Diagnosis, Classification, and Pathogenesis of Diabetes Mellitus
J Clin Psychiatry 2001;62(suppl 27):5-9
© Copyright 2016 Physicians Postgraduate Press, Inc.
Access to this article is available to valid users
Still can't log in? Contact the Circulation Department at 1-800-489-1001 x4 or send email
Register: If you do not have one already, register for a free account.
Diabetes mellitus is a metabolic disorder that is characterized by inappropriate hyperglycemia and
is associated with both acute and chronic complications. Currently, diabetes mellitus is diagnosed by
blood or plasma glucose levels. A random plasma glucose level ≥ 200 mg/dL in an individual with
classic symptoms is sufficient to make the diagnosis. Otherwise, a fasting plasma glucose level ≥ 126
mg/dL or a 2-hour plasma glucose level ≥ 200 mg/dL after an oral glucose challenge of 75 g on 2
occasions is sufficient evidence upon which to diagnose diabetes mellitus. The major types of diabetes
mellitus are type 1 diabetes (insulin deficient) and type 2 diabetes (combination of insulin resistance
and insulin deficiency). In both types, there is a genetic predisposition as well as environmental factors
that contribute to the expression of the genetic predisposition. In type 1 diabetes, the primary abnormality
is extensive deficiency of beta cell function. In type 2 diabetes, insulin resistance occurs,
and the marked compensatory increases in insulin secretion necessary to maintain normal glucose tolerance
cannot be achieved or maintained. As beta cell function continues to decrease, the individual
progresses from normal glucose tolerance to impaired glucose tolerance to diabetes with primarily
postprandial hyperglycemia to diabetes with fasting hyperglycemia. Drugs can cause diabetes by interfering
with beta cell insulin secretion, by increasing insulin resistance, or by a combination of both.
Atypical antipsychotic drugs have been reported to cause diabetic ketoacidosis, obesity and insulin
resistance, type 2 diabetes, and hypertriglyceridemia. A monitoring system should be in place in patients
started on treatment with these agents to detect metabolic abnormalities as they are evolving so
that adequate and timely treatment can be initiated.