Abstract
Rituximab hypersensitivity reactions are rare but are one of the main causes of rituximab elimination from antilymphoma immunochemotherapy treatments. While the clinical picture may be indistinguishable from other infusion-related reactions, hypersensitivity reactions (HSR) do not disappear and instead become more intense with subsequent administrations. Objective. To describe the use of the 12-step protocol for desensitization to intravenous rituximab in clinical practice and the complementary study of a possible IgE-mediated HSR in the context of B-cell lymphoma treatment. Methods. A 12-step rituximab desensitization protocol was performed prospectively within clinical practice in 10 patients with a history of severe infusion reactions or in patients who had a repeated reaction at subsequent doses despite taking more intense preventive measures. Skin prick tests were performed at the time of reaction and at a later time to eliminate false negatives due to possible drug interference. Results. Overall, with the desensitization protocol, 70% of patients were able to complete the scheduled immunochemotherapy. Two patients had to discontinue the therapy due to clinical persistence and the third due to lymphoma progression. Intradermal tests with 0.1% rituximab were positive in only 20% of cases, demonstrating a mechanism of hypersensitivity. Conclusions. The 12-step desensitization protocol is very effective and assumable within healthcare practice. There is a need to determine the mechanism underlying the infusion reaction in a large proportion of cases due to the risk of future drug exposure.
Highlights
Rituximab is a murine/human chimeric monoclonal antibody against CD20 that has been in use for more than 20 years for the treatment of B-cell lymphomas and autoimmune disorders [1]
E main reasons for eliminating rituximab from the therapeutic protocol of lymphoma patients are severe infusion reactions (IRs) that do not remit after subsequent administrations and corrective measures
IRs are dose-dependent and, in the case of lymphomas, closely related to tumour burden, and they are limited to the first-line administration. e most frequent aetiologies are cytokine release syndrome (CRS), tumour lysis syndrome (TLS), and hypersensitivity reactions (HSRs) [5]
Summary
Rituximab is a murine/human chimeric monoclonal antibody against CD20 that has been in use for more than 20 years for the treatment of B-cell lymphomas and autoimmune disorders [1]. New monoclonal antibodies against humanized CD20 are replacing rituximab for several of its indications [2, 3] and are associated with fewer infusional adverse reactions; these new options are not affordable in many countries. E main reasons for eliminating rituximab from the therapeutic protocol of lymphoma patients are severe infusion reactions (IRs) that do not remit after subsequent administrations and corrective measures. IRs are dose-dependent and, in the case of lymphomas, closely related to tumour burden, and they are limited to the first-line administration. E most frequent aetiologies are cytokine release syndrome (CRS), tumour lysis syndrome (TLS), and hypersensitivity reactions (HSRs) [5]. IRs are dose-dependent and, in the case of lymphomas, closely related to tumour burden, and they are limited to the first-line administration. e most frequent aetiologies are cytokine release syndrome (CRS), tumour lysis syndrome (TLS), and hypersensitivity reactions (HSRs) [5].
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