Prevalence and characteristics of type 2 diabetes mellitus in 9-18 year-old children with diabetic ketoacidosis.
ABSTRACT To estimate the prevalence of type 2 diabetes mellitus (DM2) in 9-18 year-old children with diabetic ketoacidosis (DKA) and to describe the presenting biochemical characteristics and response to standardized DKA treatment.
Data were collected from a consecutive sample of 9-18 year-old children presenting with DKA. DKA was defined as hyperglycemia and ketosis with an initial pH <7.3, or bicarbonate <15 mmol/l. Patients were classified as having DM2 if they had negative autoantibody status and normal or elevated fasting C-peptide.
The prevalence of DM2 in patients with DKA was 13.0% (6.1-23.3%). There was no significant difference in the presenting pH (7.14 vs 7.15), but blood glucose was higher (735 vs 587 mg/dl) in patients with DM2, than in patients with type 1 DM (DM1). The duration of insulin infusion until resolution of acidosis (17.3 vs 13.2 h) and intensive care unit stay (2.4 vs 1.6 days) were longer in patients with DM2. Seven of the nine patients with DM2 did not require insulin at 1-year follow-up.
Children with DM2 can present with DKA and constitute a significant percentage in the above 9-year age group. The need for insulin must be carefully re-evaluated as DKA resolves in these patients. Adolescents with DM2 and their families need to be educated about DKA.
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- Paediatrics & child health 02/2007; 12(1):43-4. · 1.55 Impact Factor
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ABSTRACT: We previously characterized patients presenting with diabetic ketoacidosis prospectively into four subgroups of ketosis-prone diabetes mellitus (KPDM), based on the presence or absence of beta-cell autoimmunity (A+ or A-) and beta-cell functional reserve (B+ or B-). The A+B- KPDM subgroup comprises patients with classic, autoimmune type 1 diabetes, whereas the A+B+ KPDM subgroup has only partial beta-cell loss and a distinct clinical phenotype. We hypothesized that epitope specificity of autoantibodies directed against the 65-kDa isoform of glutamate decarboxylase (GAD65) reflects differences in beta-cell destruction. Sera of sequential GAD65Ab-positive KPDM patients admitted for diabetic ketoacidosis (n = 36) were analyzed for their epitope recognition using five GAD65-specific recombinant Fab and their ability to inhibit GAD65 enzymatic activity. All patients were followed longitudinally to assess beta-cell functional reserve and insulin dependence. Binding to an amino-terminal epitope defined by monoclonal antibody DPD correlated positively with fasting serum C-peptide levels at baseline (P = 0.0008) and after 1 yr (P = 0.007). Binding to the DPD-defined epitope also correlated positively with area under the curve for C-peptide after glucagon stimulation (P = 0.007) and with homeostasis model assessment percent B at 1 yr (P = 0.03). Binding to the DPD-defined epitope was significantly stronger in A+B+ than in A+B- patients (P = 0.001). Sera of 16 patients (44%) significantly inhibited GAD65 enzymatic activity, but this did not correlate with beta-cell function. DPD-defined epitope specificity is correlated directly with preserved beta-cell functional reserve in GAD65Ab-positive patients and is associated with the milder clinical phenotype of A+B+ KPDM.Journal of Clinical Endocrinology & Metabolism 03/2007; 92(2):462-7. DOI:10.1210/jc.2006-1719 · 6.31 Impact Factor