Neonatal Endocrinology

Prof Dr. Olcay Evliyaoğlu

Transition to extrauterine life-Hypothermia, hypoglycemia, hypocalcemia Adrenal cortex – autonomic nervous system

including the paraaortic chromaffin system- essential!

Cortisol Surge:Occurs near term.a) Increased cortisol production by the fetal

adrenal.b) Decreased rate of conversion of cortisol to

cortisone.

Cortisol Surge1. Augments surfactant synthesis in lung tissue.2. Increases adrenomedullary phenylethanolamine

N-methyl-transferase activity increases methylation of norepinephrine to epinephrine.

3. Increases hepatic iodothyronine outer ring MDI activity increases conversion of T4 to T3.

4. Decreases sensitivity of the ductus arteriosus to prostaglandins facilitates ductus closure.

5. Induces maturation of several enzymes and transport processes of the small intestine.

6. Stimulates maturation of hepatic enzymes.

Secondary effects of cortisol surge Increased T3 levels

stimulate ß-adrenergic receptor binding and potentiate surfactant synthesis in lung tissue and

increase the sensitivity of brown adipose tissue to norepinephrine.

Catecholamine Surge:

Norepinephrine epinephrine dopamine

1. Critical cardiovascular adaptations (increased blood pressure, increased cardiac ventricular inotropic effects)

2. Increased glucagon secretion3. Decreased insulin secretion4. Increased brown adipose tissue thermogenesis

with increased plasma fatty acid levels.5. Pulmonary adaptation (including mobilization of

pulmonary fluid and increased surfactant release.)

Neonatal brown adipose tissue thermogenesis

Brown adipose tissue is the major site for thermogenesis in the newborn.

Largest masses: envelope the kidneys and adrenal glands.

Smaller masses: surround the blood vessels of the mediastinum and neck.

Norepinephrine, via ß-adrenergic receptors, stimulates brown adipose tissue thermogenesis and optimal responsiveness of this tissue to NE is thyroid hormone dependent.

Calcium homeostasis High concentrations of fetal calcium are

maintained by active placental transport from maternal blood.

Fetal parathyroid PTHRP acts on the placenta to stimulate maternal-fetal calcium transfer.

High total and ionized calcium in fetal blood PTH levels relatively low – CT concentrations high.

25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol are transported accross the placenta, and free vitamin D concentrations in the fetal circulation are similar to or higher than maternal values.

Calcium homeostasis : Intrauterin high PTH supressed, calcitonin

increased BirthCa decline PTH supressed, calcitonin

increased Postnatal adoptation PTH increase, calcitonin

decrease Delay in maturation

Newborn hypocalcemia

In the first days low glomerular filtration rate renal response to PTH weak phosphate excretion is

limitted :hyperphosphatemia

In prematures and SGA (small for gestational age) infants

PTH lower Calcitonin higher kidney functions more immature

Hypocalcemia more prominent

Calcium homeostasis and PTH secretion usually normalize within 1-2 wk in full-term infants but normalization may require 2-3 wk in the small premature infants.

Glucose homeostasis The low glucose and high catecholamine levels

stimulate glucagon secretion and a transient peak in plasma glucagon level occurs within 2h after birth.

Plasma insulin levels are low at birth and tend to fall further secondary to hypoglycemia.

The early glucagon and catecholamine surges rapidly deplete hepatic glycogen stores so that return of plasma glucose levels to normal is after 12-18 h and requires maturation of hepatic gluconeogenesis under the stimulus of a high plasma glucagon/insulin ratio.

Glucagon secretion gradually increases during the early hours after birth, especially with protein feeding.

Premature infants have more severe and prolonged hypocalcemia because of relatively reduced glycogen stores and impaired hepatic gluconeogenesis.

For the healthy term infant, glucose homeostasis is achieved within 5 to 7 d of life, in premature infants 1-2 wk may be required.

Thyroid functionsJust after birth due to cold and stress

In the first 30 min TSH increase to 60-80 mIU/ml

In 1-2 days decrease gradually In 5-7 days decrease to normal levels(<8 mIU/ml)

After TSH increaseT3 andT4 increase to thyrotoxic levels(first 24 hours)

T4 : 15-19 g/dl, T3 :300 ng/dl This is called as ‘physiological hyperthyroidism’