• Disturbances of growth are the most common presenting complaints in the pediatric endocrine clinic.
  • Fetal growth is dependent on maternal factors (placental sufficiency, maternal nutrition, etc.), insulin-like growth factor-2 (IGF-2) and insulin.
  • Growth in late infancy and childhood is dependent on growth hormone/IGF-1 axis and thyroid hormone. Growth is more rapid during infancy—up to 20 cm per year. It is common to see shifts in the growth curve in the first 18 months when children are adjusting to their genetic potential growth isopleth. During childhood, growth rate is fairly constant at approximately 2 inches (approximately 5 cm) per year.
  • Pubertal growth is dependent on sex hormones as well as growth hormone/IGF-1 axis and the thyroid gland. There is a mild deceleration in growth velocity before initiation of pubertal growth spurt.
• Abnormal growth and stature: criteria
  • Child’s growth curve is crossing percentiles.
  • Child’s growth rate is <2 inches or 5 cm per year.
  • Height is >2 standard deviations (SDs) (4 inches/10 cm) below from midparental height.
• If poor weight gain and lack of nutrition is the problem without affecting height velocity, it is unlikely to be an endocrine cause and patient may warrant a gastrointestinal evaluation instead.

The serum calcium level is low (5–7 mg/dL), and the phosphorus level is elevated (7–12 mg/dL).

Blood levels of ionized calcium (usually approximately 45% of the total) more nearly reflect physiologic adequacy but also are low.

The serum level of alkaline phosphatase is normal or low, and the level of 1,25[OH]₂D₃ is usually low, but high levels have been found in some children with severe hypocalcemia.

The level of magnesium is normal but should always be checked in hypocalcemic patients.

Levels of PTH are low when measured by immunometric assay.

Administration of the synthetic 1–34 fragment of human PTH (teriparatide acetate) results in increased urinary levels of cyclic adenosine monophosphate and phosphate. This response differentiates hypoparathyroidism from pseudohypoparathyroidism. With the advent of very sensitive PTH assays, this test is usually not necessary.

Radiographs of the bones occasionally reveal an increased density limited to the metaphyses, Continue reading »

As diabetes develops, symptoms steadily increase, reflecting the decreasing ?-cell mass, worsening insulinopenia, progressive hyperglycemia, and eventual ketoacidosis. Initially, when only insulin reserve is limited, occasional hyperglycemia occurs. When the serum glucose increases above the renal threshold, intermittent polyuria or nocturia begins. With further ?-cell loss, chronic hyperglycemia causes a more persistent diuresis, often with nocturnal enuresis, and polydipsia becomes more apparent. Female patients may develop monilial vaginitis due to the chronic glycosuria. Calories are lost in the urine (glycosuria), triggering a compensatory hyperphagia. If this hyperphagia does not keep pace with the glycosuria, loss of body fat ensues, with clinical weight loss and diminished subcutaneous fat stores.

An average, healthy 10-yr-old child consumes about 50% of 2,000 daily calories as carbohydrate. As that child becomes diabetic, daily losses of water and glucose may be 5 L and 250 g, respectively, representing 1,000 calories, or 50%, of the average daily caloric intake. Despite the child’s compensatory increased intake of food, the body starves because unused calories are lost in the urine.

When extremely low insulin levels are reached, keto acids accumulate. At this point, the child Continue reading »