ABSTRACT
Diabetes mellitus is a complex of syndromes characterized by hyperglycemia and altered glucose metabolism associated with specific microvascular and macrovascular complications as well as neuropathy (1). There are many etiologies of elevated plasma glucose and impaired glucose tolerance (2). This review will concentrate on what has been termed type 1A diabetes, or the form of diabetes resulting from immunemediated destruction of the cells that produce insulin (3-6). This is the most common form of childhood diabetes in the United States, but type 1A diabetes can present at any age. The term Type 2 diabetes probably encompasses several genetic disorders and is characterized phenotypically by insulin resistance, an association with obesity, an absence of an absolute requirement for insulin and thus a diminished incidence of ketoacidosis. Diabetic syndromes with a known genetic etiology such as several forms of maturity onset diabetes of the young (MODY) are distinct from both type 2 and type 1 diabetes. The clearest distinction between these forms of diabetes relate to the detection of known genetic mutations (e.g. the MODY3 HNF-1α mutation (7) or the presence of anti-islet autoantibodies for type 1A diabetes. Type 1 diabetes or insulin-dependent diabetes mellitus of children is characterized by a more rapid onset of hyperglycemia, a tendency to ketoacidosis, and total dependence on insulin to survive and maintain health. Such a dependence usually only develops several years after diabetes onset. There has been considerable progress in reaching a consensus that the major subset of type 1 diabetes is of immune etiology and thus the designation type 1A diabetes for “immunemediated” diabetes (2). Type 1B diabetes refers to diabetic syndromes with loss of insulin-producing cells, but where the loss is not immune-mediated.
