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      Exogenous insulin antibody syndrome (EIAS): a clinical syndrome associated with insulin antibodies induced by exogenous insulin in diabetic patients

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          Abstract

          Insulin has been used for diabetes therapy and has achieved significant therapeutic effect. In recent years, the use of purified and recombinant human insulin preparations has markedly reduced, but not completely suppressed, the incidence of insulin antibodies (IAs). IAs induced by exogenous insulin in diabetic patients is associated with clinical events, which is named exogenous insulin antibody syndrome (EIAS). The present review is based on our research and summarizes the characterization of IAs, the factors affecting IA development, the clinical significance of IAs and the treatments for EIAS.

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          Immunological responses to exogenous insulin.

          S Edwin Fineberg, Thomas T Kawabata, Deborah Finco-Kent … (2007)
          Regardless of purity and origin, therapeutic insulins continue to be immunogenic in humans. However, severe immunological complications occur rarely, and less severe events affect a small minority of patients. Insulin autoantibodies (IAAs) may be detectable in insulin-naive individuals who have a high likelihood of developing type 1 diabetes or in patients who have had viral disorders, have been treated with various drugs, or have autoimmune disorders or paraneoplastic syndromes. This suggests that under certain circumstances, immune tolerance to insulin can be overcome. Factors that can lead to more or less susceptibility to humoral responses to exogenous insulin include the recipient's immune response genes, age, the presence of sufficient circulating autologous insulin, and the site of insulin delivery. Little proof exists, however, that the development of insulin antibodies (IAs) to exogenous insulin therapy affects integrated glucose control, insulin dose requirements, and incidence of hypoglycemia, or contributes to beta-cell failure or to long-term complications of diabetes. Studies in which pregnant women with diabetes were monitored for glycemic control argue against a connection between IAs and fetal risk. Although studies have shown increased levels of immune complexes in patients with diabetic microangiopathic complications, these immune complexes often do not contain insulin or IAs, and insulin administration does not contribute to their formation. The majority of studies have shown no relationship between IAs and diabetic angiopathic complications, including nephropathy, retinopathy, and neuropathy. With the advent of novel insulin formulations and delivery systems, such as insulin pumps and inhaled insulin, examination of these issues is increasingly relevant.
          Article 0 comments Cited 57 times – based on 0 reviews     Review now
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            Immunological mechanism underlying the immune response to recombinant human protein therapeutics.

            Melody Sauerborn, Vera Brinks, Wim Jiskoot … (2010)
            Recombinant human (rhu) protein therapeutics are powerful tools to treat several severe diseases such as multiple sclerosis and diabetes mellitus, among others. A major drawback of these proteins is the production of anti-drug antibodies (ADAs). In some cases, these ADAs have neutralizing capacity and can interfere with the efficacy and safety of the drug. Little is known about the immunological mechanisms underlying the unwanted immune response against human homolog protein therapeutics. This article aims to provide current insights into recent immunological developments and to link this with regard to production of ADAs. A particular focus is given to aggregates being present in a rhu protein formulation and their impact on the immune system, subsequently leading to breakage of tolerance and formation of ADAs. Aggregation is one of the key factors in immunogenicity and by reducing aggregation one can reduce immunogenicity and make drugs safer and more efficient. Copyright 2009 Elsevier Ltd. All rights reserved.
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              Insulin-I131 metabolism in human subjects: demonstration of insulin binding globulin in the circulation of insulin treated subjects.

              S BERSON, R S YALOW, A. Bauman … (1956)
              Article 0 comments Cited 47 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Endocr Connect
                Journal ID (iso-abbrev): Endocr Connect
                Journal ID (hwp): EC
                Title: Endocrine Connections
                Publisher: Bioscientifica Ltd (Bristol )
                ISSN (Electronic): 2049-3614
                Publication date Collection: January 2018
                Publication date (Electronic): 12 December 2017
                Volume: 7
                Issue: 1
                Pages: R47-R55
                Affiliations
                [1 ]Department of Endocrinology The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China
                [2 ]Department of Endocrinology Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
                Author notes
                Correspondence should be addressed to F Chen: cfl1993@ 123456126.com
                Article
                Publisher ID: EC170309
                DOI: 10.1530/EC-17-0309
                PMC ID: 5776673
                PubMed ID: 29233817
                SO-VID: a2d7610a-d8d5-47ce-a7c2-c10e487a7838
                Copyright © © 2018 The authors
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                Date received : 01 December 2017
                Date accepted : 12 December 2017
                Categories
                Subject: Review

                Keywords: insulin antibodies,exogenous insulin antibody syndrome,diabetes,hypoglycaemia,hyperglycaemia
                Data availability:
                Keywords: insulin antibodies, exogenous insulin antibody syndrome, diabetes, hypoglycaemia, hyperglycaemia

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