Thyroid for Dummies (39 page)

Alice is a cousin of Stacy, Karen, Sarah, and

she is checked for thyroid-stimulating hormone

Margaret – friends from earlier chapters. She is

receptor stimulating antibodies. The test result is

four weeks pregnant and notices that her heart

very positive. Alice starts taking the antithyroid

is beating very fast all the time and she is also

medication, propylthiouracil. Within three weeks,

feeling very warm. She has lost a few pounds in

Alice begins to feel better. At six weeks, she is

weight, and her husband notices that her neck

gaining weight and her heart has slowed notice-

seems enlarged.

ably. Alice is able to come off the propylthiouracil

during the second half of her pregnancy, which

Alice and her husband go to their GP, who obtains

proceeds normally. Her baby is checked care-

thyroid blood tests to rule out hyperthyroidism.

fully for hyperthyroidism, which fortunately, does

To her surprise, her doctor rules in the possibility

not develop.

of hyperthyroidism when results show that the

free T4 level in Alice’s blood is elevated while her

After the delivery, Alice again needs antithyroid

TSH level is suppressed. The doctor immediately

medication, which she takes for a year. She

refers Alice to a thyroid specialist clinic where

does well.

Lab tests show that a hyperthyroid mother has high levels of free T4 and low levels of TSH. In this situation, a total T4 test (refer to Chapter 4) is not helpful at all, because the total T4 is always elevated in view of the increase in thyroid-binding globulin in the mother’s system.

Hyperthyroidism needs to be controlled during pregnancy, otherwise it can lead to:

ߜ Premature delivery

ߜ Foetal malformations

ߜ Low birth weight

ߜ Hyperthyroidism in the infant

ߜ High blood pressure and other problems in the mother The development of hyperthyroidism during a pregnancy is relatively uncommon and is thought to affect around 1 in every 500 pregnancies.

This type of hyperthyroidism is associated with antibodies that stimulate the TSH receptors on thyroid cells and trigger the production of more thyroid hormone. In some cases, Graves’ disease (refer to Chapter 6) occurs before 25_031727 ch18.qxp 9/6/06 10:44 PM Page 227

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pregnancy and reappears despite successful treatment with radioactive iodine, surgery, or antithyroid drugs. And, although mum may have normal thyroid function, she may still have antibodies that can pass through the placenta to the foetus, giving the foetus hyperthyroidism and a probable goitre.

Finding hyperthyroidism in the foetus

A number of signs suggest that the foetus has hyperthyroidism, most of which are determined during an ultrasound scan of the developing foetus.

These signs include:

ߜ Foetal goitre

ߜ Very rapid foetal heart rate (over 160 beats per minute) ߜ Increased movement of the foetus

ߜ Changes in foetal bones (increased bone maturity)

ߜ Slowed foetal growth

If you are pregnant after successful treatment for Graves’ disease, your foetus can become hyperthyroid because you still have thyroid-stimulating antibodies that can pass through the placenta. It’s important for your doctor to monitor the foetus for signs of hyperthyroidism and check you for TSH

receptor antibodies early in pregnancy. If your TSH receptor antibodies are elevated, but no signs of foetal hyperthyroidism is present, both are usually checked again after six months.

Treatment of hyperthyroidism in the foetus involves giving antithyroid drugs to the mother; the medication then passes through the placenta to decrease the thyroid function of the foetus. The mother may need to take thyroid hormone replacement as a result, however, because her thyroid function is reduced during the antithyroid treatment, as well.

The foetus may also show hyperthyroidism at birth if the mother has Graves’

disease that is not well controlled or has a lot of TSH receptor stimulating antibodies. A mother who has a baby with neonatal hyperthyroidism is at especially high risk of having another in a subsequent pregnancy.

Hyperthyroidism in the newborn may not appear until the antithyroid drugs, obtained through the placenta, have cleared out of the baby’s system. The baby will then have the usual signs of hyperthyroidism plus signs specific to a newborn, such as failure to thrive, increase in the yellow colour of the skin (jaundice due to increased bilirubin), and increased irritability. After the mother’s thyroid-stimulating antibodies clear from the baby’s blood, the baby will have normal thyroid function.

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Treating the mother during pregnancy

Autoimmune hyperthyroidism tends to improve through the course of a pregnancy because of a general decline in the mother’s autoimmunity. Other factors aiding the improvement of autoimmune hyperthyroidism include an increase in thyroxine-binding globulin, an increased loss of iodine in the urine, and an increase in TSH receptor blocking antibodies as the TSH receptor stimulating antibodies decline.

Radioactive iodine is not used to treat Graves’ disease during a pregnancy, because the radiation can create malformations in the foetus and destroy the foetal thyroid gland.

The usual treatment for Graves’ disease during pregnancy is the use of antithyroid drugs: propylthiouracil or carbimazole. The dose of antithyroid drug that is used is the least amount that can keep the free T4 in the upper part of the normal range (refer to Chapter 4 and Chapter 6). When this is done, the foetus receives the right amount of T4 from the mother.

A study of goitres in babies at birth found that 8 out of 11 were due to hypothyroidism in the baby, while 3 were due to hyperthyroidism. Of the 8 hypothyroid babies, 5 were due to excessive amounts of antithyroid drugs given to the mother during pregnancy. This evidence emphasises how important it is to give the least amount of antithyroid drug that allows the mother’s thyroid function to return to normal.

A few circumstances require surgery rather than antithyroid drugs, including: ߜ Repeated failure to take antithyroid drugs.

ߜ When the mother needs exceptionally high doses of medication.

ߜ When a slow foetal heart rate suggests the foetus may have hypothyroidism due to the mother’s antithyroid drug.

ߜ The mother has extremely severe hyperthyroid symptoms.

ߜ The mother experiences side effects, like a fall in white blood cells, from the drug.

If surgery is needed, the best time is between three and six months of pregnancy (second trimester), when it is least harmful to the foetus and the mother.

To prepare for surgery, the mother is sometimes given iodine. Iodine passes easily through the placenta to the foetus, where it can cause goitre and hypothyroidism. Iodine is also found in topical compounds and dyes used for better observation of the growing foetus. The use of iodine is necessary in these situations, but talk with your doctor about the consequences of excessive use.

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Checking mother and child after birth

After a baby is born, a mother with Graves’ disease can expect a worsening of her symptoms as her immune function increases and autoimmunity becomes severe again. Getting your thyroid function checked with blood tests after the delivery is important.

The easiest way to check the thyroid status of a newborn is to check the levels of free T4 and TSH in the umbilical cord blood. Treatment depends upon the findings.

Breastfeeding with Graves’ disease

For many years, doctors believed that mothers who were being treated with antithyroid drugs for Graves’ disease should not breastfeed because the drugs would enter her milk and pass to the baby. Recent studies have proved that this is not the case. You can breastfeed safely if you are taking antithyroid drugs for hyperthyroidism as long as the baby’s development is closely monitored, and the lowest effective dose of drug is used.

Postpartum Graves’ disease

Postpartum Graves’ disease is not the same as postpartum thyroiditis (refer to Chapter 11). Graves’ disease is associated with increased production of thyroid hormones due to stimulation by TSH receptor stimulating antibodies, whereas postpartum thyroiditis occurs when preformed thyroid hormone spills from a damaged thyroid. Treatment for these two conditions is therefore entirely different – postpartum Graves’ disease is treated with anti-thyroid drugs, whereas postpartum thyroiditis, in which symptoms are usually mild, is treated with a beta-blocker if necessary. Postpartum thyroiditis is differentiated from Graves’ disease by detecting a low uptake of injected technetium during a thyroid scan. Breast-feeding is usually only stopped for 30 hours after this investigation.

Postpartum thyroiditis is associated with thyroid autoantibodies. Some specialists recommend that all pregnant women have tests for thyroid autoantibodies early in pregnancy, as about 50 per cent of those with positive tests go on to develop postpartum thyroiditis.

Gestational transient thyrotoxicosis

Holly is a 27-year-old woman who is pregnant for the first time. She has a lot of morning sickness during the first few weeks of her pregnancy. She loses some weight, but believes this loss is due to the morning sickness. However, in the last few days, she notices other symptoms of a rapid heartbeat, fatigue, 25_031727 ch18.qxp 9/6/06 10:44 PM Page 230

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trouble sleeping, and a feeling of warmth all the time. She checks with her GP

who suggests that Holly has Graves’ disease. Thyroid function tests seem to confirm this and she is referred to a thyroid specialist clinic.

The doctor at the clinic notices that Holly’s thyroid is not enlarged. He is concerned about the amount of vomiting that Holly describes and checks her for TSH receptor stimulating autoantibodies. The result is negative and Holly is told she probably has a condition called
gestational transient thyrotoxicosis
(GTT), which usually improves quickly. Holly takes a low dose of propranolol, a drug that relieves her symptoms, along with a drug for her vomiting. Over the next few weeks, Holly returns to normal and has no further trouble with hyperthyroid symptoms. Her thyroid function tests also return to normal.

Gestational transient thyrotoxicosis is actually more common than Graves’

disease in pregnancy, occurring as often as two to three times in 100 pregnancies. Fortunately, GTT is generally mild. But sometimes the condition is more serious, and is occasionally confused with Graves’ disease, leading to incorrect treatment.

GTT is due to the hormone called
human chorionic gonadotrophin
(HCG), which is produced by the placenta to maintain early pregnancy. HCG is at its highest level in the mother’s circulation at around 10 weeks of pregnancy, but remains elevated throughout, and may appear in a form that is cleared very slowly from the mother’s circulation. HCG can act as a thyroid stimulant, leading to increased free T4 and decreased TSH, which produces a diagnosis of hyperthyroidism. No TSH receptor stimulating antibodies are found in GTT.

About half of women with GTT show the typical symptoms of hyperthyroidism.

In addition, many experience a significant increase in vomiting, sometimes called hyperemesis gravidarum. A goitre does not usually develop.

Most women with GTT need minimal treatment with a beta-blocker like propranolol (refer to Chapter 6). Sometimes, the mother is given fluids to replen-ish what she loses from vomiting. Occasionally, antithyroid drugs are needed for a short time, until levels of HCG begin to fall (usually after 10 weeks of pregnancy). However, in twin pregnancies, HCG levels may remain particularly high for a longer time period. Some studies have not shown a difference in the level of HCG between pregnant women who vomit a lot and those who do not. This evidence suggests that women who experience a lot of vomiting may make a form of HCG that is especially stimulating to the thyroid.

The most severe vomiting associated with GTT occurs when the level of thyroid hormone, the level of HCG, and the level of oestrogen in the pregnant mother are all at a maximum.

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If you have symptoms of hyperthyroidism plus vomiting in early pregnancy, the likely diagnosis is GTT rather than Graves’ disease. GTT usually improves after several weeks, while Graves’ disease requires treatment throughout the pregnancy in many cases.

Hydatidiform mole and choriocarcinoma

Occasionally, as a result of some abnormality of the mother’s egg or in fertilization, the placenta forms a series of grape-like clusters called a hydatidiform mole. No viable foetus develops from this mole, but in about 10 per cent of cases it can secrete large amounts of HCG and cause hyperthyroidism. The mother often experiences vaginal bleeding, and her uterus is not the correct size for the stage of the pregnancy (it’s usually too large).

An ultrasound study in this situation shows the mole very clearly. Because no viable foetus is present, the pregnancy is terminated.

Very rarely – about 2 per cent of the time – the mole changes into a cancer called a choriocarcinoma, which can also make a large amount of HCG.

Fortunately, this cancer is very treatable, and the patient can usually go on to have further children in the future.

Finding New Thyroid Nodules

during Pregnancy

Because pregnant women have frequent exams, thyroid nodules are sometimes discovered during pregnancy. Treatment depends upon the tissue found in the nodule and the stage of the pregnancy.

The first step is to do a fine needle aspiration biopsy of the nodule (refer to Chapter 7). If the biopsy shows that a nodule is definitely cancer, and the patient is less than six months pregnant, she is usually offered thyroid surgery at that time. Between three and six months of pregnancy (second trimester) is the best time for this surgery because it offers the least chance of interfering with the development of the baby or of causing premature labour.