Prediabetic markers in children with stress hyperglycemia
D. M. Bhisitkul, A. I. Vinik, A. L. Morrow, J. X. She, J. Shults, A. C. Powers and N. K. Maclaren
Division of Pediatric Emergency Medicine, Children's Hospital of the King's Daughters, Norfolk, VA 23507, USA.
BACKGROUND: Previous studies have shown that children with stress
hyperglycemia have an increased risk for development of type I or
insulin-dependent diabetes mellitus. OBJECTIVE: To determine whether stress
hyperglycemia in prospectively screened pediatric patients represents a
prediabetic state. DESIGN: Prospective, cohort analytic study. SETTING: The
Children's Hospital of the King's Daughters is an urban pediatric emergency
department at a tertiary care, university-based children's hospital in
Norfolk, Va. PATIENT POPULATION: All patients who required a venipuncture
for evaluation of an acute illness or injury from October 1992 through
March 1993 were screened prospectively for hyperglycemia (blood glucose
level > or = 8.3 mmol/L [> or = 150 mg/dL]). Each hyperglycemic
patient was age matched to a stress control subject (defined as a
nonhyperglycemic but acutely ill child) from the emergency department and a
healthy control subject from a well-child clinic. INTERVENTION: Blood
samples were obtained at the time of initial evaluation in the emergency
department from 30 hyperglycemic patients (age range, 4 weeks to 12.4
years; median, 2 years), 30 stress control subjects, and 30 healthy control
subjects. All samples were tested for islet cell antibodies, insulin
autoantibodies, glutamic acid decarboxylase (GAD) antibodies, and HLA
typing, specifically the genotypes at the DQB1 gene. MAIN OUTCOME MEASURES:
The presence of immunologic or genetic markers for insulin-dependent
diabetes mellitus and/or the clinical development of insulin-dependent
diabetes mellitus. RESULTS: No patients or control subjects were positive
for islet cell antibodies. One hyperglycemic patient and 3 stress control
subjects were positive for insulin autoantibodies; all 4 of these subjects
had sickle-cell disease and fever. Four of the 8 patients with sickle-cell
disease had insulin autoantibodies, compared with none of the 52 patients
and stress control subjects without sickle-cell disease (P < .001). One
healthy control subject had antibodies to GAD65. The patient group did not
show increased genotypes at the DQB1 gene that were indicative of an
enhanced risk for insulin-dependent diabetes mellitus. Of the 32
hyperglycemic patients, 27 healthy control subjects, and 25 stress control
subjects contacted for follow-up at 31 to 36 months, none has developed
insulin-dependent diabetes mellitus. CONCLUSIONS: Children with stress
hyperglycemia do not have an increased prevalence of immunologic or genetic
markers of insulin-dependent diabetes mellitus and thus do not appear to be
at an increased risk for development of insulin-dependent diabetes
mellitus. Our data suggest that insulin autoantibodies develop in children
subject to sickle cell crises.
