HYPOTHYROIDISM IN THE FETUS AND NEONATE
Najjar S.S.
Faculty of Medicine - American University
of Beirut - Lebanon
Thyroid hormone (TH) is essential for the
normal development of the Central Nervous System of the fetus and in the
first three years of life.
The causes of TH deficiency are: Iodine (I)
deficiency, Maternal hypothyroxinemia, Congenital hypothyroidism.
I.
Iodine deficiency: I is essential for the
synthesis of TH and for brain development. Significant I deficiency impairs
TH synthesis and directly damages the CNS resulting in irreversible mental
retardation, neurologic damage, hypothyroidism and deaf-mutism. I
deficiency is considered by WHO as the most common preventable cause of
mental retardation. The worldwide population at risk has been estimated at
30 to 100 million. It results in a global loss of 10 to 15 intellectual
quotient point per affected individual. To prevent these catastrophic
events mothers should be I sufficient before pregnancy.
II. Maternal Hypothyroxinemia: The fetal thyroid becomes functional at
about 18 weeks of gestation. Prior to that the source of thyroxine (T4) to
the embryo is maternal. Maternal hypothyroxenemia in the first trimester
poses an increased risk for poor neuropsychologic development of the fetus,
irrespective of maternal levels of TSH and T3. Mothers who have low free T4
should be treated with T4 and not T3 as soon as possible. Maternal
screening for low serum T4 (Free T4 ≤ 10th percentile) in the
first trimester is highly recommended. The frequency of poor mental
development in offsprings of hypothyroxenemic mothers has been estimated to
be 150 times that of congenital hypothyroidism.
III. Congenital Hypothyroidism (CH): CH whether due to an anatomic defect of
the thyroid gland or an enzymatic defect in the synthesis of T4 will result
in permanent mental retardation unless treated in the first two weeks of
life and not later than one month of age. Such an early diagnosis can only
be achieved by a neonatal screening program because symptoms and signs of
hypothyroidism take weeks and months to appear. Treatment with T4 after 2
to 4 weeks of age will not prevent mental retardation secondary to severe
hypothyroidism. The incidence of CH is 1:4000-1:5000 newborn but maybe as
high as 1:1500 in areas of iodine deficiency. Adequate replacement of T4
can be assessed only by determining serum levels of T4 or free T4 and TSH.
Serum T4 concentration should be maintained in the upper half of the normal
range. Absence of clinical signs and symptoms are not indicators of
adequate serum T4 concentration.