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Source: Triplitt CL, Reasner CA. Diabetes Mellitus. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. http://www.accesspharmacy.com/content.aspx?aid=7990956. Accessed July 7, 2012.

  • Juvenile-onset diabetes mellitus (DM)
  • Insulin-dependent DM

  • Disorder of carbohydrate regulation caused by markedly reduced or absent insulin production by pancreas.

  • Autoimmune disorder usually developing in childhood or early adulthood probably initiated by exposure of genetically susceptible individual to unknown environmental agent.
  • Idiopathic type 1 DM is nonimmune form often seen in minorities, especially Africans and Asians, with intermittent insulin requirements.

  • Immune-mediated destruction of pancreatic β-cells usually resulting in absolute deficiency of insulin.
  • β-cell destruction thought to occur during long preclinical period (9–13 years) associated with presence of immune markers.
  • Hyperglycemia occurs when 80–90% of β-cells are destroyed.
  • A transient remission (“honeymoon phase”) may precede established disease with associated risks for complications and death.
  • Factors initiating the autoimmune process unknown, but process mediated by macrophages and T lymphocytes with a utoantibodies to β-cell antigens (e.g., islet cell antibody, insulin antibodies).

  • Approximately 1 million Americans have disease.
  • About 15,600 young people diagnosed each year.
  • Affects 1 in every 400–600 children and adolescents.
  • Accounts for 5–10% of all cases of DM.
  • Constitutes about 5% of diabetes cases in adults.

  • Presently no means of prevention.
  • Routine screening not recommended; screening for islet autoantibody status in high-risk family members may be appropriate in context of clinical trials.

  • Parent or sibling with type 1 DM
  • Mother who had preeclampsia during pregnancy
  • Respiratory infection shortly after birth

Signs and Symptoms

  • Patients often thin and prone to develop diabetic ketoacidosis (DKA) if insulin withheld or under conditions of stress.
  • 20–40% of patients present with DKA several days of:
    • Polyuria
    • Polydipsia
    • Polyphagia
    • Weight loss

Laboratory Tests

  • Criteria for diagnosis of DM include any one of the following:
    • A1C ≥6.5%
    • Fasting plasma glucose ≥126 mg/dL (7.0 mmol/L)
    • 2-hour plasma glucose ≥200 mg/dL (111.1 mmol/L) during oral glucose tolerance test (OGTT) using 75 g anhydrous glucose in water
    • Random plasma glucose concentration ≥200 mg/dL (111.1 mmol/L) with symptoms of hyperglycemia
  • In absence of unequivocal hyperglycemia, confirm criteria 1 through 3 by repeat testing.
  • Normal fasting plasma glucose (FPG) <100 mg/dL (5.6 mmol/L).
  • Impaired fasting glucose defined as FPG of 100–125 mg/dL (5.6–6.9 mmol/L).
  • Impaired glucose tolerance diagnosed when 2-hour postload sample of OGTT is between 140–199 mg per dL (7.8–11.0 mmol/L).

Differential Diagnosis

  • Ameliorate symptoms of hyperglycemia.
  • Reduce risk of microvascular and macrovascular complications.
  • Reduce mortality.
  • Improve quality of life.
  • Achieve desirable plasma glucose and A1C levels (Table 1).

Table 1. Glycemic Goals of Therapy

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