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Type 1.5 diabetes (a.k.a. — latent type 1 diabetes in adults)
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My patient is a 57-year-old man who presented with a 10-year history of diabetes that had, until the last six months, been well controlled with oral therapy.
Over the last six months he had lost 25 lbs and now weighed 156 lbs. He was 68” and had a BMI of 24. He had felt generally unwell and tired but never experienced thirst or polyuria and was able to fully continue his work as a laborer. There was no family history of diabetes and he had no symptoms of complications of diabetes. For most of the past decade he had controlled his diabetes well by careful attention to diet and exercise together with metformin 1,000 mg twice a day.
As his diabetes became more difficult to control sitagliptin (Januvia, Merck) had been added but with only limited success. A careful history yielded no information that his weight loss might be related to an underlying malabsorption syndrome or malignancy.
On examination he was a thin muscular gent in no distress, pulse 68 and regular, BP 130/75 and no abnormal physical findings in any organ system. In particular there was no clinical evidence of hyperthyroidism, organomegaly or lymphadenopathy. His lab studies included fasting blood glucose of 340 and C-peptide of 0.7 (reference interval 0.9 to 7.1). ESR was 5, electrolytes, eGFR, AST/ALT and complete blood count were all normal.
Prior to getting these lab results I had made a presumptive diagnosis of type 1.5 diabetes, discontinued the sitagliptin and began therapy with glargine. In essence he now has type 1 diabetes.
This type of diabetes often presents in adults as type 2 diabetes and over time responsivity to oral therapy declines. Some patients present with diabetic ketoacidosis, which might be the result of glucose toxicity or the transition from type 1 to type 2, as in my patient (fortunately without diabetic ketoacidosis). Usually this transition occurs earlier than 10 years after the initial diagnosis of diabetes and can be confirmed by the low C-peptide, limited response of C-peptide to stimulation with glucagon, and the presence of antibodies to islet cells and/or glutamic acid decarboxylase, with glutamic acid decarboxylase antibodies being slightly more prevalent.