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Type 2 Diabetes Mellitus in Children: A New Challenge for Diagnosis and Prevention

Type 2 Diabetes Mellitus in Children: A New Challenge for Diagnosis and Prevention

Type 2 diabetes mellitus is becoming an increasing problem among children and adolescents.1,2 Type 1 diabetes mellitus is caused by deficiency of insulin secretion from pancreatic beta-cell damage. Type 1A is characterized by autoimmune destruction of pancreatic beta cells; type 1B refers to insulin-dependent diabetes not of immune cause. Type 2 diabetes occurs most often in adults and is associated with insulin resistance and a relative insufficiency of insulin.

In the past, 2% to 3% children with diabetes were thought to have type 2 disease.3 However, an increasing number of cases are being seen in pediatric clinics and in the general population. This increase in frequency is linked to the increase in childhood obesity. A study in 2000 from Ohio showed that 33% of African American and Caucasian children aged 10 to 19 years with diabetes had type 2 disease.4 It has been estimated that 4.1 per 1000 American children aged 12 to 19 years have diabetes and that 30% of these children have type 2 diabetes.5

Type 2 diabetes in children is associated with obesity, family history of type 2 diabetes, female sex, and ethnic background.4 In Canada, various aboriginal communities have been studied. One study found a high prevalence of childhood obesity that resulted in an increased risk of diabetes or impaired fasting glucose.6 Among the risk factors described, childhood obesity is the only one that can be altered and therefore should be the target for prevention strategies.

The early onset of type 2 diabetes is a serious health concern for children, since a significant portion of their life will be spent controlling this disease. Complications of diabetes are common; poor glycemic control of long duration can lead to significant morbidity, including macrovascular (peripheral vascular disease, coronary artery disease, and stroke) and microvascular (retinopathy, neuropathy, and nephropathy) complications.7 Obesity in itself can also lead to macrovascular complications and hypertension.

The new challenge to physicians is to prevent these problems from occurring through aggressive management of childhood obesity. Here we provide guidelines on detecting type 2 diabetes and on close monitoring of children with the disease.

Diagnosis of Type 2 Diabetes in Children

Detection of type 2 diabetes and close monitoring of children at risk is key to preventing complications.8 The Canadian Diabetes Association has defined a fasting plasma glucose level of 7 mmol/L or more as diabetes, 6.1 to 6.9 mmol/L as impaired fasting glucose, and between 4 and 6 mmol/L as normal. These are the same criteria currently in use for the adult population.9

It has been recommended that the fasting (no food for at least 8 hours) plasma glucose be used for the initial screening test. The test is fast, easy to perform, inexpensive, and more convenient than the oral glucose tolerance test.

 

75-g oral glucose tolerance test may be necessary when clinical suspicion is high but the fasting plasma glucose level is normal. With the oral glucose tolerance test, a 2-hour blood glucose value of 11.1 mmol/L or higher is considered a positive result for diabetes, 7.8 to 11 mmol/L is impaired glucose tolerance, and less than 7.8 mmol/L is normal. In the absence of significant symptoms and unequivocal metabolic decompensation, a confirmatory laboratory glucose test (either a fasting plasma glucose, casual plasma glucose or oral glucose tolerance test) must be done on a separate day.9

 

Children, like adults, may be asymptomatic for a long period before presenting with signs or symptoms of hyperglycemia in type 2 diabetes. Although diabetic ketoacidosis is commonly seen in type 1 diabetes, children with type 2 diabetes may present with diabetic ketoacidosis.10

Children should be screened for type 2 diabetes if they have a family history of type 2 diabetes, are from a high-risk ethnic group, are obese, or have polycystic ovary syndrome. Important historical and physical examination findings and laboratory investigations are shown in Tables 1, 2, and 3.

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