Case Study: Inadequate Glycemic Control for 5 Years

Case Study: Misdiagnosed With Type 2 Diabetes
Case Study: Misdiagnosed With Type 2 Diabetes

Ms. W, 50 years old, was seen for ongoing care of type 2 diabetes, diagnosed five years earlier. In addition to being evaluated by a nutritionist, she had attended diabetes-education classes and was adhering to dietary guidelines. She exercised 30-45 minutes three or more times a week. In spite of receiving maximal doses of metformin and a sulfonylurea, she remained hyperglycemic. Her hemoglobin A1c level (9.2%) revealed inadequate control.


Ms. W weighed 166 lb and was 68 in tall, for a BMI of 25.2. Her waist was 34 in, BP 120/80 mm Hg, LDL 160 mg/dL, triglycerides 148 mg/dL, and HDL 48 mg/dL. Physical examination revealed no acanthosis or skin tags. However, she was already manifesting background retinopathy with microaneurysms and reduced deep tendon reflexes of the lower extremities. When the patient expressed concern over poor glycemic control to her previous provider, she was told that she had type 2 diabetes (obvious by her lack of ketoacidosis) and would not need insulin.

Diagnostic Workup

Laboratory studies revealed C peptide 1 ng/mL (normal fasting range 0.78-1.89) and glutamic acid decarboxylase antibodies (GADab).

Normal C-peptide levels indicate some degree of beta-cell function, i.e., insulin is still being released by the pancreas, which would be unexpected in type 1 diabetes. In type 2 diabetes, C-peptide levels are usually well above normal. A positive GADab is a well-recognized sensitive and specific marker of autoimmune beta-cell destruction and predictive of declining beta-cell function and eventual failure.

The absence of obesity and/or metabolic syndrome, lack of acanthosis or skin tags, relatively normal triglyceride and HDL levels, early presence of microvascular complications, and inability to achieve optimal glycemic control despite maximal doses of hypoglycemic agents led to a reconsideration of the diagnosis. In all probability, this patient had latent autoimmune diabetes of adulthood (LADA).

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