Thyroid for Dummies (24 page)

Postpartum and silent thyroiditis are most likely variations of the same disease. Postpartum thyroiditis occurs usually three to six months after a pregnancy, while silent thyroiditis can happen to anyone at any time.

This disease is classed as an autoimmune disorder because high levels of peroxidase autoantibodies are found in the blood (refer to Chapter 4). In this condition, the antibodies seem to damage thyroid cells, causing a release of thyroid hormone that leads to temporary hyperthyroidism. So far, scientists have not managed to link any single gene with this form of thyroiditis.

Postpartum thyroiditis is very common; it occurs after 5–10 per cent of all pregnancies. With this condition, unlike subacute thyroiditis, a new mother has no symptoms of fever or weakness, although she may complain of feeling warm. A rapid heartbeat and palpitations are part of the condition. The thyroid itself is not painful, although it’s often abnormally large. The changes that occur in thyroid function are similar to those that occur with subacute 17_031727 ch11.qxp 9/6/06 10:45 PM Page 128

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thyroiditis, however. First hyperthyroidism occurs, followed by normal function, followed by hypothyroidism. The hypothyroidism may resolve, but the person can develop permanent hypothyroidism.

Women who develop postpartum thyroiditis show a high rate of recurrence in later pregnancies, and 25 per cent of them are permanently hypothyroid after three to five years. As many as 50 per cent of women are hypothyroid seven to nine years after pregnancy. The recurrence rate of silent thyroiditis is also very high.

Ten per cent of women with postpartum thyroiditis experience depression.

Therefore, testing thyroid function in any woman complaining of postpartum depression is important.

Interpreting lab results

The lab test that best distinguishes someone with subacute thyroiditis from a person with postpartum or silent thyroiditis is the test of erythrocyte sedimentation rate (ESR). This test measures how quickly the blood cells in a thin column of a person’s blood settle down to the bottom – simply a measure of the stickiness of that person’s blood due to the presence of inflammatory substances. With subacute thyroiditis, the ESR is high, but with postpartum or silent thyroiditis, the rate is normal.

Thyroid function tests from people with postpartum or silent thyroiditis are initially high, then normal, then low. As in subacute thyroiditis, the hyperthyroid phase of the disease is due to leakage from the thyroid. Because the ratio of T4 to T3 is much higher in the thyroid than in the blood, the ratio of T4 to T3 temporarily becomes high in the blood as well. The TSH and the radioactive uptake of iodine are also on the low side during the hyperthyroid phase.

Getting treatment

Treatment for postpartum and silent thyroiditis depends on the stage at which the disease is diagnosed. If someone is diagnosed during the hyperthyroid phase, she is given the beta-blocker propranolol, which helps to control the symptoms of hyperthyroidism. Antithyroid drugs aren’t useful in this case because they won’t prevent hyperthyroidism due to the leakage of thyroid hormone. When the hypothyroidism phase occurs, thyroid hormone replacement is given with the understanding that it probably isn’t needed on a permanent basis.

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Chapter 11: Spotting Thyroid Infections and Inflammation
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Identifying Acute Thyroiditis

Patrick is a 45-year-old man who suddenly develops severe pain in his neck, fever, and chills. The pain is so severe that he has to bend his neck forward to cope with it. He can’t swallow without pain. He also feels weak.

Patrick goes off to see his doctor, who notes that he is very sick. His thyroid gland is extremely tender, and he has a fever. The doctor sends him urgently to the thyroid specialist clinic, where the consultant notes that the tender area is somewhat soft. He puts a fine needle into the area and removes a quantity of pus. The pus is sent for culture and for staining to determine which type of bacteria is causing the infection, and Patrick is placed on an antibiotic, along with aspirin.

In a few days, Patrick is feeling much better. The pus grows a type of bac-terium that is sensitive to the antibiotic used, and this medication is continued for 10 days. Patrick recovers fully.

Acute thyroiditis is much rarer than subacute thyroiditis but is easily confused with subacute, depending on the way the disease appears in the patient. Most doctors will only see a few cases during their working life.

Describing the disease

Many different organisms can infect the thyroid gland to cause acute thyroiditis. Bacteria are present about 70 per cent of the time. The type of bacteria found varies from pneumococcus (which often causes pneumonia) to strep-tococcus (associated with strep throat) and staphylococcus (which causes skin infections). About 15 per cent of the time, a fungus is the infecting organism; tuberculosis is the cause 10 per cent of the time, and various other bugs are the culprits much less frequently.

Besides the tender thyroid, nearby structures such as the trachea (air passage), larynx (voice box), and oesophagus (swallowing tube) are inflamed, and local lymph glands in the neck are tender. In many people, a connection from the outside (such as the throat) to the thyroid tissue is found, through which the infection invades. This tiny, abnormal opening is called a
fistula
and is a result of a developmental defect that is present from birth. A fistula results when the thyroid tissue moves from the back of the tongue down into the neck (check out Chapter 3 for more on how the thyroid gland develops in a embryo) and acts as an open pipe to the thyroid through which infections can pass. If a fistula is found in association with acute thyroiditis, the fistula is always removed as infection will inevitably recur. In fact, infection of the thyroid is so rare that a fistula is actively sought in every case.

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Someone with acute thyroiditis looks obviously sick. The individual complains of a pain in the neck and may have to bend her neck forward to decrease it. She has a fever and chills. The thyroid is enlarged (usually on one side), hot, and tender. Depending on how large the thyroid gets, the patient may have trouble swallowing or even breathing. Lymph nodes are often enlarged, swollen, and tender as well.

Confirming the diagnosis with lab tests

In a person with acute thyroiditis, general blood tests for infection, such as the white blood cell count and the erythrocyte sedimentation rate, are abnormally high. These results confirm that an infection or inflammation is present.

When thyroid tests such as the free T4 and the TSH are done, the results are generally normal, although once in a while the destruction of the thyroid is so great that enough hormone leaks to cause hyperthyroidism. Thyroid uptake of radioactive iodine is normal, and thyroid autoantibodies are negative.

The best test for acute thyroiditis is a needle biopsy. Usually, the biopsy shows inflammation and the infecting organism, but occasionally, no inflammation is seen. Then the diagnosis is much more difficult. Sometimes the thyroid has an abscess, which is drained via the needle.

Treating acute thyroiditis

The treatment for this condition is to give the appropriate antibiotic based upon the suspected organism. The biopsy can provide a good idea of what type of organism is causing the infection, which is later confirmed from a culture of the biopsy tissue. The right antibiotic generally cures the infection and restores normal thyroid function. Sometimes the infection does not respond, and surgery to remove the infected part of the thyroid or the whole thyroid is necessary.

When acute thyroiditis recurs, this event suggests that a fistula is allowing bacteria to get into the thyroid from the outside. In that situation, the person has a barium swallow test, during which X-rays show a trail of barium going from the throat into the thyroid gland. Surgery is then required to eliminate the fistula.

Occasionally, acute thyroiditis causes such damage to the thyroid tissue that hypothyroidism results, and treatment with replacement thyroid hormone is needed.

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Diagnosing a Rare Form of Thyroiditis

Christopher is a 42-year-old man who comes to his doctor complaining of gaining weight and feeling tired, weak, cold, and sleepy. He also says that his neck feels very tight. He has trouble swallowing and breathing.

His doctor examines him and notes that his neck feels very dense. His thyroid barely moves when he swallows. The doctor does not feel swelling in the lymph nodes in his neck.

The doctor runs thyroid function tests, which show a low free T4 and a high TSH. At the same time, he obtains a calcium level, and this test result is low as well. A test of the hormone made in the parathyroid glands called parathyroid hormone is run, and the result of that test is low. The doctor refers Chris to the thyroid specialist clinic where a barium swallow shows compression on the oesophagus. The consultant attempts to do a fine needle biopsy of Chris’s thyroid, but is unable to get tissue. The doctor makes a presumptive diagnosis of Riedel’s thyroiditis, and starts Chris on treatment with corticosteroids, thyroid hormone, and calcium. Chris’s symptoms gradually decrease, but the hypothyroidism and the hypoparathyroidism (low parathyroid function resulting in low calcium) remain. Chris continues to take thyroid hormone replacement and vitamin D for the rest of his life.

This final form of thyroiditis is included for completeness, although it’s so rare that most doctors will not come across the condition during their career.

The disease is called
Riedel’s thyroiditis
and its cause is unknown. The condition is associated with elevated levels of antithyroid autoantibodies so autoimmunity is probably playing some role, especially in view of the good response to corticosteroids. Some specialists believe that Riedel’s thyroiditis is a variant of chronic autoimmune thyroiditis (refer to Chapter 5). Both conditions are associated with autoantibodies and both are often associated with other autoimmune diseases in the same person.

Riedel’s thyroiditis is probably twice as frequent in men as in women, but as so few cases are recorded it’s hard to tell. It tends to occur between ages 30

and 60.

First, the thyroid develops fibrosis – the replacement of thyroid tissue by hard fibres – that is often so dense that thyroid function is lost and the patient becomes hypothyroid. The fibrous tissue firmly attaches the thyroid to the trachea and the nearby muscles so that it doesn’t move in the neck. Even a small needle can’t penetrate the woody, fibrous tissue, so fine needle aspiration biopsy is impossible.

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If the fibrosis continues, it involves the parathyroid glands, which sit behind the thyroid. If these glands are destroyed, the patient also develops hypoparathyroidism. Because the parathyroid glands are important for maintaining calcium levels, the result of this disease is a fall in calcium. Symptoms of tingling and numbness in the hands and feet and tingling around the mouth begin to occur. As the calcium falls, it can result in severe muscle spasms.

Sometimes, the fibrosis stops and the person remains stable. Other times, it continues to cause trouble with breathing, swallowing, and even talking.

When the doctor does thyroid function tests early in the disease, they are often normal. Later, the patient becomes hypothyroid, although the erythrocyte sedimentation rate remains normal.

Because the fibrosis is so invasive, Riedel’s thyroiditis is sometimes confused with anaplastic carcinoma, an extremely rapid-growing, invasive form of thyroid cancer (refer to Chapter 8). A biopsy generally shows the difference, but sometimes the condition is not recognised until the patient is in the operating room about to have surgery for what the surgeon thinks is cancer.

If severe neck symptoms occur, surgery is sometimes necessary to free up the tissues. Sometimes, so much fibrosis is present that surgery isn’t successful in removing the tissue. A trial of corticosteroids often slows or stops progression of the disease. The other agent that has shown some success is the anti-oestrogen drug, tamoxifen.

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Chapter 12

Overcoming Iodine

Deficiency Disease

In This Chapter

ᮣ Grasping the extent of the problem

ᮣ Understanding iodine’s place in mental and physical development

ᮣ Identifying endemic cretinism

ᮣ Dealing with the crisis

In the movie
Love and Death,
Woody Allen describes a convention of village idiots in Russia. If such a convention actually occurred, sadly, most of the people in attendance would probably have iodine deficiency disease.

As you discover in this chapter, iodine deficiency disease is the world’s most common and preventable cause of impaired mental ability. What stops it from elimination is more often politics than medicine. The situation is very similar to the problem of infectious diseases that are preventable with immunisation.

The science of the condition is clearly understood, including the treatment.

What’s missing is the means to transfer that knowledge into action.

A case in point is the story of the former East Germany. Prior to 1980, 50 per cent of East German adolescents developed
goitres
. A goitre is an enlargement of the thyroid that’s sometimes debilitating. In 1980, the country started to add minute amounts of iodine to common table salt, and the percentage of adolescents with goitre dropped to less than 1 per cent. Unfortunately, with the reunification of Germany, iodisation became voluntary, and the goitre rate began to rise again.

This chapter gives you a greater appreciation of the major role of thyroid hormone in the growth and development of the human body, particularly mental development. When you finish this chapter, you won’t have any chance of getting invited to that convention in Russia.