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BACKGROUND

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Insulin is produced by beta cells in the islets of Langerhans in the pancreas. Insulin secretion is regulated by glucose influx into the beta cell, which is dependent on the serum glucose level. Insulin acts on target tissues including liver, fat, and muscle to stimulate glucose uptake and inhibit gluconeogenesis, glycogenolysis, lipolysis, and ketogenesis.

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The prevalence of diabetes mellitus in the United States in youth less than 20 years of age is 0.182%.1 Type 1 diabetes accounts for 85% of these cases, while type 2 diabetes accounts for 12%, and maturity-onset diabetes of the young (MODY) accounts for 1% to 2%. The incidences of type 1 diabetes and type 2 diabetes in children are both increasing, although the United States has seen a particularly striking increase of type 2 diabetes in children and young adults in the past several years.

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PATHOPHYSIOLOGY

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Hyperglycemia results from abnormal insulin production, abnormal insulin action, or both. In type 1 diabetes, autoimmune destruction of beta cells results in an absolute insulin deficiency. Approximately 90% of patients with type 1 diabetes have measurable serum antibodies against islet cells, glutamic acid decarboxylase (GAD), or insulin.2 However, although autoimmunity is an essential component of the pathogenesis of type 1 diabetes, it alone is not sufficient; environmental factors including diet, prenatal influences, infectious exposures, stress, and genetic factors contribute to development of this disease.

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Type 2 diabetes is characterized by insulin resistance, often due to obesity, with resulting beta cell dysfunction and glucotoxicity that results in a relative insulin deficiency despite hyperinsulinemia. Although the etiology of type 2 diabetes is multifactorial, there is a stronger genetic component than for type 1 diabetes.2

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CLINICAL PRESENTATION

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Patients with hyperglycemia often have a history of polyuria, polydipsia, polyphagia, weight loss, and/or fatigue. Depending on the duration of illness and the underlying pathophysiology, the patient may or may not have ketosis or acidosis as a consequence of absolute or relative insulin deficiency. Although more common in type 1 diabetes, ketosis and acidosis can also occur in type 2 diabetes.

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Children with newly diagnosed diabetes may present to the hospital in advanced stages of metabolic decompensation because the symptoms of hyperglycemia were not recognized. Treatment of diabetic ketoacidosis (DKA) in childhood requires strict attention to fluid balance and neurologic status because of the increased risk of cerebral edema in the pediatric population. Early detection of diabetes can reduce these risks.

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DIFFERENTIAL DIAGNOSIS

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The cause of hyperglycemia is not always apparent at initial presentation. The differential diagnosis includes type 1 diabetes, type 2 diabetes, MODY, “stress hyperglycemia” from illness or trauma, pancreatitis, other pancreatic dysfunction (e.g. cystic fibrosis), and drug effect (glucocorticoids, antipsychotics, etc.). Less commonly, hyperglycemia may be seen in the setting of other endocrine disorders such as excess endogenous glucocorticoid, growth hormone, ...

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