A complete history and physical examination were obtained at the diabetes clinic. No known drug allergies were noted. Since the initiation of metformin six days earlier, Adam’s home glucose values measured >200 mg/dL throughout the day. Ketone monitoring was not ordered. The family implemented a diet eliminating concentrated sweets.

The patient’s father had recently been diagnosed with T2DM. No endocrine or autoimmune disorders were reported in other family members. A review of systems was notable for continued fatigue, polyuria, polydipsia, and polyphagia.


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On physical exam, Adam was alert, interactive, and in no apparent distress. Height was 160 cm, weight 70 kg, BMI 27.3, BP 107/56 mm Hg, and heart rate 76 beats per minute. Skin was warm and dry with no rash or stria. Mild acanthosis nigricans (AN) was noted on the posterior neck.

Laboratory studies obtained by pediatric endocrinology are listed in Table 2.

Adam’s HbA1c and glucose levels were elevated. He showed no clinical symptoms or laboratory analyses suggesting diabetic ketoacidosis (DKA). However, based on these laboratory findings and the presence of classic clinical symptoms, he clearly had diabetes. Due to an extremely elevated HbA1c, intensive insulin therapy was initiated during his initial clinic visit, pending further laboratory analysis.

Because of Adam’s age, family history, and clinical presentation, it is important to determine whether he had T1DM or T2DM. Given such physical findings as high BMI and mild AN, along with his positive family history of T2DM, the patient was started on metformin. While the presence of mild AN suggests insulin resistance and hyperinsulinemia, Adam’s C-peptide level was not elevated. The AN was more likely related to his high BMI.4

Laboratory findings did not show acidosis, which would support the possibility of T2DM. Although Adam’s C-peptide level fell within the normal range, given his degree of hyperglycemia, a normal C-peptide may actually have demonstrated insulin deficiency — a characteristic of T1DM. Two of the diabetes autoantibody studies (glutamic acid decarboxylase [GAD] and insulinoma associated [IA]-2) were positive, demonstrating pancreatic autoimmunity, which is also suggestive of T1DM.1 Finally, Adam’s insulin autoantibody was negative, but since he was insulin (exogenous)-naïve, this was not unexpected.5 Considering his history and laboratory assessment, Adam was diagnosed with T1DM.