Patients with type 1 diabetes (T1D) require exogenous insulin for survival and should be identified as soon as possible to avoid high morbidity due to a delay in insulin treatment.
T1D should be suspected in pediatric patients with hyperglycemia, particularly if they are younger than 10 years; the majority of these patients have T1D, regardless of race or ethnicity. Among adolescents and young adults, the ratio of T1D to T2D shifts. In the 2014 Centers for Disease Control and Prevention (CDC) Diabetes Statistics report, the proportions of youth 10-19 years of age with newly diagnosed T1D were: Native Americans, 18%; Asians, 39%; non-Hispanic blacks, 40%; Hispanics, 52%; and non-Hispanic whites, 85% (1).
Body mass index was once thought to be suggestive diabetes type, but as obesity rates have risen, patients’ physical characteristics are no longer reliable diagnostic indicators. Among 6222 adult participants in the T1D Exchange, a clinic registry of patients with T1D, 23% were obese (body mass index [BMI] ≥30 kg/m2), and another 35% were overweight. Of 8394 children and adolescents, 14% were obese and 23% were overweight (2).
Table 1 offers recommendations for the differential diagnosis of T1D and T2D (3,4). T1D is usually characterized by absolute insulin deficiency and should be confirmed by the presence of autoantibodies to glutamic acid decarboxylase, pancreatic islet β cells (tyrosine phosphatase IA-2), zinc transporter (ZnT8), and/or insulin. Documenting the levels of insulin and C-peptide and the presence or absence of immune markers in addition to the clinical presentation may help establish the correct diagnosis to distinguish between T1D and T2D in children or adults (3).
Table 1. Clinical and Laboratory Characteristics Used to Distinguish Type 1 and Type 2 Diabetes
|
Type 1 Diabetes |
Type 2 Diabetes |
Usual clinical course |
Insulin-dependent |
Initially noninsulin dependent |
Usual age of onset |
~50% of patients younger than 20 years at diagnosis |
>40 years but incidence in younger patients is rising due to rising obesity rates |
Body weight |
Often lean but ~50% overweight or obese |
Usually obese |
Onset |
Often acute |
Subtle, slow |
Ketosis prone |
Yes |
No |
Family history |
Less common; ≤15% have first-degree relative with diabetes |
Common |
Frequency of HLA-DR3, DR4, DQB1*0201, DQB1*0302 |
Increased |
Not increased |
Islet autoantibodies (GADA, ICA, IA-2A, IAA) |
Present |
Absent |
Abbreviations: GADA = glutamic acid decarboxylase; HLA = human leukocyte antigen; IAA = autoantibodies to insulin; IA-2A = tyrosine phosphatase insulinoma antigen; ICA = islet cell antibodies; ZnT8A = zinc transporter 8.
At least 1 type of antibody is present in 85% to 95% of newly diagnosed T1D patients, but the proportion and type vary depending on patient's age, the number and quality of the assays used, and ethnicity (4).
Type 1b (idiopathic) diabetes (T1bD) is characterized by permanent insulinopenia and a propensity for ketoacidosis without evidence of autoimmunity. Only a small proportion of type 1 patients fall into this category; of those who do, most are of African or Asian ancestry (3,4).
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