The prevalence of DM2 in children is increasing in parallel with childhood obesity and is highest in children of ethnic groups with a high prevalence of DM2 in adults, including Native Americans, Hispanic Americans, and African Americans. Obesity, the metabolic syndrome, ethnicity, and a family history of DM2 are risk factors. Auto-antibodies to the pancreas are present among some clinically assumed to have DM2, compounding the difficulty in differentiating DM1 from DM2 at the time of diagnosis.
Fasting and postprandial glucose levels for diagnosis of DM2 are the same as those for DM1. The diagnosis of DM2 may be suspected on the basis of polyuria and polydipsia in a background of the metabolic syndrome. Differentiating DM2 from DM1 in children on only clinical grounds can be challenging. The possibility of DM2 should be considered in patients who are obese, have a strong family history of DM2, have other characteristics of the metabolic syndrome, or have absence of antibodies to beta cell antigens at the time of diagnosis of diabetes. Acanthosis nigricans, a dermatologic manifestation of hyperinsulinism and insulin resistance, presents as hyperkeratotic pigmentation in the nape of the neck and in flexural areas and is noted as a sign in the metabolic syndrome. Although ketoacidosis occurs far more commonly in DM1, it also can occur in patients with DM2 under conditions of physiologic stress and cannot be used as an absolute differentiating factor. DM2 can be confirmed by the evaluation of insulin orC-peptide responses to stimulation with oral carbohydrateand in the absence of islet cell autoreactivity.
DM2 is the result of a combination of insulin resistance, relative insulin deficiency, and a secretory beta cell defect. Asymptomatic patients with mildly elevated glucose values (slightly >126 mg/dL for fasting or slightly >200 mg/dL for random glucose) may be managed initially with lifestyle modifications, including nutrition therapy (dietary adjustments) and increased exercise. Exercise has been shown to decrease insulin resistance. In most children with new-onset, uncomplicated DM2, oral agents are usually the first line of therapy. Only metformin, an insulin secretagogue, is approved by the
U.S. Food and Drug Administration for use in children. A rare side effect of metformin is lactic acidosis, occurring mainly in patients with compromised renal function. The most common side effect is gastrointestinal upset. If ketonuria or ketoacidosis occurs, insulin treatment is necessary to first achieve adequate glycemic control but may be discontinued within weeks with continuation of oral medications. Insulin therapy may be required if adequate glycemic control is not achieved with lifestyle modifications and metformin.
Because DM2 may have a long preclinical course, early diagnosis is possible in subjects at risk who have the metabolic syndrome. Significant lifestyle modifications, such as improved eating habits and increased exercise, have a role in preventing or decreasing the morbidity of DM2. Finally it is critical to monitor and manage the other components of metabolic syndrome, such as advanced pubertal development, hypertension, hyperlipidemia, and polycystic ovary syndrome in females.
MODY comprises a group of dominantly inherited forms of relatively mild diabetes. Insulin resistance does not occur in these patients; instead the primary abnormality is an insufficient insulin secretory response to glycemic stimulation. Treatment depends on the type and can include the use of sulfonylureas.