Does type 1 diabetes mellitus affect bone quality in prepubertal children?

Type 1 diabetes mellitus [T1DM] in children often starts before the achievement of peak bone mass. This may constitute a landmark in predicting bone fracture risk later in their lives. This study aims to determine the serum levels of bone markers in children with T1DM in combination with their bone mineral density [BMD]. Children diagnosed with T1DM for 3 years or more without signs of puberty were included in the diabetic group. Another group of age-matched healthy non-diabetic controls was recruited froma local school. The serum levels of a group of biochemical markers for bone formation and resorption were determined in both study groups, and BMD was measured by ultrasound absorptiometry. Thirty six children with T1DM and 39 normal children were included in this study. The results showed that 24/36 [66.7%] diabetic children had a Z score below zero. Of these, five scored below -1. In contrast, 12/39 [30.8%] children from the control group had a Z score below zero, but none had a score below -1. Significantly lower levels of osteocalcin and procollagen N-terminal peptide were detected in the diabetic group. The serum levels of bone resorption markers were significantly higher in the diabetic group. T1DM decreases BMD and some bone formation and increases some bone resorption biomarkers. BMD and bone markers are useful diagnostic tools for the early detection of alterations in the bone quality of children with T1DM. This, if treated in a timely manner, may decrease future bone fracture susceptibility

Response to oral gliclazide in a pre-pubertal child with hepatic nuclear factor-1 alpha maturity onset diabetes of the young

The term "maturity onset diabetes of the young" [MODY] describes a heterogeneous group of monogenic diabetes of which hepatic nuclear factor-1 alpha [HNF-1 alpha] MODY is the most common. Patients with HNF-1 alpha mutations typically present after puberty, and oral sulfonylureas [SU] have been shown to be effective in adults with this condition. A 7-year-old boy presented with asymptomatic hyperglycemia ranging between 6.2 and 10.1 mmol/L and glycosuria for nearly a year. The child's initial HbA [1c] was 6.9% and the pancreatic Islet cell autoantibodies were negative. His response to the oral glucose tolerance test [OGTT] showed a large increment of glucose from basal level of 7.7 to 21.1 mmol/L in 120 min. The mild presentation, family history, and negative autoantibodies were suggestive of HNF-1 alpha MODY, which was confirmed by mutation analysis. Initial management with diet alone was not sufficient, but he responded well to 20 mg oral gliclazide once a day with an improvement of HbA [1c] from 7.2% to 6.5% within 3 months of treatment. The case is an illustration of the clinical utility of molecular genetic tests in the management of childhood diabetes