatologic indication were excluded. Results- Of 47 unique case reports screened, 3 were excluded for rituximab use in rheumatologic disease, 2 for pre-existing HIV, and 13 for inadequate confirmation of the PML diagnosis. In the 29 remaining cases, survival of PML was reported in only one patient. Diagnosis was made by brain biopsy (n=6), autopsy (n=6), or MRI of brain AND positive JC virus by PCR (n=17). Five cases were seen in hematopoietic transplant recipients, 4 autologous and 1 allogeneic. Of the 24 patients who were not transplanted, 10 had purine analog exposure. Thirteen of the 14 patients that did not receive transplant or a purine analog received an alkylating agent, with 7 receiving standard R-CHOP. The median age of the 29 patients was 63.5 years (range 32–89), 15 were female and 14 male. Indications for rituximab were: large B-cell lymphoma (n=6), follicular lymphoma (n=6), CLL (n=5), Waldenstrom (n=2) and other non-Hodgkin lymphomas (n=10). Median time to diagnosis of PML from first and last rituximab doses was 10 and 5 months respectively. The median number of rituximab doses was 6. Quality comparison of source data is contained in table 1. Overall completeness ratio for literature and observed reports vs. FDA and manufacturer reports was 1.48. Conclusions: We have found 29 cases of rituximab-associated PML, of which 14 were not associated with transplantation or purine analog exposure, suggesting an association of rituximab therapy independent of these other treatment related risk factors. FDA and manufacturer reports are inferior to those available in published case reports or through active surveillance. Further examination of the relationship of rituximab to PML, using an active surveillance strategy, is warranted. Type of Information Literature and Observed Cases (n=10) %Reporting FDA and Manufacturer Cases (n=19) %Reporting Completeness Ratio Outcome 90 63 1.42 Date of Lymph 80 68 1.18 Diagnosis Date of Death 78 53 1.47 HIV Status 60 16 3.75 Specific Lymphoma Type 100 84 1.19 Dose of Rituximab 80 63 1.27 Date of 1st Dose 70 94 .74 Date of Last Dose 70 84 .83


2019 ◽  
Vol 12 ◽  
pp. 2632010X1982926 ◽  
Author(s):  
Mary-Jane OU Williams ◽  
Hossein Akhondi ◽  
Omar Khan

Sub-acute liver failure is a term that describes the relatively sudden loss of liver function, usually >21 days and <26 weeks, with impaired synthetic function and associated encephalopathy in a person with no pre-existing liver disease or cirrhosis. It is commonly caused by viruses and drugs, less so by malignancy. Our patient is a 71-year-old Japanese man who presented with signs of sub-acute liver failure. A subsequent liver biopsy demonstrated involvement by B-cell non-Hodgkin lymphoma. Evaluation of the bone marrow demonstrated significant marrow involvement by B-cell lymphoma. The fluorescence in situ hybridization (FISH) returned positive for t(14; 18). Noted was the patient’s clinical presentation of cholestasis secondary to hepatic lymphoma with no evidence of lymphadenopathy or peripheralized lymphoma. Given the disease distribution, the overall findings are consistent with primary hepatic follicular lymphoma as described in few case reports and small case series in the literature.


Blood ◽  
2019 ◽  
Vol 133 (1) ◽  
pp. 70-80 ◽  
Author(s):  
Kamil Bojarczuk ◽  
Kirsty Wienand ◽  
Jeremy A. Ryan ◽  
Linfeng Chen ◽  
Mariana Villalobos-Ortiz ◽  
...  

Abstract Inhibition of the B-cell receptor (BCR) signaling pathway is a promising treatment strategy in multiple B-cell malignancies. However, the role of BCR blockade in diffuse large B-cell lymphoma (DLBCL) remains undefined. We recently characterized primary DLBCL subsets with distinct genetic bases for perturbed BCR/phosphoinositide 3-kinase (PI3K) signaling and dysregulated B-cell lymphoma 2 (BCL-2) expression. Herein, we explore the activity of PI3K inhibitors and BCL-2 blockade in a panel of functionally and genetically characterized DLBCL cell line models. A PI3K inhibitor with predominant α/δ activity, copanlisib, exhibited the highest cytotoxicity in all BCR-dependent DLBCLs. The proapoptotic effect of copanlisib was associated with DLBCL subtype-specific dysregulated expression of BCL-2 family members including harakiri (HRK) and its antiapoptotic partner BCL extra large (BCL-xL), BCL2 related protein A1, myeloid cell leukemia 1 (MCL-1), and BCL2 interacting mediator of cell death. Using functional BH3 profiling, we found that the cytotoxic activity of copanlisib was primarily mediated through BCL-xL and MCL-1–dependent mechanisms that might complement BCL-2 blockade. For these reasons, we evaluated single-agent activity of venetoclax in the DLBCLs and identified a subset with limited sensitivity to BCL-2 blockade despite having genetic bases of BCL-2 dysregulation. As these were largely BCR-dependent DLBCLs, we hypothesized that combined inhibition of PI3Kα/δ and BCL-2 would perturb BCR-dependent and BCL-2–mediated survival pathways. Indeed, we observed synergistic activity of copanlisib/venetoclax in BCR-dependent DLBCLs with genetic bases for BCL-2 dysregulation in vitro and confirmed these findings in a xenograft model. These results provide preclinical evidence for the rational combination of PI3Kα/δ and BCL-2 blockade in genetically defined DLBCLs.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A938-A939
Author(s):  
Mustafa Alam ◽  
Mohamad Hosam Horani

Abstract Case Presentation: The patient is a 60 year old male with a past medical history of celiac disease, paroxysmal Afib, iron deficiency, and CAD who presented with lightheadedness, dizziness, and fatigue. Notable workup revealed that the patient had Afib with RVR, a TSH of 0.189, Free t4 0.51an LDH of 2726, hemoglobin of 8.7, AST of 155, ALT of 19, WBC of 4.5, and serum iron of 20. The patient’s cardizem dose was adjusted and repeat transthoracic echocardiogram was unremarkable compared to history. The patient presented again with complaints of abdominal distension, postural dizziness, occasional night sweats, and fevers. Repeat workups revealed pancytopenia, proteinuria, hypotension, and anasarca most pronounced in the lower extremity and scrotum. Ultimately, a kidney biopsy revealed an intravascular B cell non-Hodgkin lymphoma (IVBCL). Notable repeat labs include a CRP of 44 and a failed ACTH stimulation test. A brain MRI revealed a 6mm pituitary microadenoma. The patient placed on an R-CHOP regiment and is scheduled for repeat MRI to rule out pituitary involvement. Discussion: IVBCL’s are a rare form of diffuse B cell lymphoma and remain a diagnostic challenge due to the variety of involved systems including skin, CNS, and endocrine. IVBCL is also known to not produce a mass or lymphadenopathy. Celiac disease is a known risk factor for non-Hodgkin’s lymphoma. A literature search reveals a few case reports with common themes of increased LDH and inflammatory markers, anemia, and hepatic and renal dysfunction. Postural hypotension can also be a presenting symptom due to IVBCL’s ability to infiltrate neurovascular tissue to cause autonomic neuropathy. However, in this case, the patient’s history of primary adrenal insufficiency makes this unlikely. Hypothyroidism secondary to pituitary and thyroid involvement was suspected due to TSH level suppressed enough for central hypothyroidism. Repeated MRI showed resolution of Pituitary Microadenoma post Chemo therapy. Sylvain Raoul Simeni Njonnou, Bruno Couturier, Yannick Gombeir, Sylvain Verbanck, France Devuyst, Georges El Hachem, Ivan Theate, Anne-Laure Trepant, Virginie De Wilde, Frédéric-Alain Vandergheynst, “Pituitary Gland and Neurological Involvement in a Case of Hemophagocytic Syndrome Revealing an Intravascular Large B-Cell Lymphoma”, Case Reports in Hematology, vol. 2019, 6 pages, 2019. https://doi.org/10.1155/2019/9625075 Catassi C, Fabiani E, Corrao G, et al. Risk of Non-Hodgkin Lymphoma in Celiac Disease. JAMA. 2002;287(11):1413 Khan MS, McCubbin M, Nand S. Intravascular Large B-Cell Lymphoma: A Difficult Diagnostic Challenge. J Investig Med High Impact Case Rep. 2014 Mar 6;2(1):2324709614526702. Pearce C, Hope S, Butchart J. Intravascular lymphoma presenting with postural hypotension. BMJ Case Rep. Published 2018 Jan 29.


2014 ◽  
Vol 25 ◽  
pp. iv151 ◽  
Author(s):  
R. Plummer ◽  
D. Dua ◽  
N. Cresti ◽  
A. Suder ◽  
Y. Drew ◽  
...  

Hematology ◽  
2005 ◽  
Vol 2005 (1) ◽  
pp. 321-328 ◽  
Author(s):  
Michele Ghielmini

Abstract Rituximab was the first humanized antibody widely used on patients, so research on its optimal use was a clinical challenge. Many studies have been performed to optimize its dose and schedule, and more are ongoing. The dose of 375 mg/m2 has become standard, mainly because it shows activity and has little associated toxicity. The combination of rituximab with chemotherapy has been shown to prolong remission in all types of lymphomas, and in patients with diffuse large B-cell lymphoma it can improve survival. As a single agent, particularly when the treatment is prolonged over several months, results are similar to chemotherapy but with fewer side effects. Finally, used as maintenance therapy it can prolong the duration of chemotherapy-obtained remissions. Based on available data, the administration of 375 mg/m2 before each chemotherapy cycle can be recommended for first line treatment of patients with curable B-cell lymphomas and for patients with high-risk indolent lymphoma who are rituximab-naïve. Single-agent treatment at a prolonged schedule is recommended for cases of indolent disease not in need of urgent response and for patients who are unlikely to tolerate chemotherapy.


2019 ◽  
pp. 1-5 ◽  
Author(s):  
Harriet S. Walter ◽  
Christopher S. Trethewey ◽  
Matthew J. Ahearne ◽  
Ross Jackson ◽  
Sandrine Jayne ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document