This form of diabetes is defined by insulin deficiency due to destruction of the fi cells of the pancreas. It was formerly designated ''insulin-dependent diabetes,'' but efforts are being made to eliminate this name because many patients with other types of
Table 3 Classification of diabetes mellitus3
I. Type 1 diabetes (formerly designated insulin-dependent diabetes)
II. Type 2 diabetes (formerly designated non-insulin-dependent diabetes)
III. Secondary diabetes
A. Genetic defects of 0 cell function (e.g., maturity onset diabetes of youth)
B. Genetic defects of insulin action pathway
C. Exocrine pancreatic disease
D. Endocrinopathies (e.g., Cushing's syndrome and acromegaly)
E. Drugs or chemicals
F. Infections (e.g., congenital rubella)
G. Other genetic syndromes (e.g., Down's and Klinefelter's syndromes)
Classification proposed by the Expert Committee on the Diagnosis and the Classification of Diabetes Mellitus under the sponsorship of the American Diabetes Association (Diabetes Care 27: S5-S10, 2004).
diabetes also require insulin for adequate control. The predominant cause is believed to be an autoimmune attack against the insulin-producing 0 cells within the islets of Langerhans (diabetes type 1A). At the time of diagnosis, most patients demonstrate antibodies to certain pancreatic autoantigens, which include antibodies to islet cell cytoplasmic components, glutamic acid decarboxylase, insulin, and tyrosine phosphatases IA-2 and IA-20. Such auto-antibodies, when present, help to confirm the diagnosis. This disease also has strong HLA antigen associations, which may either predispose to or protect from the development of diabetes. In a minor subset of patients classified as idiopathic type 1 diabetes (type 1B), the presentation and clinical course is similar to autoimmune type 1A diabetes, but all tests for autoimmune markers are negative.
Early diagnosis of autoimmune diabetes Type 1 diabetes has a variable presymptomatic phase that may extend for several years, during which time it is possible to make a diagnosis. This form of diagnostic testing is reserved for research purposes because the disease is not sufficiently common to warrant widespread screening strategies and because practical methods for preventing the progression to overt diabetes are not available. Because type 1 diabetes is occasionally familial, screening of individuals with strong family histories can be performed by measuring levels of the specific pancreatic autoantigens described previously; subjects with high titers of antibodies who possess unfavorable HLA subtypes, indicating significant risk of later development of diabetes, may then undergo intravenous glucose tolerance testing with quantitation of the insulin response. Diminution of the early phases of insulin release can be seen even years before the onset of symptoms of disease. Currently, such diagnosis is important only to enable participation in clinical trials of diabetes prevention.
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