Transient subclinical hyperthyroidism occurs in 10-20 per cent of normal pregnant women during the period serum HcG concentration is the highest. Hyperemesis gravidarum is often associated with biochemical hyperthyroidism. Trophoblastic hyperthyroidism occurs in about 60 per cent of women with hydatidiform mole or chorion carcinoma.

Hyperthyroidism complicating pregnancy occurs in 0.2% of pregnancies most often (95%) Grases' Graves' thyroid disease (autoimmune disease with stimulating antibodies). Other causes are toxic adenomas and subacute lymphocystic thyroidism. Some antibodies can inhibit fetal thyroidism.
Autoimmune thyroid disease is common in pregnancy. The thyroid peroxidase antibodies (TPA) or antibodies against thyreoglubin is associated with a significant increase in miscarriage rate.
Pregnancy complicated with poorly controlled hyperthyroidism is associated with increase rate of spontaneous abortion, preterm delivery, IUGR, stillbirth, preeclampsia, congestive heart failure.
Crisis are seldom: Precipitated by , infection and preeclampsia.
Exacerbation may occur in the first trimester and improvement in the last half of pregnancy (TSH receptor stimulating antibodies may fall).
Diagnosis
Raised T3 and T4 and TSH fall (see normal lab values) present of TRAb and goiter and present of TRAb autoimmunity.
Normally diagnosed before pregnancy but can be revealed in pregnancy (most often take place in the first or the beginning of the second trimester).
Symptoms
Exophthalmos (may occur before hyperthyroidism) tremor, lid lag, weight loss, tachycardia.
Treatment
The goal is to keep the mothers euthyroid with free T4 in the high normal range using the lowest drug dose.
Thionamides
Both prophylthiouracil (PTU) and Methimazole (MMI) cross the placenta and can cause fetal hypothyroidism and goiter. PTU has generally been preferred because it has not been associated with fetal scalp defects - aplasia cutis or choanal or esophageal atresia which very rarely has been seen with MMI. PTU has a shorter halflife and more bound to albumin which may result in less fetal hypothyroidism.
Women on maintenance dose of MMI need not be switch to PTU in pregnancy.
Newly diagnosed thyrotoxicosis should be aggressively treated with PTU 450 mg or MMI 45 mg for 4-6 weeks before reduction in dose.
Doses of PTU £ 150 mg/day or MMI £ 45 are unlikely to cause problems in the fetus. And these doses are safe for breastfeeding (only 0.07% of the maternal dose is consumed by the fetus). If higher dose, the thyroid function should be checked in the neonate.
Combined therapy with Thyroxin "block and replace therapy" has no place (fetal thyroidism).
b-blockers
Often used in early management for symptoms and discontinued once there is clinical improvement, usually after 3 weeks.
Can occasionally cause IUGR, hypoglycemia, respiratory depression and tachycardia.
Surgery
Rarely indicated. Usually reserved for those with dysplasia or stridor and those who has or develop allergies to antithyroid drugs (1-5%). Best performed in the II trimester, if necessary. May be associated with increased risk of abortion and preterm labor.
Radioactive Iodine
Contraindicated in pregnancies and 4 months after treatment.
Fetal and neonatal Grave“s disease
1-5% have hyperthyroidism due to transplacental transfer of TSH receptor-stimulating antibodies (TRAb).
Half life is long (Weeks) and symptoms seen up to 6 weeks post partum. Values five-fold and more are predictive. Low < 20 l minimal risk.
Symptoms:
Symptoms: High fetal heart rate (> 160 beats/min, fetal goiter, fetal hydrops, pretem delivery, advanced bone age, IUGR fetal deaths and craniosynostosis are manifestations of fetal thyrotoxicosis (seldom).
Fetal blood sampling for thyroid function test may be considered.
Propylthiouracil and Methimaxol as well as betablockers (Propranolol) may be given to mothers to treat fetuses who have severe tachycardia or very poor growth. The pediatrician should be informed whenever there is a history of maternal thyroid disease without treatment, as the mortality rate of the newborn is almost 15%.
The treatment is only needed for a few weeks.
NB! In case of unexplained fetal tachycardia and goiter, TRAB should be measured.
In case of struma and treatment with antithyreoid medicine which can block the infants thyreoid gland. The infant can develop slight but transiant hypofunction. If the mother has TRAb antibodies the baby can later develop hyperthyroidism.
Yodine uptake: recommended dose 2250 µ/d. The prevalende: overt (0,3-0,5%), subclinical 2-3%

IUGR, pretern birth, abortion, congenital anomalies, (10=20%) perinatal mortality and neuro-psychological impairment. Even a free T4 concentration below 10th percentile caused an increased risk for slightly lower I.Q.
Overt hypothyroidism are rare because of anovulation and first trimester abortion. The fetus depending on maternal thyroid hormone until thyroid fetal function begins around 12 weeks of gestation.
Women with thyroid autoimmunity and euthyroid are at risk of developing hypothyreodism and should be monitored by TSH.
Symptoms:
Lethargy, tiredness, hairless, dry skin, constipation, carpal tunnel syndrome, fluid retention and goiter
Cases:
Most common Hashimoto's thyroiditis or and Grave's disease. Others are atropic thyoriditis or iatrogenic (thyroidectomy, radioactive therapy) and related to drugs (iodine, lithium anti-thyroid drugs).
Diagnosis:
Low free T4 and raised TSH (see normal lab values) suggest primary hypothyreodisme, overt if free T4 are clearly below normal and subclinical if free T4 is normal.
Treatment:
The goal of therapy is to normalize the mother's serum TSH concentration, low in the normal range and free Ty in the upper 1/3 of the normal range. Small amount of thyroxine cross the placenta but no risk for thyrotoxicosis of the fetus. Most have maintenance dose of 100-150 mg/day. Starting dose normal 100-150 mg/day.

Very rare. Most cases caused by agenesis or dysgenesis of the fetal thyroid, congenital ages = hormonogenesis, or iodine deficiencies in endemic areas. And woman with atrophic thyroiditis due to transplacental TSH receptor-blocking antibodies (TRAb) causing transient fetal goiter.

Incidence 5-10% and in up to 25% with type 1 diabetes, also high if previous Grave's disease and high antibody peroxidase concentration. Most common in families with history of hypothyroidism and type I diabetes and those with thyroid peroxidase (antimicrosomal) antibodies in whom 50-70% will develop postpartum thyroiditis and one third develop permanent hypothyroidism within 4 years.
Two patterns can be defined: Subacute lymphocytic (postpartum) thyroiditis and postpartum exacerbation of chronic lymphocytic (Hashimoto's) thyroiditis.
The clinical presentations are: (a) Monophasic: producing transient hypothyroidism (40%) or hyperthyroidism (40%) or (b) Biphasic (20%) producing hyperthyroidism and the more prolonged hypothyroidism (4-8 month postpartum) but permanent hypothyroidism in 3-4%.

• Flare up of Grave's disease .
• Distinguish postpartum by iodine or technetium scan high uptake in Grave's disease) and absent thyroid stimulating antibodies in postpartum thyroiditis.

About 1% of woman and up to 40% malignant (most often papillary carcinoma) especially if tumor are fixated, rapid growth of painless tumor (very sudden onset suggest bleeding into a cystic lesion), solid lymphadenopathy, voice change, Homer's syndrome.
Diagnosis:
Should be evaluated in the same way as if the woman is not pregnant. Radionuclide scanning is contraindicated.
Thyroid function test should be performed to exclude a toxic nodule or Hashimoto's thyroiditis.
A raised Thyroglobulin titre (-100 mg (L) is suggestive of malignancy.
Ultrasound:
Cystic lesions more likely to be benign.
Surgery in case of malignancy performed in the II or III trimester with Thyroxine given postoperative to suppress TSH since residual tumor is usually TSH dependent.

Feel free to mail me or the webmaster Dr Lars Krag Moeller if you have suggestions or corrections that you believe could improve the manual. (njsecher@dadlnet.dk)
Terms of use for the site