Diabetes is classified into two types. Type 1 diabetes is characterized by destruction of the pancreatic beta cells, leading to absolute insulin deficiency. This is usually due to autoimmune destruction of the pancreatic beta cells (type 1A). Testing for islet-cell antibodies (ICA) or other autoantibodies (antibodies to glutamic acid decarboxylase [anti-GAD], insulin, and to the tyrosine phosphatase IA-2) in serum may be helpful if establishing the diagnosis is important; a positive result is indicative of immune-mediated or type 1A diabetes. However, some patients have no evidence of autoimmunity and have no other known cause for beta-cell destruction. They are said to have idiopathic or type 1B diabetes mellitus.
Type 2 diabetes is responsible for over 80 percent of cases of diabetes in the United States, Canada, and Europe; type 1 diabetes accounts for another 5 to 10 percent, with the remainder due to other causes. New information has led to increased understanding of genetic defects related to diabetes, and the formerly termed MODY syndromes (maturity onset diabetes of the young) have now been linked to specific genetic defects.
Type 2 diabetes is by far the most common type of diabetes, and is characterized by variable degrees of insulin deficiency and resistance. However, it is occasionally difficult to distinguish between type 1 and atypical presentations of type 2 diabetes. Many patients with type 2 diabetes lose beta cell function over time and require insulin for glucose control. Thus, need for insulin does not distinguish between type 1 and type 2 diabetes. Patients with type 2 diabetes typically present with hyperglycemia, although ketoacidosis can occur.
Fibrocalculous pancreatic diabetes — Fibrocalculous pancreatic diabetes is a unique form of diabetes secondary to tropical pancreatitis that is endemic in certain parts of the world (eg, southern India). In a prospective evaluation of 370 patients all of the macrovascular and microvascular complications typically associated with diabetes were found.
Gestational diabetes occurs when a woman's pancreatic function is not sufficient to overcome both the insulin resistance created by the anti-insulin hormones secreted by the placenta during pregnancy (eg, estrogen, prolactin, human chorionic somatomammotropin, cortisol, and progesterone) and the increased fuel consumption necessary to provide for the growing mother and fetus.
©2004-2010 All Rights Reserved. • Diabetes