Q: How can I tell the difference between type 1 and type 2 diabetes in children?
A: At first glance, it would appear to be relatively easy to distinguish type 1 diabetes (T1D) from type 2 diabetes (T2D).
T1D, caused by autoimmune destruction of the pancreatic beta cells, typically presents with a relatively brief prodrome of increased thirst and urination. Weight loss is common, and up to one third of children with T1D present with ketoacidosis. T1D is more common in Caucasians of northern European background; the peak age at presentation is early adolescence, with a lesser peak in the group younger than 5 years.
T2D, which has been increasing steadily in the pediatric population during the past 10 years, is more prevalent in African American, Latino, and American Indian youth. T2D typically has a more insidious onset and is frequently diagnosed during routine screening. Weight loss is less common; indeed, obesity plays a significant role in the development of T2D in children. Insulin resistance from obesity (and perhaps underlying genetic factors) requires compensatory increases in insulin secretion to maintain normal glucose tolerance. Once the demand for insulin exceeds the capacity of the beta cell, overt diabetes occurs.1
Table – Differentiating type 1 from type 2 diabetes
| Type 1 diabetes | Type 2 diabetes | |||||||||||||||||||||||||
| Onset | Acute, symptomatic | Insidious, often asymptomatic | ||||||||||||||||||||||||
| Clinical Presentation | Polyuria, polydipsia, weight loss | Obesity, acanthosis nigricans, polycystic ovary syndrome | ||||||||||||||||||||||||
| Ketosis | Almost always present | Usually absent | ||||||||||||||||||||||||
| Race/ethnicity | Caucasian | African Amercian, Latino, American Indian | ||||||||||||||||||||||||
| Family history | Often absent | Usually present | ||||||||||||||||||||||||
| Antibodies | ICA-,GAD-, ICA512-positive | ICA-,GAD-, ICA512-negative | ||||||||||||||||||||||||
| Therapy | Insulin | Oral hypoglycemic agents |
Despite their markedly disparate etiologies and seemingly different clinical presentations, however, it can be difficult to differentiate T1D from T2D in some children. For example:
•With the increasing prevalence of obesity among young people, more children with T1D are obese at presentation. It is also thought that the increased demands placed on the beta cell may accelerate the autoimmune destructive process in children with a genetic predisposition to T1D.2
•While ketoacidosis and pancreatic autoantibodies are classic indicators of T1D, it is now evident that some African American youth with T2D may present with diabetic ketoacidosis.3 Also, markers of autoimmunity may not be as reliable in some non-white populations with T1D.4
•It now appears that there may be some overlap in the diagnosis. In so-called double diabetes, children with clinical characteristics of T2D have autoimmune markers characteristic of T1D.5
•Monogenic forms of diabetes (maturity-onset diabetes of youth [MODY]), which typically occur in lean, Caucasian teens or young adults with a family history of diabetes, may easily be misdiagnosed as either T1D or T2D.6
So, what is the clinician to do? It is still reasonable to consider the typical clinical characteristics at presentation (Table), supplemented by appropriate laboratory testing at diagnosis in specific situations (eg, measurement of pancreatic autoantibodies to differentiate T1D from T2D in an African American adolescent, or molecular diagnostics to confirm MODY in a non-obese teenager with mild T2D).
With the availability of more therapeutic options for youth with diabetes--such as insulin sensitizers for T2D and sulfonylureas for MODY—the issue of classification of diabetes has never been more important.