Thyroid Disease in Pregnancy

District 1 ACOG Medical Student Teaching Module 2011

Physiologic Changes in Thyroid Function During Pregnancy

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

**initial screening

test**

Free T4 Free Thyroxine Index (FTI)

Total T4 Total T3 Resin Triiodo-

thyronine Uptake (RT3U)

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

Begins concentrating iodine at 10-12 weeks

Controlled by pituitary TSH by approximately 20 weeks

Hyperthyroidism 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

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) 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

Most common cause of hyperthyroidism is Graves’ disease 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: Excess TSH production, gestational trophoplastic

disease, hyperfunctioning thyroid adenoma, toxic goiter, subacute thyroiditis, extrathyroid source of TH

Treatment of Hyperthyroidism

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 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

Effect of treatment on fetal thyroid function: 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

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

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 Type 1 DM -> 5-8% risk of hypothyroidism; 25%

postpartum thyroid dysfunction

Hypothyroidism: Fetal & Neonatal Effects

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

Causes: 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

Treat with Levothyroxine in sufficient dose to return TSH to normal

Adjust dosage every 4 weeks Check TSH every trimester

ACOG Recommendations

Screening of all pregnant women with a personal history, physical examination, or symptoms of a thyroid disorder.

Prolog Question #1

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: 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

A) Begin levothyroxine 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.