This article aimed to review and describe clinical presentations, underlying mechanisms of rituximab hypersensitivity as well as management including rapid drug desensitization (RDD). Comprehensive reviews focused on rituximab-induced HSRs are scarce. The drug is considered to be of good and accepted tolerability, ( Vidal et al., 2011 Makatsori et al., 2014) however, increased use of rituximab has been associated with HSRs ( Brennan et al., 2009 Patel and Khan, 2017 Picard and Galvão, 2017 Isabwe et al., 2018). Rituximab treatment results in two main categories of adverse reactions, including immunodeficiency and hypersensitivity reactions (HSRs). Later on, it became a bright treatment opportunity instead of the conventional treatment for chronic granulomatosis and inflammatory diseases ( Wong and Long, 2017). It was initially approved as an anti-neoplastic agent ( Vikse et al., 2019). Rituximab is a chimeric IgG mAb directed against CD20 antigen that is expressed on normal and malignant B cells ( Plosker and Figgitt, 2003). Monoclonal antibodies (mAbs) have become mandatory for neoplastic targeted therapies as well as chronic inflammatory and autoimmune diseases ( Beck et al., 2010 Li et al., 2013 Patel and Khan, 2017 Picard and Galvão, 2017 Özyiğit et al., 2020). We aimed to review clinical presentations, underlying mechanisms of rituximab hypersensitivity, as well as management including rapid drug desensitization. Severe delayed type IV hypersensitivity reactions including non-severe maculopapular rash to severe reactions such as Stevens–Johnson syndrome and toxic epidermal necrolysis have been rarely reported following rituximab injection. The classic serum sickness triad (fever, rash, and arthralgia) has been observed in patients mainly with an underlying rheumatologic condition. Classified as Type III reaction, rituximab-induced serum sickness reactions have been reported in patients with autoimmune diseases and hematological malignancies. In some cases, clinical manifestations of IgE-mediated reactions and cytokine-release reactions partially overlap, which is called a mixed reaction. Recent studies have shown the presence of serum anti-rituximab antibodies, either represented by the IgG or IgE isotype. Some of the immediate infusion reactions are due to a cytokine-release but some reactions raise concerns for type I (IgE/non-IgE) hypersensitivity. However, in about 10% of patients, severe infusion-related reactions develop, which prevent its use. Immediate infusion-related reactions to rituximab are quite common and decrease in frequency with subsequent infusions. However, increased use of rituximab has been associated with hypersensitivity reactions (HSRs), which can be classified as infusion-related, cytokine-release, type I (IgE/non-IgE), mixed, type III, and type IV reactions. It has been used for the treatment of various lymphoid malignancies, lymphoproliferative diseases, and rheumatologic disorders. Rituximab is a chimeric monoclonal antibody (mAb) against CD20 molecule which is expressed on human B cells.
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