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Is Latent Autoimmune Diabetes in Adults Distinct from Type 1 Diabetes Or Just Type 1 Diabetes at an Older Age? Jerry P

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Is Latent Autoimmune Diabetes in Adults Distinct from Type 1 Diabetes Or Just Type 1 Diabetes at an Older Age? Jerry P Is Latent Autoimmune Diabetes in Adults Distinct From Type 1 Diabetes or Just Type 1 Diabetes at an Older Age? Jerry P. Palmer,1,2 Christiane S. Hampe,1 Harvey Chiu,1,2 Amit Goel,1,2 and Barbara M. Brooks-Worrell1,2 Diabetes is classified clinically into two types: type 1 and the antibodies commonly found in type 1 diabetes; this type 2 diabetes. Type 1 diabetes is an autoimmune diabe- subset has been said to have type 1.5 diabetes, latent tes, whereas, in contrast, type 2 diabetes is nonautoim- autoimmune diabetes in adults (LADA), slowly progres- mune. However, there is a group of phenotypic adult type 2 sive IDDM, latent type 1 diabetes, youth-onset diabetes of diabetic patients (ϳ10%) who have islet autoantibodies maturity, latent-onset type 1 diabetes, and antibody-posi- similar to type 1 diabetes. These patients are said to have tive non-insulin-dependent diabetes (4–6) (Table 1). Al- latent autoimmune diabetes in adults (LADA) or type 1.5 though the different names have caused some confusion, diabetes. T-cells reacting with islet proteins have been demonstrated in type 1 and type 1.5 diabetic patients. In the finding of this subset of phenotypic type 2 diabetic contrast, classic autoantibody-negative type 2 diabetic pa- patients by many different investigators rather than just tients are also negative for T-cell responses to islet pro- one or two groups confirms their existence as an impor- teins. Therefore, we questioned whether type 1 and type tant subset of phenotypic type 2 diabetic patients. 1.5 diabetes are similar or different autoimmune diseases. Probably the greatest area of confusion involves the We have investigated the immunological and metabolic distinction of LADA from type 1 diabetes occurring in differences between type 1, type 1.5, and classic type 2 individuals over the age of 30–35 years. Epidemiologic diabetic patients. We have identified autoantibody differ- evidence suggests that type 1 diabetes peaks around ences, differences in islet proteins recognized by T-cells, puberty and again around age 40 years (7), and Nerup and and differences in insulin resistance. We have also identi- fied a small group of patients who have T-cells responsive colleagues (8) have suggested that the incidence of type 1 to islet proteins but who are autoantibody negative. These diabetes is approximately equivalent below and above age patients appear to be similar to type 1.5 patients in having 20 years. We have discussed some of these nomenclature decreased stimulated C-peptide values. These immunolog- issues in an editorial (9), and most recently the Immunol- ical differences between type 1 and type 1.5 diabetes ogy of Diabetes Society proposed several criteria to try to suggest at least partially distinct disease processes. standardize those patients referred to as having LADA. Diabetes 54 (Suppl. 2):S62–S67, 2005 The Immunology of Diabetes Society proposed that pa- tients be Ն30 years of age, positive for at least one of the four antibodies commonly found in type 1 diabetic pa- tients (ICAs and autoantibodies to GAD65, IA-2, and he finding nearly simultaneously by two groups insulin), and not treated with insulin within the first 6 in 1974 (1,2) that islet cell antibodies (ICAs) months after diagnosis. The latter requirement, although were common in the sera of patients with type 1 admittedly subjective and likely to vary depending on the diabetes (type 1 diabetes) provided strong evi- treating physician, is meant to distinguish LADA and T ␤ Ͼ dence that the -cell lesion of type 1 diabetes was auto- type 1 diabetes occurring in patients 30 years of age immune in nature. Shortly thereafter, it was published that (S. Fourlanos, F. Dotta, C. Greenbaum, J.P.P., O. Rolands- ϳ11% of patients with type 2 diabetes were also positive son, P.G. Colman, L.C. Harrison, unpublished data). for ICAs and that this ICAϩ subset of type 2 diabetic Another area of controversy involves the role of obesity patients tended to fail sulfonylurea therapy and needed and consequently the degree of insulin resistance in LADA. insulin treatment earlier than ICAϪ type 2 diabetic patients Kahn et al. (10) described the normal curvilinear relation- (3). Many other groups have also identified a subset of ship between insulin resistance and insulin secretion. phenotypic type 2 diabetic patients who are positive for Normal ␤-cells compensate for insulin resistance by se- creting more insulin, and the product of insulin sensitivity and insulin secretion is normally a constant that Kahn (11) From the 1Department of Medicine, Division of Metabolism, Endocrinology and Nutrition, University of Washington, Seattle, Washington; and the 2De- has termed the disposition index. The primary importance partment of Veterans Affairs Puget Sound Health Care System, Seattle, of this physiology is that insulin-resistant patients will Washington. present with hyperglycemia with a less severe degree of Address correspondence and reprint requests to Jerry P. Palmer, MD, DVA Puget Sound Health Care System, Endocrinology (111), 1660 S. Columbian absolute insulin deficiency than insulin-sensitive patients. Way, Seattle, WA 98108. E-mail: [email protected]. Because LADA patients span the spectrum from lean to Received for publication 4 March 2005 and accepted in revised form 28 April obese, it is likely that differences in insulin sensitivity are 2005. an important variable in the physiology of LADA. We have This article is based on a presentation at a symposium. The symposium and the publication of this article were made possible by an unrestricted educa- become interested in this topic and will present some of tional grant from Servier. our initial findings later in this article. GADA, GAD antibody; ICA, islet cell antibody; LADA, latent autoimmune Whether the immunological damage to and destruction diabetes in adults; MICA, major histocompatibility complex class I chain– ␤ related gene A. of the pancreatic -cells involves the same mechanisms in © 2005 by the American Diabetes Association. all patients with autoimmune diabetes is unknown. That S62 DIABETES, VOL. 54, SUPPLEMENT 2, DECEMBER 2005 J.P. PALMER AND ASSOCIATES TABLE 1 Type 1.5 diabetes Latent autoimmune diabetes of adults (LADA) Antibody-positive type 2 diabetes Latent-onset type 1 diabetes Slowly progressive IDDM (SPIDDM) Youth overt diabetes of maturity (YODM) Progressive insulin-dependent diabetes mellitus (PIDDM) question is addressed in the title of this article: “Is LADA different pathophysiologically from classic childhood type 1 diabetes or is LADA merely type 1 diabetes presenting at an older age?” This question is the focus of this review. This question also has important therapeutic implications. Because LADA is more common than classic childhood type 1 diabetes and because immunomodulatory thera- pies, such as anti-CD3, have been identified that are efficacious in modulating the type 1 diabetes disease process (12), it will be of great interest to see whether FIG. 1. Clustering of autoantibodies in autoantibody-positive patients. Numbers (%) refer to the percentage of the antibody-positive patients these treatments are similarly effective in LADA. who were positive for the respective antibodies. Reproduced with The genes predisposing to and protecting from classic permission from Juneja et al., Metabolism 50:10081–10013, 2001. type 1 diabetes have been extensively studied. Also, the islet autoantibodies in classic type 1 diabetes and as predictors of subsequent clinical diabetes in at-risk indi- that some unidentified antigens are more commonly in- viduals have been very well characterized. Furthermore, volved in LADA than type 1 diabetes. because type 1 diabetes is largely a T-cell–mediated dis- In a relatively large study (n ϭ 569, type 2 diabetes), ease, several groups, including our own, have begun to GAD65/67 chimeric molecules were used to test for pos- describe the T-cell abnormalities characteristic of type 1 sible associations of GADA epitope specificity and clinical diabetes. Similarities or differences between classic type 1 characteristics. Of the 11% of type 2 diabetic patients who diabetes and LADA in terms of genes, islet autoantibodies, were GADA positive, ϳ80% had antibodies directed to and T-cells would provide important evidence to the both middle and COOH-terminal epitopes. These patients question posed above: “Is LADA different pathophysiologi- had a lower BMI, lower basal C-peptide, and a higher cally from type 1 diabetes or just type 1 diabetes present- frequency of insulin treatment than GADAϪ patients. The ing at an older age?” This article will review these data. 20% of GADAϩ patients with antibodies directed solely at the mid-portion of GAD65 were indistinguishable from ANTIBODIES GADAϪ type 2 diabetic patients (17). The presence of islet autoantibodies in both LADA and In collaboration with Chris Hampe and Åke Lernmark, classic type 1 diabetes provides strong evidence that the we investigated whether there are differences in epitope underlying disease processes are both autoimmune, but specificity of GADAs in LADA versus type 1 diabetes. differences in antibodies in LADA and type 1 diabetes Using recombinant 35S-GAD65/67 fusion proteins, we suggest potentially important immunological differences. found that sera from over 90% of type 1 diabetes bound to All four islet autoantibodies—ICAs, GAD antibodies the middle or COOH-terminal portion of GAD65, whereas (GADAs), IA-2 antibodies, and insulin autoantibodies—are this was the case for only 65% of sera from LADA patients. common in childhood type 1 diabetes, with many patients In contrast, the NH2-terminal portion of GAD65 was rec- being positive for multiple autoantibodies. And, in nondi- ognized by 20% of LADA patients compared with 5% of abetic relatives of patients with type 1 diabetes, risk of type 1 diabetic patients (18). More recently, we have found future type 1 diabetes is directly proportional to the similar results using GAD65-specific recombinant Fabs.
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