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Published on: July 30, 2011
Diabetes in the parents of children with Type I diabetes
I F Douek1, K M Gillespie, P J Bingley
1Diabetes and Metabolism, Division of Medicine, University of Bristol, Bristol, UK.
Insights
This study found that diabetes in parents of children with Type I diabetes is often autoimmune (Type I), not the non-autoimmune Type II diabetes previously assumed. This suggests no excess of Type II diabetes in these families.
Area of Science:
- Endocrinology
- Immunology
- Genetics
Background:
- Previous research indicated a higher prevalence of Type II diabetes in parents of children with Type I diabetes.
- This observation raised questions about potential shared genetic or environmental factors influencing diabetes development within families.
Purpose of the Study:
- To investigate the clinical and immunogenetic characteristics of diabetes in parents of children diagnosed with Type I diabetes.
- To critically evaluate the hypothesis suggesting an increased incidence of Type II diabetes among this parental group.
Main Methods:
- Clinical data from 3164 parents in the Bart's-Oxford study were analyzed.
- Immunogenetic analysis included islet cell antibodies, GAD, IA-2 antibodies, and HLA class II genotyping in a subset of parents.
- Diabetes classification was based on clinical presentation and autoantibody measurements.
Main Results:
- Of 184 diabetic parents, 141 (4.5%) were classified as Type I diabetes based on autoantibodies or insulin use, and 31 (0.98%) as Type II diabetes.
- Autoimmune markers (islet autoantibodies) were present in 59% of tested parents.
- A significant proportion of parents initially classified as non-insulin-dependent (Type II) showed evidence of autoimmunity.
Conclusions:
- Autoimmune diabetes (Type I) can manifest later in life and may not initially require insulin treatment in parents of children with Type I diabetes.
- The study challenges previous assumptions, indicating no excess of non-autoimmune (Type II) diabetes in families with childhood Type I diabetes.
- Misclassification of late-onset autoimmune diabetes as Type II diabetes may have occurred in earlier studies.
Aims/Hypothesis:
Previous studies have reported an excess of Type II (non-insulin-dependent) diabetes mellitus in parents of children with Type I (insulin-dependent) diabetes mellitus. We set out to characterise the clinical and immunogenetic features of diabetes in parents of affected children, and to test the hypothesis that there is no excess of Type II diabetes within this population.
Methods:
Clinical details were collected from 3164 parents of 1641 children with Type I diabetes participating in the Bart's-Oxford study of childhood diabetes. Islet cell antibodies, antibodies to GAD and IA-2, and HLA class II genotype were determined in a subset of this group. Individuals were assigned a classification of Type I diabetes on the basis of clinical features and measurement of islet autoantibodies.
Results:
Of 184 parents with diabetes, 138 (75 %) were on insulin. At least one islet autoantibody was detected in 90 (59 %) of 152 parents tested, and of 116 who were HLA-typed, 23 (20 %) had the highest risk genotype HLA-DRB1(*)03-DQA1*0501-DQB1(*)0201 / DRB1*04-DQA1(*)0301-DQB1*0302. Of 46 non-insulin-treated parents, 12 had islet autoantibodies. Of all parents, 141 (4.5 %) were therefore classified as having Type I diabetes, and 31 (0.98 %) as Type II diabetes; 12 could not be classified because of missing data or samples.
Conclusion/Interpretation:
Autoimmune diabetes can present late and without immediate need for insulin treatment in parents of children with the disease. Previous studies have categorised this as Type II diabetes. Our study suggests that there is no excess of non-autoimmune diabetes in the families of children with Type I diabetes.
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