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Title: Types of pediatric diabetes mellitus defined by anti-islet autoimmunity and random C-peptide at diagnosis

Author
item REDONDO, MARIA - Texas Children'S Hospital
item RODRIGUEZ, LUISA - Children'S Nutrition Research Center (CNRC)
item ESCALANTE, MIRNA - Texas Children'S Hospital
item SMITH, E - Children'S Nutrition Research Center (CNRC)
item BALASUBRAMANYAM, ASHOK - Baylor College Of Medicine
item HAYMOND, MOREY - Children'S Nutrition Research Center (CNRC)

Submitted to: Pediatric Diabetes
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/4/2013
Publication Date: 8/1/2013
Citation: Redondo, M.J., Rodriguez, L.M., Escalante, M., Smith, E.O., Balasubramanyam, A., Haymond, M.W. 2013. Types of pediatric diabetes mellitus defined by anti-islet autoimmunity and random C-peptide at diagnosis. Pediatric Diabetes. 14(5):333-340.

Interpretive Summary: Type 1 diabetes mellitus is the result of the immune destruction of the insulin making cells of the pancreas. Why this occurs is not known. A study was done in children with newly diagnosed type 1 diabetes to examine the different type of antibodies thought to be responsible for this destruction. The children with evidence of continued insulin secretion had better glucose control at 2 years than those with little or no evidence of insulin secretion. This was true regardless of the presence or absence of auto antibodies which are frequently used to distinguish between type 1 and type 2 diabetes mellitus. We concluded that using the presence of anti-islet cell autoantibodies and a random blood measure of insulin secretion at diagnosis defines four distinct type (phenotypes) of pediatric diabetes which has prognostic value in their management. Such findings are important for the pediatric community in better managing the treatment approaches of children with diabetes.

Technical Abstract: The objective of this study was to test the hypothesis that anti-islet autoantibody expression and random serum C-peptide obtained at diagnosis define phenotypes of pediatric diabetes with distinct clinical features. We analyzed 607 children aged <19 yr consecutively diagnosed with diabetes after exclusion of 13% of cases with secondary diabetes (e.g., cystic fibrosis related, steroid induced) and 7.3% of cases lacking measurement of C-peptide and/or autoantibodies. Autoantibody positivity (A+) was defined as >=1 positive out of GAD65, insulin, and ICA512 antibodies. Preserved beta-cell function (beta+) was defined as random serum C-peptide at diagnosis greater than or equal to 0.6 ng/mL. Body mass index (BMI) was measured at median 1.2 months after diagnosis. Characteristics at diagnosis and 2 yr (range 18–30 months) after diagnosis were compared among groups. Autoantibody expression and C-peptide at diagnosis defined the following groups: A+beta- (52.1% of the children), A+beta+ (32.8%), A-beta+ (12.5%), and A-beta- (2.6%). These four groups differed in gender, race/ethnicity, and clinical characteristics at diagnosis [i.e., age, pubertal development, obesity/overweight, diabetic ketoacidosis, glycemia, and hemoglobin A1c (HbA1c)] and at 2 yr (i.e., clinical diagnosis, treatment, and (HbA1c) (all p<0.0001). Among all beta+ children, C-peptide >2 ng/mL was associated with lower HbA1c at onset (p=0.0001) and, in the A+beta+ subgroup, with higher frequency of achieving HbA1c<7% at 2 yr (p=0.03). All three patients (0.7% of total) with monogenic diabetes (maturity onset diabetes of the young, MODY) were A-beta+ with C-peptide between 0.6 and 2 ng/mL. Anti-islet autoantibodies status and serum random C-peptide at diagnosis define four distinct phenotypes of pediatric diabetes with prognostic value.