Iodide
fortification of table salt and bread
products has diminished and iodide deficiency has been identified in some of the population. Adequate iodide is requisite for normal fetal neurological development
beginning soon after conception.
The
recommended daily intake during pregnancy
is at least 220 ug/day
. Severe deficiency is associated with endemic cretinism. Although not quantified it is presumed that moderate deficiency has intermediate
and variable effects on intellectual and psychomotor function.
Although it is doubtful that mild
deficiency causes intellectual impairment supplementation prevents
fetal goiter
CLINICAL HYPOTHYROIDISM
Clinical
or overt hypothyroidism complicates
approximately 2 per 1000
pregnancies . Clinical
hypothyroidism is diagnosed
when an abnormally high
serum thyrotropin level is
accompanied by an abnormally low
free thyroxine level. The most
common etiology is glandular destruction
by autoantibodies or
Hashimoto thyroiditis . Thyroid peroxidase
antibodies have been identified
in 5 to 15 percent of
pregnant women up to half of whom later in life develop an autoimmune thyroiditis.
Overt
hypothyroidism is
associated with infertility. When pregnancy
does occur there are increased rates of maternal and fetal complications to include preeclampsia
placental abruption cardiac dysfunction stillbirth
and prematurity . Fortunately
perinatal outcomes are usually normal with adequate treatment . Replacement therapy
is with thyroxine 50 to 100
ug daily . Serum TSH and free thyroxine levels
are measured at 4 to 6 week
intervals and thyroxine adjusted
by 25 to 50 ug increments until
normal values are reached. Pregancy is
associated with an increase in
thyroxine requirements of about
a third however care should be individualized as not all
women require an adjustment in therapy.
SUBCLINICAL HYPOTHYROIDISM
Subclinical hypothyroidism is defined
by an abnormally elevated TSH level
with normal serum free T in an asymptomatic
woman. The prevalence of
subclinical hypothyroidism in pregnancy
is approximately 2.3 percent. Approximately 2 to 5 percent
of reproductive age women with subclinical disease per year
progress to overt thyroid failure. Heredity is a potent risk
factor . Other risk factors for
thyroid failure include type -1
diabetes and thyroid peroxidase
antibodies . Effects of subclinical hypothyroidism on pregnancy outcome are not clear. Pregnancies with subclinical hypothyroidism on pregnancy outcome are not clear. Pregnancies with
subclinical hypothyroidism may
be at increased risk for preterm
birth or placental abruption. Effect of maternal hypothyroidism on the fetus and infant . Hypothyroidism – either overt
or subclinical - has been reported
to cause sub normal mental development
Elevated
maternal TSH values have been associated with
offspring who have diminished
school performance reading
recognition and intelligence quotient
scores as compared with matched
controls.
Some
organization have recommended
prenatal screening and treatment for subclinical disease. However the American College of Obstetricians and Gynecologists continues to recommend against routine screening . Randomized placebo controlled
trials to determine risks or benefits
of detecting and treating subclinical
thyroid dysfunction in pregnancy are in progress.
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