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      Treatment of Secondary Immune Thrombocytopenia with Non-Hodgkin Lymphoma: A Case Report and Literature Review

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          Abstract

          Secondary immune thrombocytopenic purpura (ITP) with non-Hodgkin lymphoma (NHL) is a rare disease. Although some treatment regimens are available for primary ITP, the treatment strategy for secondary ITP remains unconfirmed. We herein report a 79-year-old man who was diagnosed with secondary ITP with mantle cell lymphoma. Although intravenous immunoglobulin (IVIG) has been considered an effective option for secondary ITP, similar to the treatment of primary ITP, our patient did not benefit from IVIG. A literature review including the current report revealed that IVIG was ineffective in all treated patients. Secondary ITP with NHL should be treated differently from primary ITP.

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          Intravenous gammaglobulin suppresses inflammation through a novel T(H)2 pathway.

          Robert M Anthony, Toshihiko Kobayashi, Fredrik Wermeling … (2011)
          High-dose intravenous immunoglobulin is a widely used therapeutic preparation of highly purified immunoglobulin G (IgG) antibodies. It is administered at high doses (1-2 grams per kilogram) for the suppression of autoantibody-triggered inflammation in a variety of clinical settings. This anti-inflammatory activity of intravenous immunoglobulin is triggered by a minor population of IgG crystallizable fragments (Fcs), with glycans terminating in α2,6 sialic acids (sFc) that target myeloid regulatory cells expressing the lectin dendritic-cell-specific ICAM-3 grabbing non-integrin (DC-SIGN; also known as CD209). Here, to characterize this response in detail, we generated humanized DC-SIGN mice (hDC-SIGN), and demonstrate that the anti-inflammatory activity of intravenous immunoglobulin can be recapitulated by the transfer of bone-marrow-derived sFc-treated hDC-SIGN(+) macrophages or dendritic cells into naive recipients. Furthermore, sFc administration results in the production of IL-33, which, in turn, induces expansion of IL-4-producing basophils that promote increased expression of the inhibitory Fc receptor FcγRIIB on effector macrophages. Systemic administration of the T(H)2 cytokines IL-33 or IL-4 upregulates FcγRIIB on macrophages, and suppresses serum-induced arthritis. Consistent with these results, transfer of IL-33-treated basophils suppressed induced arthritic inflammation. This novel DC-SIGN-T(H)2 pathway initiated by an endogenous ligand, sFc, provides an intrinsic mechanism for maintaining immune homeostasis that could be manipulated to provide therapeutic benefit in autoimmune diseases. ©2011 Macmillan Publishers Limited. All rights reserved
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            The ITP syndrome: pathogenic and clinical diversity.

            Eline Luning Prak, J Bussel, Kelly Liebman … (2009)
            Immune thrombocytopenia (ITP) is mediated by platelet autoantibodies that accelerate platelet destruction and inhibit their production. Most cases are considered idiopathic, whereas others are secondary to coexisting conditions. Insights from secondary forms suggest that the proclivity to develop platelet-reactive antibodies arises through diverse mechanisms. Variability in natural history and response to therapy suggests that primary ITP is also heterogeneous. Certain cases may be secondary to persistent, sometimes inapparent, infections, accompanied by coexisting antibodies that influence outcome. Alternatively, underlying immune deficiencies may emerge. In addition, environmental and genetic factors may impact platelet turnover, propensity to bleed, and response to ITP-directed therapy. We review the pathophysiology of several common secondary forms of ITP. We suggest that primary ITP is also best thought of as an autoimmune syndrome. Better understanding of pathogenesis and tolerance checkpoint defects leading to autoantibody formation may facilitate patient-specific approaches to diagnosis and management.
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              Expansion of CD4+CD25+ regulatory T cells by intravenous immunoglobulin: a critical factor in controlling experimental autoimmune encephalomyelitis.

              Sandrine Delignat, Karen Cohen, Amal Ephrem … (2008)
              The clinical use of intravenous immunoglobulin (IVIg) based on its immunomodulatory and anti-inflammatory potential remains an ongoing challenge. Fcgamma receptor-mediated effects of IVIg, although well elucidated in certain pathologies, cannot entirely account for its proven benefit in several autoimmune disorders mediated by autoreactive T cells. In this study, we show that prophylactic infusion of IVIg prevents the development of experimental autoimmune encephalomyelitis (EAE), an accepted animal model for multiple sclerosis (MS). The protection was associated with peripheral increase in CD4+CD25+Foxp3+ regulatory T cell (Treg) numbers and function. The protection was Treg-mediated because IVIg failed to protect against EAE in mice that were depleted of the Treg population. Rather than inducing de novo generation from conventional T cells, IVIg had a direct effect on proliferation of natural Treg. In conclusion, our results highlight a novel mechanism of action of IVIg and provide a rationale to test the use of IVIg as an immunomodulatory tool to enhance Treg in early onset MS and other autoimmune and inflammatory conditions.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Intern Med
                Journal ID (iso-abbrev): Intern Med
                Title: Internal Medicine
                Publisher: The Japanese Society of Internal Medicine
                ISSN (Print): 0918-2918
                ISSN (Electronic): 1349-7235
                Publication date (Electronic): 15 May 2021
                Publication date (Print): 15 May 2021
                Volume: 60
                Issue: 10
                Pages: 1583-1588
                Affiliations
                [1 ]Department of Hematology and Oncology, Graduate School of Medicine, The University of Tokyo, Japan
                [2 ]General Education Center, The University of Tokyo Hospital, Japan
                [3 ]Department of Cell Therapy and Transplantation Medicine, The University of Tokyo Hospital, Japan
                Author notes

                Correspondence to Dr.　Mineo Kurokawa, kurokawa-tky@ 123456umin.ac.jp

                Article
                DOI: 10.2169/internalmedicine.5611-20
                PMC ID: 8188037
                PubMed ID: 33994446
                SO-VID: e2e76fbd-5245-45cd-810a-6f117ce75bee
                Copyright © Copyright © 2021 by The Japanese Society of Internal Medicine
                License:

                The Internal Medicine is an Open Access journal distributed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. To view the details of this license, please visit ( https://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 14 June 2020
                Date accepted : 4 October 2020
                Categories
                Subject: Case Report

                Keywords: secondary immune thrombocytopenia,intravenous immunoglobulin,chemotherapy,non-hodgkin lymphoma
                Data availability:
                Keywords: secondary immune thrombocytopenia, intravenous immunoglobulin, chemotherapy, non-hodgkin lymphoma

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