| TABLE 1: |
| |
1st Trimester |
2nd Trimester |
3rd Trimester |
| TSH |
Normal or Decreased |
Normal |
Normal |
| Free T4 |
Normal |
Normal |
Normal |
| Free T3 |
Normal |
Normal |
Normal |
| Total T4 |
High |
High |
High |
| Total T3 |
High |
High |
High |
| T3 Resin Uptake (Inverse measure of protein
binding) |
Low |
Low |
Low |
| Free T4 Index (FT4I, FTI) |
Normal |
Normal |
Normal |
What is the interaction between
the thyroid function of the mother and the baby?
For the first 10-12 weeks of pregnancy, the baby is completely
dependent on the mother for the production of thyroid hormone. By
the end of the first trimester, the baby’s thyroid begins
to produce thyroid hormone on its own. The baby, however, remains
dependent on the mother for ingestion of adequate amounts of iodine,
which is essential to make the thyroid hormones. The World Health
Organization recommends iodine intake of 200 micrograms/day during
pregnancy to maintain adequate thyroid hormone production. The normal
diet in the United States contains sufficient iodine so additional
iodine supplementation is rarely necessary. |
| What
are the most common causes of hyperthyroidism during pregnancy?
Overall, the most common cause (80-85%) of maternal hyperthyroidism
during pregnancy is Graves’ disease (see Graves’
Disease brochure) and occurs in 1 in 1500 pregnant patients.
In addition to other usual causes of hyperthyroidism (see Hyperthyroid
brochure), very high levels of hCG, seen in severe forms of
morning sickness (hyperemesis gravidarum), may cause transient
hyperthyroidism. The diagnosis of hyperthyroidism can be somewhat
difficult during pregnancy, as 123I thyroid scanning
is contraindicated during pregnancy due to the small amount of radioactivity,
which can be concentrated by the baby’s thyroid. Consequently,
diagnosis is based on a careful history, physical exam and laboratory
testing.
What are the risks of Graves’
Disease/hyperthyroidism to the mother?
Graves’ disease may present initially during the first
trimester or may be exacerbated during this time in a woman known
to have the disorder. In addition to the classic symptoms associated
with hyperthyroidism, inadequately treated maternal hyperthyroidism
can result in early labor and a serious complication known as pre-eclampsia.
Additionally, women with active Graves’ disease during pregnancy
are at higher risk of developing very severe hyperthyroidism known
as thyroid storm. Graves’ disease often improves during the
third trimester of pregnancy and may worsen during the post partum
period.
What are the risks of Graves’
Disease/hyperthyroidism to the baby?
The risks to the baby from Graves’ disease are due to one
of three possible mechanisms:
- Uncontrolled maternal hyperthyroidism: Uncontrolled maternal
hyperthyroidism has been associated with fetal tachycardia (fast
heart rate), small for gestational age babies, prematurity, stillbirths
and possibly congenital malformations. This is another reason
why it is important to treat hyperthyroidism in the mother.
- Extremely high levels of thyroid stimulating immunogloblulins
(TSI): Graves’ disease is an autoimmune disorder caused
by the production of antibodies that stimulate thyroid gland referred
to as thyroid stimulating immunoglobulins (TSI). These antibodies
do cross the placenta and can interact with the baby’s thyroid.
Although uncommon (2-5% of cases of Graves’ disease in pregnancy),
high levels of maternal TSI’s, have been known to cause
fetal or neonatal hyperthyroidism. Fortunately, this typically
only occurs when the mother’s TSI levels are very high (many
times above normal). Measuring TSI in the mother with Graves’
disease is often done in the third trimester.
In the mother with Graves’ disease requiring antithyroid
drug therapy, fetal hyperthyroidism due to the mother’s
TSI is rare, since the antithyroid drugs also cross the placenta.
Of potentially more concern to the baby is the mother with prior
treatment for Graves’ disease (for example radioactive iodine
or surgery) who no longer requires antithyroid drugs. It is very
important to tell you doctor if you have been treated for Graves’
Disease in the past so proper monitioring can be done to ensure
the baby remains healthy during the pregnancy.
- Anti-thyroid drug therapy (ATD). Methimazole (Tapazole) or
propylthiouracil (PTU) are the ATDs
available in the United States for the treatment of hyperthyroidism
(see Hyperthyroidism
brochure). Both of these drugs cross the placenta and can
potentially impair the baby’s thyroid function and cause
fetal goiter. Historically, PTU has been the drug of choice for
treatment of maternal hyperthyroidism, possibly because transplacental
passage may be less than with Tapazole. However, recent studies
suggest that both drugs are safe to use during pregnancy. It is
recommended that the lowest possible dose of ATD be used to control
maternal hyperthyroidism to minimize the development of hypothyroidism
in the baby or neonate. Neither drug appears to increase the general
risk of birth defects. Overall, the benefits to the baby of treating
a mother with hyperthyroidism during pregnancy outweigh the risks
if therapy is carefully monitored.
What are the treatment options for
a pregnant woman with Graves’ Disease/hyperthyroidism?
Mild hyperthyroidism (slightly elevated thyroid hormone levels,
minimal symptoms) often is monitored closely without therapy as
long as both the mother and the baby are doing well. When hyperthyroidism
is severe enough to require therapy, anti-thyroid medications are
the treatment of choice, with PTU being the historical drug of choice.
The goal of therapy is to keep the mother’s free T4 and free
T3 levels in the high-normal range on the lowest dose of antithyroid
medication. Targeting this range of free hormone levels will minimize
the risk to the baby of developing hypothyroidism or goiter. Maternal
hypothyroidism should be avoided. Therapy should be closely monitored
during pregnancy. This is typically done by following thyroid function
tests (TSH and thyroid hormone levels) monthly.
In patients who cannot be adequately treated with anti-thyroid
medications (i.e. those who develop an allergic reaction to the
drugs), surgery is an acceptable alternative. Surgical removal of
the thyroid gland is only very rarely recommended
in the pregnant woman due to the risks of both surgery and anesthesia
to the mother and the baby.
Radioiodine is contraindicated to treat hyperthyroidism during
pregnancy since it readily crosses the placenta and is taken up
by the baby’s thyroid gland. This can cause destruction of
the gland and result in permanent hypothyroidism.
Beta-blockers can be used during pregnancy to help treat significant
palpitations and tremor due to hyperthyroidism. They should be used
sparingly due to reports of impaired fetal growth associated with
longterm use of these medications. Typically, these drugs are only
required until the hyperthyroidism is controlled with anti-thyroid
medications.
What is the natural history of
Graves’ Disease after delivery?
Graves’ disease typically worsens in the postpartum
period, usually in the first 3 months after delivery. Higher doses
of anti-thyroid medications are frequently required during this
time. At usual, close monitoring of thyroid function tests is necessary.
Can the mother with Graves’
disease, who is being treated with anti-thyroid drugs, breastfeed
her infant?
Yes. PTU is the drug of choice because it is highly protein bound.
Consequently, lower amounts of PTU cross into breast milk compared
to Tapazole. It is important to note that the baby will require
periodic assessment of his/her thyroid function to ensure maintenance
of normal thyroid status. |
| What
are the most common causes of hypothyroidism during pregnancy?
Overall, the most common cause of hypothyroidism is the autoimmune
disorder known as Hashimoto’s thyroiditis (see Hypothyroidism
brochure). Hypothyroidism can occur during pregnancy due to
the initial presentation of Hashimoto’s thyroiditis, inadequate
treatment of a woman already known to have hypothyroidism from a
variety of causes, or over-treatment of a hyperthyroid woman with
anti-thyroid medications. Approximately, 2.5% of women will have
a slightly elevated TSH of greater than 6 and 0.4% will have a TSH
greater than 10 during pregnancy.
What are the risks of hypothyroidism
to the mother?
Untreated, or inadequately treated, hypothyroidism has been associated
with maternal anemia (low red blood cell count), myopathy (muscle
pain, weakness), congestive heart failure, pre-eclampsia, placental
abnormalities, low birth weight infants, and postpartum hemorrhage
(bleeding). These complications are more likely to occur in women
with severe hypothyroidism. Most women with mild hypothyroidism
may have no symptoms or attribute symptoms they may have as due
to the pregnancy.
What are the risks of maternal hypothyroidism
to the baby?
Thyroid hormone is critical for brain development in the
baby. Children born with congenital hypothyroidism (no thyroid function
at birth) can have severe cognitive, neurological and developmental
abnormalities if the condition is not recognized and treated promptly.
These developmental abnormalities can largely be prevented if the
disease is recognized and treated immediately after birth. Consequently,
all newborn babies in the United States are screened
for congenital hypothyroidism so they can be treated with thyroid
hormone replacement therapy as soon as possible.
The effect of maternal hypothyroidism on the baby’s brain
development is not as clear. Untreated severe hypothyroidism in
the mother can lead to impaired brain development in the baby. This
is mainly seen when the maternal hypothoidism is due to iodine deficiency,
which also affects the baby However, recent studies have suggested
that mild brain developmental abnormalities may be present in children
born to women who had mild untreated hypothyroidism during pregnancy.
At this time there is no general consensus of opinion regarding
screening all women for hypothyroidism during pregnancy. However,
some physician groups recommend checking a woman’s TSH value
either before becoming prenant (pre-pregnancy counseling) or as
soon as pregnancy is confirmed. This is especially true in women
at high risk for thyroid disease, such as those with prior treatment
for hyperthyroidism, a positive family history of thyroid disease
and those with a goiter. Clearly, woman with established hypothyroidism
should have a TSH test once pregnancy is confirmed, as thyroid hormone
requirements increase during pregnancy, often leading to the need
to increase the levothyroxine dose. If the TSH is normal, no further
monitoring is typically required. This issue should be discussed
further with your health care provider, particularly if you are
contemplating pregnancy. Once hypothyroidism has been detected,
the woman should be treated with levothyroxine to normalize her
TSH and Free T4 values (see Hypothyroidism
brochure).
How should a woman with hypothyroidism
be treated during pregnancy?
The treatment of hypothyroidism in a pregnant woman is the same
as for a man or non-pregnant woman, namely, adequate replacement
of thyroid hormone in the form of synthetic levothyroxine (see Hypothyroidism
brochure). It is important to note that levothyroxine requirements
frequently increase during pregnancy, often times by 25 to 50 percent.
Occasionally, the levothyroxine dose may double. Ideally, hypothyroid
women should have their levothyroxine dose optimized prior to becoming
pregnant. Women with known hypothyroidism should have their thyroid
function tested as soon as pregnancy is detected and their dose
adjusted by their physician as needed to maintain a TSH in the normal
range. Thyroid function tests should be checked approximately every
6-8 weeks during pregnancy to ensure that the woman has normal thyroid
function throughout pregnancy. If a change in levothyroxine dose
is required, thyroid tests should be measured 4 weeks later. As
soon as delivery of the child occurs, the woman may go back to her
usual pre-pregnancy dose of levothyroxine. It is also important
to recognize that prenatal vitamins contain iron that can impair
the absorption of thyroid hormone from the gastrointestinal tract.
Consequently, levothyroxine and prenatal vitamins should not be
taken at the same time and should be separated by at least 2-3 hrs.
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