Endocrinology of Growth

Growth hormonal does have a major effect on post-birth growth but has much less of an effect in pre--birth growth. Babies born without growth hormone are of normal or close to normal length.

The release of growth hormone (GH) is stimulated by the hypothalamic hormone growth hormone releasing hormone (GHRH). GH has some direct effects such as creation of insulin resistance, but most of its action is mediated via the liver's production of Insulin Like Growth Factor-1 (IGF-1). Growth hormone levels are usually low all day and rise at certain times, which is absent in growth hormone deficient patients. Thus, random GH levels are not useful unless the levels are high such as in states of growth hormone resistance or acromegaly. Circulating growth hormone levels are bound to growth hormone binding proteins. In classic growth hormone resistance (Laron dwarfism) the serum GHBP values are low and the GH levels are high. In other GH deficiencies the function of the GH receptor is defective.

In GH deficiency the bone age development is delayed but the upper-to-lower segment ratio is normal for bone age. This is different to hypothyroidism in which bone age is severely delayed but the upper-to-lower segment ratio is increased since the limbs did not grow.

IGF's were previously called somatomedins. They are produced in tissue throughout the body. IGF-1 is most closely associated with growth of cells in the body. Plasma values of IGF-1 are low in growth hormone deficiency. Normally IGF-1 levels are low in infants and increase slowly through childhood until a peak is reached in puberty. IGF-1 levels are not closely related to growth rate. Measuring IGF-1 levels used in the diagnosis of growth hormone deficiency should be done with great caution since they can vary widely.

Thyroid hormone is essential for post-birth growth but has little effect on fetal length growth. Congenital hypothyroidism is associated with normal or slightly greater than normal birth length. Thyroid hormone is essential for normal secretion of growth hormone as hypothyroid patients may not respond to GH-stimulation tests, thereby confusing the diagnosis of hypothyroidism with GH deficiency. Hypothyroid patients who also have GH deficiency cannot respond well to GH therapy unless they are on thyroid hormone replacement.

Sex steroids advance growth, skeletal age, and pubertal development in the post-birth state. They are responsible for the pubertal growth spurt and are responsible for half of the growth of puberty. If there are excessive sex steroids such as in congential adrenal hyperplasia, then the bone growth plates epiphyses will fuse prematurely, and the previously tall child will become a short adult. The absence of sex steroids will delay skeletal maturation and decrease the pubertal growth spurt, but then in some cases will lead to a taller than predicted adult stature.

Glucocorticoids are the most effective growth hormone suppressors when they are in high concentrations or doses. Cushings syndrome can cause growth to stop and cause short stature. Adrenal insufficiency should not cause growth changes.

Insulin excess can increase the growth rate in the fetus. An example is mothers with gestational diabetes or patients with insulinomas.

Genetic factors are also important in growth. The correlation of mid-parental-heightand a child's height can be used to predict future height for a child.

Finally nutrition issues such as anorexia or malnutrition, chronic medical conditions such as rheumatoid arthritis, and psychological problems can lead to growth changes.