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(see Endocrinology Notes)

  1. Type I Diabetes insulin dependent, most common type in childhood
  2. prevalence: 1 in 500 children under 18 years of age
  3. etiology: genetic predisposition and environmental trigger leading to autoimmune destruction of the pancreas

Classic presentation:

  1. polyuria
  2. polydipsia
  3. polyphagia
  4. weight loss
  5. 25% present in diabetic ketoacidosis



  1. insulin, blood glucose monitoring
  2. young children more susceptible to CNS damage with hypoglycemia with fewer benefits from tight control, hence target glucose range higher at 6-12 mmol/L
  3. increasingly tighter control in older children, 4-8 mmol/L
  4. diet, exercise
  5. education, psychosocial support




  1. cause: missed/delayed meals, excess insulin, increased exercise
  2. complications: coma, seizures


  1. cause: infection, stress, diet-to-insulin mismatch
  2. complications: risk of diabetic ketoacidosis, long-term complications

diabetic ketoacidosis

  1. cause: new-onset diabetes, missed insulin doses, infection
  2. complications: dehydration, cerebral edema, decrease level of consciousness

long-term complications usually not seen in childhood

  1. present 10-20 years after onset, related to metabolic control(HbA1c)
  2. retinopathy, nephropathy, neuropathy



( see also Endocrinology Notes )

Congenital Hypothyroidism


  1. incidence: 1 in 4000 births
  2. usually caused by dysgenetic (agenesis or ectopic) malformation of the thyroid gland
  3. diagnosis through routine neonatal screening ( Guthrie test )


Usually asymptomatic in neonatal period but may have:

  1. prolonged jaundice
  2. constipation
  3. sluggish, coarse cry, lethargy, poor feeding
  4. big tongue, coarse facial features, large fontenelle, umbilical hernia



  1. excellent if treatment started within 1-2 months of birth
  2. if treatment started after 3-6 months of age may result in developmental delay

Management: thyroxine replacement

Acquired Hypothyroidism


  1. most common: Hashimoto's thyroiditis (autoimmune destruction of the thyroid)

Signs and symptoms similar to hypothyroidism in adults, but also:

  1. delayed bone age, decline in growth velocity, short stature
  2. precocious puberty
  3. does not cause permanent developmental delay



(see Endocrinology Notes)

Congenital Hyperthyroidism


  1. results from transplacental passage of maternal thyroid stimulating antibodies (mother with Grave’s)
  2. clinical manifestations in the neonate may be masked by transplacental maternal antithyroid medication craniosynostosis
  3. presents with tachycardia with CHF, irritability, craniosynostosis (condition in which one or more of the fibrous sutures in an infant skull prematurely fuses) , poorfeeding, FTT  
  4. spontaneous resolution by 2-3 months of life as antibodies cleared
  5. Management: propylthiouracil until antibodies cleared

Grave’s Disease


  1. F:M = 5:1, peak incidence in adolescence
  2. results from thyroid stimulating antibodies as with adult Grave’s
  3. may exhibit classic signs and symptoms of hyperthyroidism, but also:
    • personality changes
    • school difficulty
    • mood instability 
  4. management similar to adults: anti-thyroid drugs(propylthiouracil),radioiodine reserved for older teens, surgical thyroidectomy

Clinical Pearl


  1. Children with a solitary thyroid nodule require prompt evaluation as 30-40% have carcinoma.
  2. Rest have adenoma, abscess, cyst or multinodular goiter
Pediatrics : ENDOCRINOLOGY Pediatrics : ENDOCRINOLOGY Reviewed by Radiology Madeeasy on September 06, 2010 Rating: 5
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