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Type 1 Diabetes Through the Life Span: a Position Statement of the American Diabetes Association

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Type 1 Diabetes Through the Life Span: a Position Statement of the American Diabetes Association 2034 Diabetes Care Volume 37, July 2014 Jane L. Chiang,1 M. Sue Kirkman,2 Type1DiabetesThroughtheLife Lori M.B. Laffel,3 and Anne L. Peters,4 on behalf of the Type 1 Diabetes Sourcebook Span: A Position Statement of the Authors* American Diabetes Association Diabetes Care 2014;37:2034–2054 | DOI: 10.2337/dc14-1140 Type 1 diabetes is characterized by an immune-mediated depletion of b-cells that results in lifelong dependence on exogenous insulin. While both type 1 and type 2 diabetes result in hyperglycemia, the pathophysiology and etiology of the diseases are distinct and require us to consider each type of diabetes independently. As such, this position statement summarizes available data specific to the comprehensive care of individuals with type 1 diabetes. The goal is to enhance our ability to recognize and manage type 1 diabetes, to prevent its associated complications, and to eventually cure and prevent this disease. INCIDENCE AND PREVALENCE OF TYPE 1 DIABETES The exact number of individuals with type 1 diabetes around the world is not known, but in the U.S., there are estimated to be up to 3 million (1). Although it has long been called “juvenile diabetes” due to the more frequent and relatively POSITION STATEMENT straightforward diagnosis in children, the majority of individuals with type 1 di- abetes are adults. Most children are referred and treated in tertiary centers, where clinical data are more readily captured. The SEARCH for Diabetes in Youth study estimated that, in 2009, 18,436 U.S. youth were newly diagnosed with type 1 diabetes (12,945 non- Hispanic white, 3,098 Hispanic, 2,070 non-Hispanic black, 276 Asian-Pacific Islander, and 47 American Indian) (2). Worldwide, ;78,000 youth are diagnosed with type 1 diabetes annually. Incidence varies tremendously among countries: East Asians and American Indians have the lowest incidence rates (0.1–8 per 100,000/year) as compared with the Finnish who have the highest rates (.64.2 per 100,000/year) (3). In the U.S., the number of youth with type 1 diabetes was estimated to be 166,984 (4). The precise incidence of new-onset type 1 diabetes in those over 20 years of age is unknown. This may be due to the prolonged phase of onset and the subtleties in distinguishing the different types of diabetes. In one European study of adults aged 30–70 years, ;9% tested positive for GAD antibodies (GADA) within 5 years of a 1 diabetes diagnosis, consistent with other studies (5). American Diabetes Association, Alexandria, VA 2Department of Medicine, University of North Adults with type 1 diabetes often receive care in primary care settings rather than Carolina at Chapel Hill, Chapel Hill, NC with an endocrinologist. Unlike the consolidated care seen in pediatric diabetes man- 3Pediatric, Adolescent and Young Adult Section, agement, the lack of consolidated care in adults makes incidence and prevalence rates Joslin Diabetes Center; Department of Pediat- difficult to characterize, and therefore they are often underestimated. The number of rics, Harvard Medical School, Boston, MA 4 adults living with type 1 diabetes is increasing due to two factors: 1) the rising number Division of Endocrinology, Keck School of Med- icine of the University of Southern California, Los of new-onset cases of type 1 diabetes in adults, including those diagnosed with latent Angeles, CA autoimmune diabetes in adults (LADA), and 2) individuals with childhood-onset di- Corresponding author: Jane L. Chiang, jchiang@ abetes are living longer (6,7). diabetes.org. The position statement was reviewed and ap- CLASSIFICATION AND DIAGNOSIS proved by the Professional Practice Committee Type 1 diabetes has traditionally been diagnosed based on clinical catabolic symp- in April 2014 and approved by the Executive toms suggestive of insulin deficiency: polyuria, polydipsia, weight loss, and marked Committee of the Board of Directors in April 2014. hyperglycemia that is nonresponsive to oral agents. It is classified as an autoimmune disease with progressive b-cell destruction, resulting in a physiological dependence *A list of authors of the American Diabetes As- sociation/JDRF Type 1 Diabetes Sourcebook can on exogenous insulin. Recent studies have broadened our understanding of the be found in the ACKNOWLEDGMENTS. disease, but have made diagnosis more complex. © 2014 by the American Diabetes Association. There is tremendous variability in the initial presentation of type 1 diabetes in See http://creativecommons.org/licenses/by- both youth and adults. Children often present acutely, with severe symptoms of polyuria, nc-nd/3.0/ for details. care.diabetesjournals.org Chiang and Associates 2035 Figure 1—The percentage of antibody-positive subjects is affected by the duration of type 1 diabetes for GADA (A)andIA2A(B).Givenanincreaseinthe scatter (due to lower numbers of subjects), the x-axis is truncated at a duration of 30 years. Reproduced with permission from Tridgell et al. (16). polydipsia, and ketonemia. However, in more likely to be diagnosed as having the empiric risk of being affected is ;5% adults, type 1 diabetes presents with a type 1 diabetes, the potential for type 1 (17,18), representing a 15-fold increase more gradual onset, with a clinical pre- diabetes exists in those who phenotypi- among family members. Studies evaluat- sentation that may initially appear consis- cally appear to have type 2 diabetes. If ing children at risk for developing type 1 tent with type 2 diabetes. Distinguishing hyperglycemia persists after treatment diabetes have shown that the presence of betweentype1andtype2diabetes with noninsulin agents, which is unusual more than two autoantibodies was asso- presents diagnostic challenges. Tradition- in the treatment of newly diagnosed type ciated with a nearly 70% risk for disease ally, progressive b-cell destruction has 2 diabetes, then type 1 diabetes should development within 10 years and 84% been the hallmark of type 1 diabetes, be considered. within 15 years (19). Evaluating at-risk in- but residual C-peptide (a surrogate marker dividuals in the clinical setting is not yet for insulin secretion) may be detected over Pancreatic Autoantibodies recommended due to limited clinical in- 40 years after initial diagnosis, regardless Pancreatic autoantibodies are charac- terventions; however, ongoing research of whether the initial diagnosis was made teristic of type 1 diabetes. Highly sensi- studies are identifying at-risk individuals in childhood or in adulthood (8). tive laboratory measurements capture through genetic testing in both the lower- ;98% of individuals with autoantibod- risk general population and in the higher- Clinical Clues ies at diagnosis (10). Unfortunately, risk population of relatives of people with Much of the diagnosis will depend on most commercial laboratories do not type 1 diabetes. clinical clues, but the rising incidence have reliably sensitive or specific assays Recommendations of overweight/obesity has also con- that measure all five autoantibodies: founded the diagnosis of type 1 diabetes. Diagnosis GADA, islet cell antibodies (ICA), insulin c The American Diabetes Association’s A lean individual presenting with clinical autoantibodies (IAA), protein tyro- (ADA’s) diagnostic criteria for type 1 symptoms without a first-degree relative sine phosphatase antibodies (ICA512 and type 2 diabetes are the same with diabetes (but often with a history of or IA2A), and zinc transporter protein (Table 1). (A) distant relatives with type 1 diabetes or (ZnT8). Thus, it may be inappropriate c Consider measurement of pancreatic other autoimmune disease) is generally to report a patient as autoantibody neg- autoantibodies to confirm the diag- suggestive of type 1 diabetes. An over- “ ” ative. Another cause of false-negative nosis of type 1 diabetes. (B) weight individual (of any age) with meta- autoantibodies is testing far out from bolic syndrome and a strong family history diagnosis as antibody titers diminish Identification of At-Risk Relatives of type 2 diabetes may be assessed only over time (Fig. 1). It appears that there c Inform type 1 diabetic patients of the for the development of type 2 diabetes, is an increased incidence of type 1 di- opportunity to have their relatives even though type 1 diabetes is on the abetes in ethnic populations where au- tested for type 1 diabetes risk in the differential diagnosis. Obesity does not toantibody markers may be of variable setting of a clinical research study. (B) preclude that autoimmunity and hyper- utility, such as in Asians where autoanti- glycemia will occur even amid the rela- bodies are often negative (11–15). INITIAL EVALUATION AND tively higher levels of endogenous insulin FOLLOW-UP secretion observed in obesity. In young Family History General Considerations patients aged 10–17 years with pheno- Type 1 diabetes has a genetic predilection All patients with type 1 diabetes typic type 2 diabetes, 10% have evidence and, in some cases, can be predicted in need age-appropriate care, with an of islet autoimmunity suggesting that family members. The overall prevalence understanding of their specific needs type 1 diabetes was the likely diagnosis of type 1 diabetes in the U.S. is ;0.3%, and limitations. Infants and toddlers (9). Thus, although leaner individuals are but if a first-degree relative has diabetes, are approached quite differently from 2036 Position Statement Diabetes Care Volume 37, July 2014 Table 1—Criteria for the diagnosis of diabetes frequency in patients with type 1 diabetes (1–16% of individuals compared with A1C $6.5%. The test should be performed in a laboratory using a method that is NGSP 0.3–1% in the general population) fi certi ed and standardized to the DCCT assay.* (21,22). Symptoms of celiac disease in- OR clude diarrhea, weight loss or poor weight $ fi FPG 126 mg/dL (7.0 mmol/L). Fasting is de ned as no caloric intake for at least 8 h.* gain, abdominal pain, bloating, chronic OR fatigue, malnutrition due to malabsorp- Two-hour plasma glucose $200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test.
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