OBJECTIVE -Children with type 1 diabetes are usually asked to perform self-monitoring of blood glucose (SMBG) before meals and at bedtime, and it is assumed that if results are in target range, along with HbA 1c measurements, then overall glycemic control is adequate. However, the brief glimpses in the 24-h glucose profile provided by SMBG may miss marked glycemic excursions. The MiniMed Continuous Glucose Monitoring System (CGMS) has provided a new method to obtain continuous glucose profiles and opportunities to examine limitations of conventional monitoring.RESEARCH DESIGN AND METHODS -A total of 56 children with type 1 diabetes (age 2-18 years) wore the CGMS for 3 days. Patients entered four fingerstick blood samples into the monitor for calibration and kept records of food intake, exercise, and hypoglycemic symptoms. Data were downloaded, and glycemic patterns were identified.RESULTS -Despite satisfactory HbA 1c levels (7.7 Ϯ 1.4%) and premeal glucose levels near the target range, the CGMS revealed profound postprandial hyperglycemia. Almost 90% of the peak postprandial glucose levels after every meal were Ͼ180 mg/dl (above target), and almost 50% were Ͼ300 mg/dl. Additionally, the CGMS revealed frequent and prolonged asymptomatic hypoglycemia (glucose Ͻ60 mg/dl) in almost 70% of the children.CONCLUSIONS -Despite excellent HbA 1c levels and target preprandial glucose levels, children often experience nocturnal hypoglycemia and postprandial hyperglycemia that are not evident with routine monitoring. Repeated use of the CGMS may provide a means to optimize basal and bolus insulin replacement in patients with type 1 diabetes.

The incidence of nutritional rickets appears to be increasing in North American infants and toddlers; it is widely assumed that this is due to vitamin D deficiency. Thus, records of 43 children with nutritional rickets from greater New Haven, Connecticut, from 1986-2002 were identified. The mean age of presentation was 20 months; 86% were of African-American, Hispanic, or Middle Eastern descent. More than 93% of children had been breastfed; however, 15% had received vitamin D supplementation. Eighty-six percent of those with food histories available were weaned to diets with minimal dairy content after nursing. Serum 25-hydroxyvitamin D was 20.9 +/- 11.5 ng/ml and was less than 15 ng/ml in only 22% of patients. Three representative case histories suggest that dietary calcium intake may play a contributory role in the development of disease; 1 case documents radiographic and biochemical resolution of rachitic abnormalities after calcium treatment, but no vitamin D therapy. Clinicians should be aware that low dietary calcium intake after weaning may result in the development of nutritional rickets, and that attention to calcium intake as well as that of vitamin D is important in the establishment of optimal dietary practices for North American infants and children.

Oral Mg oxide capsules are safe and well tolerated. A positive effect of Mg supplementation on integrated hip BMC was evident in this small cohort.

Use of the Medtronic MiniMed Continuous Glucose Monitoring System (CGMS) in non-diabetic children has revealed many low and high sensor glucose (SG) values, suggesting that the original analytical algorithm (Solutions 2.0) might be overreading glycemic excursions. A revised algorithm (Solutions 3.0) was introduced in 2001. Our aim was to compare analyses of the same sensor profiles using both programs. Twenty-five lean, non-diabetic subjects (mean age 14 +/- 4 years) underwent continuous glucose monitoring with CGMS for up to 72 h. Sensor tracings were analyzed with both algorithms and compared. Separate analyses were performed for nocturnal readings (12-6 a.m.). Mean SG values were similar (103 +/- 24 mg/dL for version 2.0 vs. 100 +/- 14 for version 3.0), but the distribution was significantly different: 13.8% of total SG were <70 mg/dL by version 2.0 versus 8.2% by version 3.0 (p < 0.001), and 7.7% of total SG were >150 mg/dL by version 2.0 versus 4.7% by version 3.0 (p = 0.02). Of nocturnal SG values, 25.8% were <70 mg/dL by version 2.0 compared with 17.9% by version 3.0, and 9.4% were >150 mg/dL by version 2.0 compared with 4.0% by version 3.0. In lean non-diabetic children, Solutions 2.0 identified significantly more hypoglycemia and hyperglycemia than Solutions 3.0. Similar analyses in 40 children with type 1 diabetes revealed no significant differences. Solutions 3.0 may be a more useful algorithm for preventing over-reading of low and high SG readings in non-diabetic children, whereas both algorithms give similar results in children with diabetes.

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