The patient's clinical presentation and laboratory findings are consistent with a diagnosis of T2D.
The prevalence of T2D is increasing dramatically in children and adolescents. Like adult-onset T2D, obesity, family history, and sedentary lifestyle are major predisposing risk factors for T2D in children and adolescents. Significantly, the onset of diabetes at a younger age is associated with longer disease exposure and increased risk for chronic complications. Moreover, T2D in adolescents manifests as a severe progressive phenotype that often presents with complications, poor treatment response, and rapid progression of microvascular and macrovascular complications. Studies have shown that the risk for complications is greater in youth-onset T2D than it is in type 1 diabetes (T1D) and adult-onset T2D.
T2D has a variable presentation in children and adolescents. Approximately one third of patients are diagnosed without having typical diabetes signs or symptoms. In most cases, these patients are in their mid-adolescence are obese and were screened because of one or more positive risk factors or because glycosuria was detected on a random urine test. These patients typically have one or more of the typical characteristics of metabolic syndrome, such as hypertension and dyslipidemia.
Polyuria and polydipsia are seen in approximately 67% of youth with T2D at presentation. Recent weight loss may be present, but it is usually less severe in patients with T2D compared with T1D. Additionally, frequent fungal skin infections or severe vulvovaginitis because of Candida in adolescent girls can be the presenting complaint.
Diabetic ketoacidosis is present in less than 1 in 10 adolescents diagnosed with T2D. Most of these patients belong to ethnic minority groups, report polyuria, polydipsia, fatigue, and lethargy, and require hospital admission, rehydration, and insulin replacement therapy. Patients with symptoms such as vomiting can decline rapidly and need urgent evaluation and management.
Certain adolescent patients with obesity who present with diabetic ketoacidosis and are diagnosed with T2D at presentation can also have T1D and will require lifelong insulin treatment. Therefore, following a diagnosis of diabetes in an adolescent, it is critical to differentiate T2D from type 1 diabetes, as well as from other more rare diabetes types, to ensure proper long-term management. Given the substantial overlap between T2D and T1D symptoms, a combination of history clues, clinical characteristics, and laboratory studies must be used to reliably make the distinction. Important clues in the patient's history include:
• Age. Patients with T2D typically present after the onset of puberty, at a mean age of 13.5 years. Conversely, nearly one half of patients with T1D present before 10 years of age, regardless of race or ethnicity.
• Family history. Up to 90% of patients with T2D have an affected first- or second-degree relative; the corresponding percentage for patients with T1D is less than 10%.
• Ethnicity. T2D disproportionately affects youth of ethnic and racial minorities. Compared with White individuals, youth belonging to minority groups such as Native American, African American, Hispanic, and Pacific Islander have a much higher risk of developing T2D.
• Body weight. Most adolescents with T2D have obesity (BMI ≥ 95 percentile for age and sex), whereas those with T1D are usually of normal weight and may report a recent history of weight loss.
• Clinical findings. Adolescents with T2D usually present with features of insulin resistance and metabolic syndrome, such as acanthosis nigricans, hypertension, dyslipidemia, and polycystic ovary syndrome, whereas these findings are rare in youth with T1D. One study showed that up to 90% of youth diagnosed with T2D had acanthosis nigricans, in contrast to only 12% of those diagnosed with T1D.
Additionally, when the diagnosis of T2D is being considered in children and adolescents, a panel of pancreatic autoantibodies should be tested to exclude the possibility of autoimmune T1D. Because T2D is not immunologically mediated, the identification of one or more pancreatic (islet) cell antibodies in a diabetic adolescent with obesity supports the diagnosis of autoimmune diabetes. Antibodies that are usually measured include islet cell antibodies (against cytoplasmic proteins in the beta cell), anti-glutamic acid decarboxylase, and tyrosine phosphatase insulinoma-associated antigen 2, as well as anti-insulin antibodies if insulin replacement therapy has not been used for more than 2 weeks. In addition, a beta cell–specific autoantibody to zinc transporter 8 is frequently detected in children with T1D and can aid in the differential diagnosis. However, up to one third of children with T2D can have at least one detectable beta-cell autoantibody; therefore, total absence of diabetes autoimmune markers is not required for the diagnosis of T2D in children and adolescents.
When a diagnosis of T2D has been established, treatment should consist of lifestyle management, diabetes self-management education, and pharmacologic therapy. According to the 2022 American Diabetes Association Standards of Medical Care, the management of diabetes in children and adolescents cannot simply be drawn from the typical care provided to adults with diabetes. The epidemiology, pathophysiology, developmental considerations, and response to therapy in pediatric populations often vary from adult diabetes, and differences exist in recommended care for children and adolescents with T1D, T2D, and other forms of pediatric diabetes.
Because the diabetes type is often uncertain in the first few weeks of treatment, initial therapy should address the hyperglycemia and associated metabolic derangements regardless of the ultimate diabetes type; therapy should then be adjusted once metabolic compensation has been established and subsequent information, such as islet autoantibody results, becomes available.
Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia
Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships