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      Combined treatment with sitagliptin and vitamin D in a patient with latent autoimmune diabetes in adults

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          Summary

          Latent autoimmune diabetes in adults (LADA) is a relatively new type of diabetes with a clinical phenotype of type 2 diabetes (T2D) and an immunological milieu characterized by high titers of islet autoantibodies, resembling the immunological profile of type 1 diabetes (T1D). Herein, we report a case of a young male, diagnosed with LADA based on both clinical presentation and positive anti-glutamic acid decarboxylase antibodies (GAD-abs), which were normalized after combined treatment with a dipeptidyl peptidase-4 inhibitor (DPP-4) (sitagliptin) and cholecalciferol.

          Learning points

          • Anti-glutamic acid decarboxylase antibodies (GAD-abs) titers in young patients being previously diagnosed as type 2 diabetes (T2D) may help establish the diagnosis of latent autoimmune diabetes in adults (LADA).

          • Sitagliptin administration in patients with LADA might prolong the insulin-free period.

          • Vitamin D administration in patients with LADA might have a protective effect on the progression of the disease.

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          Most cited references17

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          Autoimmune diabetes not requiring insulin at diagnosis (latent autoimmune diabetes of the adult): definition, characterization, and potential prevention.

          P Pozzilli, U Di Mario (2001)
          Type 1 diabetes is caused by the immune-mediated destruction of islet insulin-secreting beta-cells. This chronic destructive process is associated with both cellular and humoral immune changes in the peripheral blood that can be detected months or even years before the onset of clinical diabetes. Throughout this prediabetic period, metabolic changes, including altered glucose tolerance and reduced insulin secretion, deteriorate at variable rates and eventually result in clinical diabetes. A fraction of individuals with humoral immunological changes have clinical diabetes that initially is not insulin-requiring. The onset of diabetes in these patients is usually in adult life, and because their diabetes is at least initially not insulin-requiring, they appear clinically to be affected by type 2 diabetes. Such patients probably have the same disease process as patients with type 1 diabetes in that they have similar HLA genetic susceptibility as well as autoantibodies to islet antigens, low insulin secretion, and a higher rate of progression to insulin dependency. These patients are defined as being affected by an autoimmune type of diabetes not requiring insulin at diagnosis, which is also named latent autoimmune diabetes of the adult (LADA). Special attention should be paid to diagnose such patients because therapy may influence the speed of progression toward insulin dependency, and in this respect, efforts should be made to protect residual C-peptide secretion. LADA can serve as a model for designing new strategies for prevention of type 1 diabetes but also as a target group for prevention in its own right.
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            Dipeptidyl peptidase 4 inhibitor sitagliptin maintains β-cell function in patients with recent-onset latent autoimmune diabetes in adults: one year prospective study.

            Yunjuan Zhao, Lin Yang, Yufei Xiang … (2014)
            Dipeptidyl peptidase 4 (DPP-4) inhibitors have been widely used in type 2 diabetes. An important unanswered question concerns the effect of DPP-4 inhibition on β-cell function in patients with autoimmune diabetes.
            Article 0 comments Cited 48 times – based on 0 reviews     Review now
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              1,25-Dihydroxyvitamin D3 protects human pancreatic islets against cytokine-induced apoptosis via down-regulation of the Fas receptor.

              R Riachy, B Vandewalle, S Belaich … (2006)
              Beta cell loss occurs at the onset of type 1 diabetes and after islet graft. It results from the dysfunction and destruction of beta cells mainly achieved by apoptosis. One of the mediators believed to be involved in beta cell apoptosis is Fas, a transmembrane cell surface receptor transducing an apoptotic death signal and contributing to the pathogenesis of several autoimmune diseases. Fas expression is particularly induced in beta cells by inflammatory cytokines secreted by islet-infiltrating mononuclear cells and makes cells susceptible to apoptosis by interaction with Fas-ligand expressing cells. We have previously demonstrated that 1,25(OH)2D3, the active metabolite of vitamin D, known to exhibit immunomodulatory properties and prevent the development of type 1 diabetes in NOD mice, is efficient against apoptosis induced by cytokines in human pancreatic islets in vitro. The effects were mainly mediated by the inactivation of NF-kappa-B. In this study we demonstrated that 1,25(OH)2D3 was also able to counteract cytokine-induced Fas expression in human islets both at the mRNA and protein levels. These results were reinforced by our microarray analysis highlighting the beneficial effects of 1,25(OH)2D3 on death signals induced by Fas activation. Our results provides additional evidence that 1,25(OH)2D3 may be an interesting tool to help prevent the onset of type 1 diabetes and improve islet graft survival.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Endocrinol Diabetes Metab Case Rep
                Journal ID (iso-abbrev): Endocrinol Diabetes Metab Case Rep
                Journal ID (pmc): edm
                Journal ID (publisher-id): EDM Case Reports
                Title: Endocrinology, Diabetes & Metabolism Case Reports
                Publisher: Bioscientifica Ltd (Bristol )
                ISSN (Electronic): 2052-0573
                Publication date (Electronic): 27 May 2016
                Publication date (Print): 2016
                Volume: 2016
                Electronic Location Identifier: 150136
                Affiliations
                [1 ]Diabetes Center of 1st Department of Internal Medicine, AHEPA University Hospital , Thessaloniki, Greece
                [2 ]1st Department of Internal Medicine, AHEPA University Hospital , Thessaloniki, Greece
                Author notes
                Correspondence should be addressed to K Kotsa Email: kalmanthou@ 123456yahoo.gr
                Article
                Publisher ID: EDM150136
                DOI: 10.1530/EDM-15-0136
                PMC ID: 4888610
                PubMed ID: 27252860
                SO-VID: bac1feb0-a498-49fe-b1d6-cab45883f898
                Copyright © © 2016 The authors
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.

                History
                Date received : 24 April 2016
                Date accepted : 6 May 2016
                Categories
                Subject: Insight into Disease Pathogenesis or Mechanism of Therapy

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