Suboptimal Glycaemic control in Type 1 diabetes explained by insulin antibodies — ASN Events

Suboptimal Glycaemic control in Type 1 diabetes explained by insulin antibodies (#362)

Amanthi Shamani Mendis 1
  1. Concord Repatriation General Hospital, Croydon, NSW, Australia

Insulin auto antibodies (IA2) in association with other antibodies (GAD, Islet cell) have been reported extensively in literature as markers to predict future type 1a diabetes, in genetically predisposed individuals. However, antibodies to insulin after insulin therapy can lead to extreme insulin resistance and frequent hyperglycemia. Insulin antibodies (IA) to humanised insulin analogues are less common when compared to porcine insulin, but can be clinically relevant in patients with difficult to control hyperglycaemia especially in type 1 diabetes.

We report a case of a 57 year old gentleman with difficult to control type 1 diabetes mellitus and positive insulin antibodies.

He was initially diagnosed at the age of 21 when he presented with significant weight loss and typical hyperglycaemia related symptoms without ketoacidosis. He required significantly large doses of insulin consisting of Lantus 44 units nocte and Actrapid 20 units three times daily pre-meal. This was complicated by occasional hypoglycaemic episodes which most recently had resulted in a hospital admission and more frequent post prandial hyperglycaemia. His only diabetic complication was that of diabetic retinopathy for which he had not received laser therapy. There was a 10 year history of erectile dysfunction. His past medical history was significant for a diagnosis of Hashimoto’s thyroiditis for which he had undergone a thyroidectomy and was now on thyroxine 300 mcg 6 days of the week. In regards to family history, his son also had a diagnosis of type 1 diabetes mellitus.

On examination he had an obese BMI of 35 kg/m2 with a weight of 111.5 kg and waist circumference of 115cm. On examination of his feet he had palpable peripheral pulses, normal monofilament testing and no ulcerations. There was no lipodystrophy. Pathology revealed positive GAD antibodies, normal inulin autoantibodies (IA2) and undetectable C-peptide. On further investigation he had positive insulin antibodies (IA) which were 50 times the upper limit of the normal range.

In summary, we present a case of an obese 57 year old gentleman with poorly controlled type 1a diabetes mellitus, complicated by autoimmune insulin resistance.

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