A 64-year-old man admitted for poor glycemic control and diagnosed with diabetes 20 years earlier at age 44 had been treated with glucose-lowering agents such as gliclazide and voglibose. At age 63, insulin therapy with insulin analog aspart was started due to poor glycemic control. At that time, his HbA
1c was 8.0%. Following insulin therapy, his glycemic control improved, with HbA
1c decreasing to 6.2%.
In June 2006, he reported fasting hypoglycemia and daytime hyperglycemia. We monitored glucose for 24 hours using CGM, and found an insulin antibody (NSB) of 84% with a large amount of total insulin. Scatchard analysis of the patient's insulin antibodies showed low affinity and high capacity, and it was plausible that these antibodies were the cause of his fasting hypoglycemia and daytime hyperglycemia. Analysis of insulin antibodies also showed that they could bind to both human insulin and aspart. He was diagnosed as having type 1 diabetes because his fasting serum Cpeptide was 0.65 ng/m
l and anti-GAD antibody and anti-IA-2 antibody were positive. His glycemic control improved with aspart twice a day and voglibose. CGM was thus useful tool in brittle diabetes treatment as in this case.
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