2007 Volume 50 Issue 2 Pages 145-152
An 84-year-old man with type 2 diabetes treated with human insulin from April 2000 to January 2003 experienced a progressive daily insulin dose increase up to 80 U/day during this period and 125I-insulin binding was 96%. His regimen was converted from human insulin to almost the same dose of insulin aspart. In July 2004, his blood glucose rose abruptly (FBG>300 mg/dl) and could not be controlled even with more than 90 units of insulin aspart. We then treated him with insulin lispro, after which his blood glucose rapidly decreased and was well controlled with 12 U of insulin lispro 3 times daily before each meal. We found that insulin antibodies specific to insulin aspart were 15.1% and cross-reacting to human insulin/insulin aspart were 47.2%.
Scatchard analysis of insulin antibodies showed a low-affinity constant and an extremely high binding capacity of high-affinity sites. Insulin antibody binding resembled that in insulin autoimmune syndrome. We concluded that he developed severe immunological insulin resistance caused mainly by antibodies cross-reacting to human insulin/insulin aspart. Insulin lispro seemed less reactive to his antibodies and was effective for his glycemic control.
