Transcript Thyroid Disease in Pregnancy

Thyroid Disease in Pregnancy
District 1 ACOG
Medical Student Teaching Module 2011
Physiologic Changes in Thyroid
Function During Pregnancy
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Thyroid binding globulin (TBG) increases
due to reduced hepatic clearance and
estrogenic stimulation of TBG synthesis
The test results that change in pregnancy
are influenced by changes in TBG
concentration
Plasma iodide levels decrease due to fetal
iodide use and increased maternal
clearance -> leads to notable increase in
gland size in 15% of women (without
abnormal TFTs)
Physiologic Changes in Thyroid
Function During Pregnancy
Maternal
Status
TSH
Free T4
Free
Thyroxine
Index
(FTI)
Total T4
Total T3
Resin
Triiodothyronine
Uptake
(RT3U)
**initial
screening
test**
Pregnancy
No
change
No
change
No
change
Increase
Increase
Decrease
Hyperthyroidism
Decrease
Increase
Increase
Increase
Increase
or no
change
Increase
Hypothyroidism
Increase
Decrease
Decrease
Decrease
Decrease
or no
change
Decrease
The Fetal Thyroid
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Begins concentrating iodine at 1012 weeks
Controlled by pituitary TSH by
approximately 20 weeks
Hyperthyroidism
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Occurs in 0.2% of
pregnancies; Graves’
disease accounts for
95% of cases
Look for:
-Nervousness
-Tremor
-Tachycardia
-Frequent stools
-Sweating
-Heat intolerance
-Weight loss
-Goiter
-Insomnia
-Palpitations
-Hypertension
-Lid lag/lid retraction
-Pretibial myxedema
Fetal & Neonatal Effects of
Hyperthyroidism
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Associated with preterm delivery, low
birth weight, fetal loss
Fetal thyrotoxicosis (related to disease
itself or treatment)
Risk of immune-mediated
hypo/hyperthyroidism (due to antibodies
crossing the placenta, esp. in Graves or
chronic autoimmune thyroiditis)
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Antibodies in Graves’ disease can be either
stimulatory or inhibitory
Neonates of women with Graves’ who have
been surgically/radioactively treated are at
higher risk, b/c not taking suppression
Causes & Diagnosis of
Hyperthyroidism
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Most common cause of hyperthyroidism is
Graves’ disease
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Document elevated FT4 or elevated FTI with
suppressed TSH, in absence of goiter/mass
Most patients have antibodies to TSH receptor,
antimicrosomal, or antithyroid peroxidase
antibodies, but measurement of these is not
required (though some endocrinologists
recommend measuring TSI, which are
stimulatory antibodies to TSH receptor)
Other causes:
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Excess TSH production, gestational
trophoplastic disease, hyperfunctioning thyroid
adenoma, toxic goiter, subacute thyroiditis,
extrathyroid source of TH
Treatment of Hyperthyroidism
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Goal is to maintain FT4/FTI in high normal
range using lowest possible dose
(minimize fetal exposure)
Measure FT4/FTI q2-4 weeks and titrate
Thioamides (PTU/methimazole) ->
decrease thyroid hormone synthesis by
blocking organification of iodide
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PTU also reduces T4->T3 and may work more
quickly
PTU traditionally preferred (older studies found
that methimazole crossed placenta more
readily and was associated with fetal aplasia
cutis; newer studies refute this)
Treatment of Hyperthyroidism
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Effect of treatment on fetal thyroid
function:
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Possible transient suppression of thyroid
function
Fetal goiter associated with Graves’ (usually
drug-induced fetal hypothyroidism)
Fetal thyrotoxicosis due to maternal antibodies
is rare -> screen for growth and normal FHR
Neonate at risk for thyroid dysfunction; notify
pediatrician
Breastfeeding safe when taking
PTU/methimazole
Treatment of Hyperthyroidism
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Beta-blockers can be used for
symptomatic relief (usually Propanolol)
Reserve thyroidectomy for women in
whom thioamide treatment unsuccessful
Iodine 131 contraindicated (risk of fetal
thyroid ablation especially if exposed after
10 weeks); avoid
pregnancy/breastfeeding for 4 months
after radioactive ablation
Hypothyroidism
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Symptoms: fatigue, constipation, cold
intolerance, muscle cramps, hair loss, dry
skin, slow reflexes, weight gain,
intellectual slowness, voice changes,
insomnia
Can progress to myxedema and coma
Subclinical hypothyroidism: elevated TSH,
normal FTI in asymptomatic patient
Associated with other autoimmune
disorders
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Type 1 DM -> 5-8% risk of hypothyroidism;
25% postpartum thyroid dysfunction
Hypothyroidism: Fetal & Neonatal
Effects
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Higher incidence of LBW (due to
medically indicated preterm
delivery, pre-eclampsia, abruption)
Iodine deficient hypothyroidism ->
congenital cretinism (growth failure,
mental retardation, other
neuropsychological deficits)
Causes & Diagnosis of
Hypothyroidism
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Causes:
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Hashimoto’s (chronic thyroiditis; most common
in developed countries) & iodine deficiency ->
both associated with goiter
Subacute thyroiditis -> not associated with
goiter
Thyroidectomy, radioactive iodine treatment
Iodine deficiency (most common worldwide;
rare in US)
Treatment of Hypothyroidism
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Treat with Levothyroxine in
sufficient dose to return TSH to
normal
Adjust dosage every 4 weeks
Check TSH every trimester
ACOG Recommendations
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Screening of all pregnant women
with a personal history, physical
examination, or symptoms of a
thyroid disorder.
Prolog Question #1
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A 33 year-old G3 P2 at 10 weeks GA comes to the
office for her 1st prenatal visit. She reports that she
had hypothyroidism in the distant past, but was
never treated and is asymptomatic. Physical
examination is normal. On bimanual examination
her uterus is 10 weeks size and FHR is 150 bpm.
Her TSH level is 13.1 and, free T4 level is 0.7, and
her anti-thyroid peroxidase antibody level is high.
The next best step in the patient’s care is:
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A) Begin levothyroxine
B) Repeat serum TSH and Free T4 after 20 weeks of
gestation
C) Measure serum thyroid-stimulating
immunoglobulins
D) Perform ultrasonography of the maternal thyroid
Answer
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A) Begin levothyroxine
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Although the patient is asymptomatic she has
laboratory evidence of overt hypothyroidism
with an elevated TSH and low free T4 level
She also has elevated anti-thyroid peroxidase
antibody level which indicates that the likely
cause of her hypothyroidism is chronic
autoimmune thyroditis (Hashimoto’s disease)
The anti-thyroid peroxidase antibodies also
indicate an increased risk of her developing
other autoimmune disease, such as adrena
insufficiency or type 1 DM.
Hypothyroidism in pregnancy has been
associated with pre-eclampsia, GHTN, abruptio
placentae, preterm delivery, and
neuropsychologic deficits in the child.