Complicated pathophysiology behind rituximab-induced persistent hypogammaglobulinemia

Kano, Gen; Nakatani, Takuya; Yagi, Kanae; Sakamoto, Izumi; Imamura, Toshihiko

doi:10.1016/j.imlet.2013.10.005

Cited by 16 publications

(14 citation statements)

References 7 publications

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“…While ritixumab's efficacy with autoimmune cytopenias may be in part due to its B-cell depleting properties resulting in depletion of autoantibodies, it is thought that its success in CVID patients is also partially due to its effect on T cells (110), again highlighting the importance of T cell abnormalities in CVID. There is the documented potential risk of persistent B-cell lymphopenia after treatment with rituximab (111), but this risk is offset by the ongoing use of immunoglobulin replacement therapy. Other therapies include thrombopoietin-receptor agonists, such as romiplostim and eltrombopag which were approved by the FDA in 2008 for the treatment of cirrhosis-associated thrombocytopenia, have shown success in the treatment of thrombocytopenia in CVID and other immunodeficiencies (112,113).…”

Section: Treatment Of Autoimmunity In Cvidmentioning

confidence: 99%

Current Understanding and Recent Developments in Common Variable Immunodeficiency Associated Autoimmunity

Gereige

Maglione

2019

Front. Immunol.

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Common variable immunodeficiency (CVID) is the most prevalent symptomatic primary immunodeficiency and comprises a group of disorders with similar antibody deficiency but a myriad of different etiologies, most of which remain undefined. The variable aspect of CVID refers to the approximately half of patients who develop non-infectious complications in addition to heightened susceptibility to infection. The pathogenesis of these complications is poorly understood and somewhat counterintuitive because these patients that are defined by their immune futility simultaneously have elevated propensity for autoimmune disease. There are numerous aspects of immune dysregulation associated with autoimmunity in CVID that have only begun to be studied. These findings include elevations of T helper type 1 and follicular helper T cells and B cells expressing low levels of CD21 as well as reciprocal decreases in regulatory T cells and isotype-switched memory B cells. Recently, advances in genomics have furthered our understanding of the fundamental biology underlying autoimmunity in CVID and led to precision therapeutic approaches. However, these genetic etiologies are also associated with clinical heterogeneity and incomplete penetrance, highlighting the fact that continued research efforts remain necessary to optimize treatment. Additional factors, such as commensal microbial dysbiosis, remain to be better elucidated. Thus, while recent advances in our understanding of CVID-associated autoimmunity have been exciting and substantial, these current scientific advances must now serve as building blocks for the next stages of discovery.

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Section: Treatment Of Autoimmunity In Cvidmentioning

confidence: 99%

Current Understanding and Recent Developments in Common Variable Immunodeficiency Associated Autoimmunity

Gereige

Maglione

2019

Front. Immunol.

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“…Firstly experimented and introduced in the clinical practice for the treatment of hematological malignancies, it has become a commonly used immune modulatory strategy for the treatment of many refractory or poorly controlled autoimmune or inflammatory disorders. Removal of CD20-expressing cell populations induces a dysregulation of immune homeostasis, impacting regulatory functions of normal B cells ( 20 , 21 ). Hypogammaglobulinemia represents common negative consequences of this imbalance ( 22 – 27 ), and is considered the main factor that influences the increased risk of infection in patients receiving rituximab ( 28 – 30 ).…”

Section: Iatrogenic Hypogammaglobulinemiamentioning

confidence: 99%

Immunoglobulin Replacement Therapy in Secondary Hypogammaglobulinemia

et al. 2014

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Immunoglobulin (Ig) replacement therapy dramatically changed the clinical course of primary hypogammaglobulinemias, significantly reducing the incidence of infectious events. Over the last two decades its use has been extended to secondary antibody deficiencies, particularly those related to hematological disorders as lymphoproliferative diseases (LPDs) and multiple myeloma. In these malignancies, hypogammaglobulinemia can be an intrinsic aspect of the disease or follow chemo-immunotherapy regimens, including anti-CD20 treatment. Other than in LPDs the broadening use of immunotherapy (e.g., rituximab) and immune-suppressive therapy (steroids, sulfasalazine, and mycophenolate mofetil) has extended the occurrence of iatrogenic hypogammaglobulinemia. In particular, in both autoimmune diseases and solid organ transplantation Ig replacement therapy has been shown to reduce the rate of infectious events. Here, we review the existing literature about Ig replacement therapy in secondary hypogammaglobulinemia, with special regard for subcutaneous administration route, a safe, effective, and well-tolerated treatment approach, currently well established in primary immunodeficiencies and secondary hypogammaglobulinemias.

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“…Editorial www.expert-reviews.com diseases and lymphomas, there seems to be an increasing number of persistent CVID-like phenotypes remitted for evaluation. This impression is partly supported by recent studies [19,20]. Hypogammaglobulinemia may disappear up to 18 months after cessation of rituximab therapy [21].…”

mentioning

confidence: 70%

Is there a need to redefine the diagnostic criteria for common variable immunodeficiency?

Seppänen

Aghamohammadi

Rezaei

2013

Expert Review of Clinical Immunology

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Complicated pathophysiology behind rituximab-induced persistent hypogammaglobulinemia

Cited by 16 publications

References 7 publications

Current Understanding and Recent Developments in Common Variable Immunodeficiency Associated Autoimmunity

Current Understanding and Recent Developments in Common Variable Immunodeficiency Associated Autoimmunity

Immunoglobulin Replacement Therapy in Secondary Hypogammaglobulinemia

Is there a need to redefine the diagnostic criteria for common variable immunodeficiency?

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