http://press.endocrine.org/doi/abs/10.1210/jc.2014-1759
Abstract
Context:
Insulin administration causes various types of immune responses to insulin. We previously reported 3 cases of type 1 diabetes (T1DM) triggered by insulin administration in Japanese type 2 diabetes (T2DM) patients.
Objective:
The objective of this study was to collect information and characterize insulin-triggered T1DM immunologically and genetically.
Methods:
Data for 6 patients (4 men and 2 women) with insulin-triggered T1DM aged 59.5 ± 12.8 years were collected. Serum or urinary C-peptides, islet-related autoantibodies, insulin antibody, HLA or the insulin gene VNTR genotype were analyzed. Th1- or Th2-associated responses were evaluated using an ELISPOT assay.
Results:
None of the subjects had received insulin therapy nor had an autoantibody to GAD65 before insulin administration. After insulin administration blood glucose control deteriorated acutely without any apparent cause, while C-peptide levels rapidly decreased to insulin-deficient levels. The mean duration of insulin administration to the development of T1DM was 7.7 ± 6.1 months. Islet-related autoantibodies became positive, while insulin allergy or a high titer of insulin antibody was observed in several cases. All had T1DM high-risk HLA class II (IDDM1) and the insulin gene VNTR genotype (IDDM2). GAD-reactive and insulin-peptides-reactive Th1 cells, but not Th2 cells were identified in 2 of 4 cases.
Conclusions:
The findings suggest that insulin administration may have triggered TIDM in patients with T2DM. IDDM1 and IDDM 2 as well as autoreactive T cells may contribute to the development of T1DM. Developing insulin-triggered T1DM if a patient’s blood glucose control acutely deteriorates after insulin administration should be carefully considered.