The original schema for classifying diabetes mellitus (DM) consisted of 2 categories known as type 1 diabetes mellitus and type 2 diabetes mellitus. Type 1 diabetes was also known as insulin-dependent diabetes. Patients with this type of diabetes were considered prone to develop diabetic ketoacidosis (DKA).
Patients with type 1 diabetes were found to have an absolute insulin deficiency due to autoimmune destruction of pancreatic beta cells. Patients with type 2 diabetics, or noninsulin-dependent diabetes, were not considered to be at risk for DKA. Type 2 diabetes is strongly associated with obesity and a family history of diabetes. These patients have peripheral insulin resistance with initially normal or elevated circulating levels of endogenous insulin.
Since the mid-1990s, the number of patients who presented with DKA but did not require long-term insulin therapy has increased. Many such patients had conditions that resembled traditionally defined type 2 diabetes, in that they were obese and often had a family history of diabetes. Subsequent to these observations, new ways to classify diabetes were devised.
The system of classification that most accurately predicts the need for insulin treatment 12 months after presentation with DKA is known as the Aß system. This system classifies diabetics into 4 groups as follows:
A+ß- - Autoantibodies present, β cell function absent
A+ß+ - Autoantibodies present, β cell function present
A-ß- - Autoantibodies absent, β cell function absent
A-ß+ - Autoantibodies absent, β cell function present
The commonest ketosis-prone diabetes (KPD) subgroup in a longitudinal study was A-ß+ (54%), followed by A-ß- (20%) A+ß- (18%) and A+ß+ (8%).  As noted above, in the A-ß+ subgroup of patients with KPD β cell antibodies are absent and β cell function is present. The triggering mechanisms leading to DKA in these patients are not well defined. Viral infections, other metabolic factors such as oxidative stress with concomitant G6PD deficiency, and genetic factors have been implicated. Patients who are in the A+ß+ and A-ß+ subgroups have clinical characteristics of type 2 diabetes. The American Diabetes Association (ADA) system classifies them as having type 2 diabetes.  Patients with this metabolic and clinical profile who experience DKA have ketosis prone type 2 diabetes.
There is also a modified ADA system and a system based on body mass index (BMI). 
The etiology of different diabetic conditions is an area of active research. Antibodies to glutamic acid decarboxylase exhibit different epitopes (antigenic determinants). The differences in antigenic specificity of these epitopes are related to the degree of beta-cell destruction and thus to the severity of the clinical syndrome. 
When antibodies are absent (A-ß+ phenotype), multiple etiologies have been proposed. These include viral infection, genetic variations, and oxidative stress. 
The long term prognosis of KPD varies with the Aß status. Patients who are ß- require long term insulin therapy for glycemic control. Most patients in the A-ß+ subgroup have-long term remission (do not continue to require insulin) after treatment of an initial DKA episode followed by a period of insulin therapy.
Patient education materials are available from various sources; an excellent resource is the American Diabetes Association.
Ketosis-prone type 2 diabetes is prevalent in the United States among blacks and Hispanics, who account for 20%-50% of newly diagnosed patients.  As with type 2 diabetes, most patients with ketosis-prone type 2 diabetes are obese and have a family history.
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