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Diagnosis and Classification of Diabetes Mellitus

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Diagnosis and Classification of Diabetes Mellitus POSITION STATEMENT Diagnosis and Classification of Diabetes Mellitus AMERICAN DIABETES ASSOCIATION reduction, exercise, and/or oral glucose- lowering agents. These individuals there- fore do not require insulin. Other DEFINITION AND tinal, genitourinary, and cardiovascular individuals who have some residual insu- DESCRIPTION OF DIABETES symptoms and sexual dysfunction. Patients lin secretion but require exogenous insu- MELLITUS — Diabetes mellitus is a with diabetes have an increased incidence lin for adequate glycemic control can group of metabolic diseases characterized of atherosclerotic cardiovascular, periph- survive without it. Individuals with ex- ␤ by hyperglycemia resulting from defects eral arterial, and cerebrovascular disease. tensive -cell destruction and therefore in insulin secretion, insulin action, or Hypertension and abnormalities of lipopro- no residual insulin secretion require insu- both. The chronic hyperglycemia of dia- tein metabolism are often found in people lin for survival. The severity of the meta- betes is associated with long-term dam- with diabetes. bolic abnormality can progress, regress, age, dysfunction, and failure of various The vast majority of cases of diabetes or stay the same. Thus, the degree of hy- organs, especially the eyes, kidneys, fall into two broad etiopathogenetic cate- perglycemia reflects the severity of the un- nerves, heart, and blood vessels. gories (discussed in greater detail below). derlying metabolic process and its Several pathogenic processes are in- In one category, type 1 diabetes, the cause treatment more than the nature of the volved in the development of diabetes. is an absolute deficiency of insulin secre- process itself. These range from autoimmune destruc- tion. Individuals at increased risk of de- tion of the ␤-cells of the pancreas with veloping this type of diabetes can often be CLASSIFICATION OF consequent insulin deficiency to abnor- identified by serological evidence of an DIABETES MELLITUS AND malities that result in resistance to insulin autoimmune pathologic process occur- OTHER CATEGORIES OF action. The basis of the abnormalities in ring in the pancreatic islets and by genetic GLUCOSE REGULATION — carbohydrate, fat, and protein metabo- markers. In the other, much more preva- Assigning a type of diabetes to an individ- lism in diabetes is deficient action of in- lent category, type 2 diabetes, the cause is ual often depends on the circumstances sulin on target tissues. Deficient insulin a combination of resistance to insulin ac- present at the time of diagnosis, and many action results from inadequate insulin se- tion and an inadequate compensatory in- diabetic individuals do not easily fit into a cretion and/or diminished tissue re- sulin secretory response. In the latter single class. For example, a person with sponses to insulin at one or more points in category, a degree of hyperglycemia suffi- gestational diabetes mellitus (GDM) may the complex pathways of hormone action. cient to cause pathologic and functional continue to be hyperglycemic after deliv- Impairment of insulin secretion and de- changes in various target tissues, but ery and may be determined to have, in fects in insulin action frequently coexist without clinical symptoms, may be fact, type 2 diabetes. Alternatively, a per- in the same patient, and it is often unclear present for a long period of time before son who acquires diabetes because of which abnormality, if either alone, is the diabetes is detected. During this asymp- large doses of exogenous steroids may be- primary cause of the hyperglycemia. tomatic period, it is possible to demon- come normoglycemic once the glucocor- Symptoms of marked hyperglycemia strate an abnormality in carbohydrate ticoids are discontinued, but then may include polyuria, polydipsia, weight loss, metabolism by measurement of plasma develop diabetes many years later after re- sometimes with polyphagia, and blurred glucose in the fasting state or after a chal- current episodes of pancreatitis. Another vision. Impairment of growth and suscep- lenge with an oral glucose load. example would be a person treated with tibility to certain infections may also ac- The degree of hyperglycemia (if any) thiazides who develops diabetes years company chronic hyperglycemia. Acute, may change over time, depending on the later. Because thiazides in themselves sel- life-threatening consequences of uncon- extent of the underlying disease process dom cause severe hyperglycemia, such in- trolled diabetes are hyperglycemia with (Fig. 1). A disease process may be present dividuals probably have type 2 diabetes ketoacidosis or the nonketotic hyperos- but may not have progressed far enough that is exacerbated by the drug. Thus, for molar syndrome. to cause hyperglycemia. The same disease the clinician and patient, it is less important Long-term complications of diabetes process can cause impaired fasting glu- to label the particular type of diabetes than it include retinopathy with potential loss of cose (IFG) and/or impaired glucose toler- is to understand the pathogenesis of the hy- vision; nephropathy leading to renal failure; ance (IGT) without fulfilling the criteria perglycemia and to treat it effectively. peripheral neuropathy with risk of foot ul- for the diagnosis of diabetes. In some in- cers, amputations, and Charcot joints; and dividuals with diabetes, adequate glyce- Type 1 diabetes (␤-cell destruction, autonomic neuropathy causing gastrointes- mic control can be achieved with weight usually leading to absolute insulin deficiency) ●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●● Immune-mediated diabetes. This form The information that follows is based largely on the reports of the Expert Committee on the Diagnosis and of diabetes, which accounts for only Classification of Diabetes (Diabetes Care 20:1183–1197, 1997, and Diabetes Care 26:3160–3167, 2003). 5–10% of those with diabetes, previously DOI: 10.2337/dc09-S062 © 2009 by the American Diabetes Association. Readers may use this article as long as the work is properly encompassed by the terms insulin- cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons. dependent diabetes, type I diabetes, or ju- org/licenses/by-nc-nd/3.0/ for details. venile-onset diabetes, results from a S62 DIABETES CARE, VOLUME 32, SUPPLEMENT 1, JANUARY 2009 Position Statement -Even after presenting in ketoacidosis, these patients can briefly return to normoglyء .Figure 1—Disorders of glycemia: etiologic types and stages in rare instances, patients in these categories (e.g., Vacor toxicity, typeءء ;(cemia without requiring continuous therapy (i.e., “honeymoon” remission 1 diabetes presenting in pregnancy) may require insulin for survival. cellular-mediated autoimmune destruc- els of plasma C-peptide. Immune- placement therapy in affected patients tion of the ␤-cells of the pancreas. Mark- mediated diabetes commonly occurs in may come and go. ers of the immune destruction of the childhood and adolescence, but it can oc- ␤-cell include islet cell autoantibodies, cur at any age, even in the 8th and 9th Type 2 diabetes (ranging from autoantibodies to insulin, autoantibodies decades of life. predominantly insulin resistance to glutamic acid decarboxylase (GAD65), Autoimmune destruction of ␤-cells with relative insulin deficiency to and autoantibodies to the tyrosine phos- has multiple genetic predispositions and predominantly an insulin secretory phatases IA-2 and IA-2␤. One and usually is also related to environmental factors defect with insulin resistance) more of these autoantibodies are present that are still poorly defined. Although pa- This form of diabetes, which accounts for ϳ in 85–90% of individuals when fasting tients are rarely obese when they present 90–95% of those with diabetes, previ- hyperglycemia is initially detected. Also, with this type of diabetes, the presence of ously referred to as non-insulin- the disease has strong HLA associations, obesity is not incompatible with the diag- dependent diabetes, type II diabetes, or with linkage to the DQA and DQB genes, nosis. These patients are also prone to adult-onset diabetes, encompasses indi- and it is influenced by the DRB genes. other autoimmune disorders such as viduals who have insulin resistance and These HLA-DR/DQ alleles can be either Graves’ disease, Hashimoto’s thyroiditis, usually have relative (rather than abso- predisposing or protective. lute) insulin deficiency At least initially, Addison’s disease, vitiligo, celiac sprue, In this form of diabetes, the rate of and often throughout their lifetime, these autoimmune hepatitis, myasthenia gravis, ␤-cell destruction is quite variable, being individuals do not need insulin treatment and pernicious anemia. rapid in some individuals (mainly infants to survive. There are probably many dif- and children) and slow in others (mainly Idiopathic diabetes. Some forms of type ferent causes of this form of diabetes. Al- adults). Some patients, particularly chil- 1 diabetes have no known etiologies. though the specific etiologies are not dren and adolescents, may present with Some of these patients have permanent known, autoimmune destruction of ketoacidosis as the first manifestation of insulinopenia and are prone to ketoacido- ␤-cells does not occur, and patients do the disease. Others have modest fasting sis, but have no evidence of autoimmu- not have any of the other causes of diabe- hyperglycemia that can rapidly change to nity. Although only a minority of patients tes listed above
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