Type 1 Diabetes Mellitus (T1DM) accounts for 6% of newly diagnosed diabetic cases with Type 2 Diabetes accounting for about 91% of the cases. We discuss a case of a patient presenting with insulinopenia and negative autoimmunity with signs of insulin resistance, suggesting a mixed picture of Type 1 and Type 2 diabetes.
Patient is a 29 year old male with BMI 24.6 who was diagnosed with T1DM at an outside facility. At the age of 25, he presented with nausea & vomiting and was found to have a blood glucose level of 481 with AG 28 and 3+ urine ketones and was subsequently diagnosed with Diabetic Ketoacidosis (DKA). Hemoglobin A1c was >12% and he was started on Levemir 25 units qhs (0.4 units/kg) and Novolog 7 units with meals. Workup for autoimmune T1DM included negative antibody titers against glutamic acid decarboxylase, IA2, islet cell cytoplasmic Ab. C-peptide levels were low at 0.7, suggesting low insulin secretory capacity. His triglycerides were 396, total cholesterol 180, HDL 28, LDL 73. He denied a family history of autoimmune conditions, and his parents had type 2 diabetes, unknown if requiring insulin. Glycemic control was achieved by titrating his insulin regimen to Levemir 42 units nightly and Novolog 20 units with meals, with improvement of HbA1C to 7.6%. The patient was not taking metformin 1g twice daily that was prescribed to him at the time. A consideration to add a GLP-1RA and metformin challenge was planned, but the patient was lost to follow up due to transportation costs
Type 1 diabetes usually presents with polyuria/polydipisia with only about 1/3 presenting with DKA. Type 1a is typically diagnosed with insulinopenia and the presence of auto-antibodies like anti-GAD, IA-2 Ab, insulin Ab, islet cell cytoplasmic Ab. Patients with type 1b usually have absolute insulin deficiency with unclear causes including possible viral infections. Our patient had negative auto-antibodies with an initial DKA presentation and a normal BMI which suggested a possible type 1b diabetes picture. However, with our patient having signs of metabolic syndrome such as hypertriglyceridemia and low HDL, it made it harder to differentiate between Type 1 and Type 2 diabetes. He required high doses of basal and prandial insulin, suggesting insulin resistance, in addition to insulin deficiency.
Our case is a demonstration that mixed type 1 and 2 diabetes should be considered when patients who get the diagnosis of type 1 diabetes require high doses of insulin, suggesting insulin resistance in the setting of other likely components of metabolic syndrome. A trial combination of insulin along with insulin sensitizers can be considered in these patients.
Rutgers Robert Wood Johnson
Iselin, New Jersey
Internal Medicine Resident
Rutgers-Robert Wood Johnson Medical Center
Internal Medicine Resident