Normally pregnancy cause changes in thyroid and its function because of pregnancy related hormones.

1. Hormonal Changes– Human chorionic gonadotropin (hCG) and Estrogen cause increase in thyroid hormones level in the blood.

hCG (produced by placenta) is similar to TSH and mildly stimulates the thyroid to produce more thyroid hormones. So high hCG levels in the first trimester may result in a slightly low TSH (called subclinical hyperthyroidism).

Increased estrogen produces higher levels of thyroid-binding globulin, a protein that transports thyroid hormone in the blood.

However, measurements of “Free” hormone (that not bound to protein, representing the active form of the hormone) usually remain normal. The thyroid is functioning normally if the TSH, Free T4 and Free T3 are all normal throughout pregnancy.

2. The size of thyroid increases slightly in healthy women during pregnancy, but not enough to be detected by a physical exam. Only with the help of very sensitive imaging techniques (ultrasound), it is possible to detect an increase in thyroid volume in some women.

3. Physiological changes during pregnancy such as increase in cardiac output, oxygen consumption and heat production may mimic mild hyperthyroidism and is the reason why hyperthyroidism remain undetectable during pregnancy. Even before conception, thyroid conditions that have lingered untreated can hinder a woman’s ability to become pregnant or can lead to miscarriage.

Therefore detecting a thyroid problem is important, for all those already diagnosed with a condition and if they are planning to become pregnant or are pregnant.

In a pregnant women thyroid hormone plays a very important role in the normal development of the baby’s brain and nervous system and her own expanded metabolic needs. For the first 10-12 weeks of pregnancy, the fetus is completely dependent on the mother for the production of thyroid hormone. By the end of 12 week, the baby’s thyroid begins to produce thyroid hormone on its own. But fetus is still dependent on mother for intake of adequate amount of iodine. The best way to ensure adequate amounts of iodine reach the unborn child is for the mother to take a normal diet with iodized salt, or prenatal vitamin with a sufficient amount of iodine. The WHO recommends iodine intake of 200 micrograms/day during pregnancy to maintain adequate thyroid hormone production.

Preconceptional counseling: Considering the hazards during pregnancy, preconceptional counseling is important. Adequate treatment should be instituted to bring down the thyroid function profile to normal. Radioactive iodine (131I) therapy should not be given to patients trying to get pregnant or female wants pregnancy within one year. If pregnancy occurs inadvertently, termination should be done. Oral pill is to be withheld because of accelerated metabolism and disturbed liver function.

Hyperthyroidism in pregnancy

Autoimmune hyperthyroidism (Graves’ disease) due to thyroid stimulating antibodies is the most common cause. Other causes are: Nodular thyroid disease, sub-acute thyroiditis, hyperemesis gravidarum and trophoblastic disease.

Diagnosis

• History, physical examination and lab tests.
• Measuring levels of FT4 (high), FT3 (high) and TSH (low).
• Thyroid peroxidase antibodies (TPOAb), (Anti microsomal antibodies) and thyroid stimulating immunoglobulin should be measured.
• Ultrasonography of the fetal thyroid gland is done when the mother is taking anti thyroid drugs.
• Radioactive iodine uptake and scans are contraindicated during pregnancy as it will cross the placenta and damage the fetal thyroid gland permanently.

Complications Of Untreated Hyperthyroidism

Maternal Miscarriage, preterm delivery, preeclampsia, congestive heart failure, abruptio placenta, thyroid storm and infection.

Fetal/Neonatal: IUGR, prematurity, stillbirth, hyperthyroidism, hypothyroidism, increased perinatal morbidity and mortality.

Treatment –

Mild hyperthyroidism with minimal symptoms may not require any treatment with close monitoring. Severe hyperthyroidism require to treat drugs which interfere production of thyroid hormones.

Antithyroid drugs [propylthiouracil (PTU) or methimazole (MM) is the mainstay of treatment and are very effective. 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.

Propylthiouracil is given at a daily dose of 300–450 mg and continued till the patient becomes euthyroid, the maintenance dose being 50 and 150 mg daily.

Carbimazole is given orally with a daily dose of 10–40 mg and maintained at this dose until the patient becomes euthyroid. Then it is progressively reduced to a maintenance of between 5 mg and 15 mg daily.

Side effects – Both the drugs may cause fetal goiter and hypothyroidism. Methimazole may be associated with aplasia cutis of the neonate and has the risk of embryopathy.

Therapy should be closely monitored during pregnancy. Fetal surveillance is maintained with serial USG, NST and BPP. The drugs are not contraindicated during breastfeeding provided the dose is kept relatively low and close monitoring of the neonatal thyroid functions is carried out. Cord blood should be taken for TSH and free T4 at the time of delivery to detect neonatal hyperthyroidism.

Thyroidectomy –surgical removal of thyroid is an option for the patients those who develop an allergic reaction to the drugs or who have pressure symptoms. It can be done safely in the second trimester with prior biochemical control.

Hypothyroidism in Pregnancy

 The Causes of hypothyroidism in pregnancy may be due to

• Undiagnosed before pregnancy
• Hypothyroid women who either discontinue thyroid therapy or taking inadequate doses of antithyroid drugs
• Hyperthyroid women on excessive amounts of antithyroid drugs
• Women with lithium or amiodarone therapy.
• Hashimoto thyroiditis ( autoimmune disorder )is the most common cause of Primary hypothyroidism in pregnancy

Complications or risks–

 Maternal – preeclampsia, anemia, myopathy, and congestive heart failure.

Neonatal – Miscarriage, stillbirth and prematurity and deficient intellectual development of the child.

Diagnosis–

Physical exam, clinical symptoms and lab tests

• TSH -Serum TSH should be repeated at an interval of 6–8 weeks as there is increased demand of thyroid hormone in the second half of pregnancy.
• Serum thyroid peroxidase antibodies (TPO-Ab) or antimicrosomal antibodies are elevated in autoimmune thyroiditis.

Treatment –

Synthetic levothyroxine-levothyroxine requirements frequently increase during pregnancy, so If the patient is having substitution therapy in pre-pregnant state, the dose of levothyroxine need to be increased in pregnancy. Generally, therapy is started 2 to 2.4 mcg/kg/day and then maintenance doses 75 and 150 mcg of levothyroxin per day. The serum TSH should be repeated every 2 to 6 weeks. After delivery of the child, the woman may go back to her usual pre-pregnancy dose of levothyroxine.

Levothyroxine and prenatal vitamins should not be taken at the same time because iron and calcium in the prenatal multivitamins can impair the absorption of thyroid hormone from the gastrointestinal tract and therefore should be separated by at least 2-3 hrs. Levothyroxin is safe during pregnancy.