Thyroid for Dummies (15 page)

Read Thyroid for Dummies Online

Authors: Alan L. Rubin

ߜ Blood tests for cholesterol and other fats are often lower than normal as you are burning up so much extra energy.

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Determining Whether Graves’

Disease Is the Culprit

Most cases of hyperthyroidism result from Graves’ disease, which is an autoimmune condition. Graves’ disease is most common in females and occurs 10 to 20 times more often in women than in men. Symptoms tend to start between the ages of 30 and 60, but they can occur at any age. Graves’

disease consists of any one or all of three parts:

ߜ Hyperthyroidism

ߜ Eye disease

ߜ Skin disease

Most of the signs and symptoms of Graves’ disease are the result of hyperthyroidism, which in turn results from the excessive production of thyroid hormones. Doctors can distinguish Graves’ disease from other forms of hyperthyroidism because blood tests identify autoimmunity. In addition to the symptoms of hyperthyroidism detailed earlier in this chapter, autoimmunity can lead to eye and skin disease.

Causes of Graves’ disease

About 10 per cent of the world’s population has thyroid autoantibodies (refer to Chapter 5), and these autoantibodies can lead to both hypothyroidism (underactive thyroid function) and hyperthyroidism. These conditions occur because some autoantibodies suppress the thyroid, while others stimulate it.

If you have Graves’ disease, the stimulating antibodies are in control in your body. Just why this change happens isn’t clear, but researchers have a number of theories, including the following:

ߜ The body makes many cells to prevent foreign tissue from invading and other cells that recognise the body’s own tissue. When someone has an autoimmune disorder, their body may have lost the cells meant to prevent other cells from reacting against the body’s own tissue.

ߜ Invading organisms such as viruses may share characteristics of normal body tissue. When the body creates antibodies to fight the invaders, those antibodies may react against normal tissue as well.

ߜ Certain drugs can change the immunity of the body so it reacts against itself. These drugs are used in the treatment of hepatitis and leukaemia, for example, and their effect is to activate or increase immunity. As a side effect, they may activate thyroid-stimulating immunity.

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ߜ Women, especially, may have genes that promote autoimmunity. The frequent occurrence of Graves’ disease in mothers, daughters, and sisters confirms the genetic association (head to Chapter 17).

ߜ When the thyroid is injured, for example by a viral illness, it releases chemicals into the blood that are not normally found there. The protective immunity cells may make antibodies against those chemicals, which then react back at the thyroid.

ߜ If someone with a large thyroid gland (such as a multinodular goitre; see Chapter 9) that isn’t making enough thyroid hormone takes iodine tablets, that person may undergo a sudden production of a lot of thyroid hormone that leads to hyperthyroidism.

ߜ Stress can produce a rapid heart rate, sweating, and other signs similar to hyperthyroidism. Its role in the onset of hyperthyroidism is unclear.

Signs and symptoms specific

to Graves’ disease

The eye and skin problems associated with Graves’ disease are sometimes apparent even when a person has no overt symptoms of hyperthyroidism.

Sometimes these eye and skin conditions progress even after hyperthyroidism is under control. Severe forms of both these problems are rare, but thyroid eye disease can lead to blindness.

Thyroid eye disease

Thyroid eye disease, called
infiltrative ophthalmopathy
or
exophthalmos
, is present in almost all people with Graves’ disease. Minor changes are found in up to 50 per cent of people, increasing to 90 per cent if all are investigated with ultrasound of the eye area. For some reason, smokers are more likely to develop ophthalmopathy than non-smokers. Usually, the condition is mild and does not progress after hyperthyroidism is controlled. Sometimes – in no more than 5 per cent of people with Graves’ disease – the condition does progress despite controlling the hyperthyroidism.

Someone with thyroid eye disease presents a clear-cut clinical picture. The eye, with its muscles and coverings, sits in a bony hollow within the skull, called the orbit. When eye disease is present, the skin covering the eye and the muscles within the orbit are swollen and puffy. Since limited room is available within the orbit, the swollen skin and muscles are forced to push forward. Usually both eyes are affected, but the disease can start or progress more rapidly on one side than the other. If your eye is pushed forward far enough, your eyelids cannot close fully. The result is irritation and redness of the eyeball.

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The optic nerve that carries the visual signal to your brain is stretched and sometimes damaged by thyroid eye disease, as is the back of the eye, the retina, where your eye focuses what it sees. Swelling can also compromise the blood supply to these tissues.

Additionally, the eye muscles do not function properly, so that your eyes do not move together; you may experience double vision as a result. Someone with Graves’ ophthalmopathy may first notice mild symptoms such as excess tears, intolerance of light and grittiness, or more severe symptoms such as eye pain, double vision, and reduced vision. Occasionally, the end result of this damage is blindness but this state is rare.

When the eye muscles of a person with thyroid eye disease are examined under a microscope, large numbers of autoimmune cells appear (similar to what is seen in the thyroid itself).

Treatment of thyroid eye disease is usually carried out in steps; severe measures are used only when milder measures fail. First, local measures like eye drops are given to treat the inflammation. If that fails to cure the problem, oral steroids are given to reduce your immunity. Other drugs that suppress immunity are also available.

Severe cases of thyroid eye disease usually respond to irradiation of the muscles in the orbit. If that treatment does not work or the case is severe enough, a surgeon can remove bone from the orbit; thus, decompressing the tissues.

A few simple measures can help improve eye symptoms, such as: ߜ Avoiding dust

ߜ Wearing sunglasses

ߜ Using artificial teardrops (from chemists or on prescription from your doctor)

ߜ Raising the head of your bed (to reduce swelling when lying flat at night) ߜ Wearing eye protector pads while you sleep

Thyroid skin disease

Thyroid skin disease – known medically by unpronounceable names such as
pretibial myxoedema
and
thyroid acropachy
– is seen even less often than thyroid eye disease and is very severe in only 1–2 per cent of people with Graves’ disease.

Pretibial myxoedema is an abnormal thickening of the skin, usually in the front of the lower leg. Raised patches of skin are pink in appearance. The skin problems may last for several months or longer, then gradually improve. If 11_031727 ch06.qxp 9/6/06 10:43 PM Page 73

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they become severe, they may respond to steroid creams applied under tight dressings.

With thyroid acropachy, a person’s fingers become wider, and they may experience arthritic damage to the joints of the fingers. Fortunately, these lesions usually cause only unsightly fingers and no symptoms. People with these symptoms are not given any particular treatment.

Recognising Other Causes

of Hyperthyroidism

Although the vast majority of people with hyperthyroidism have Graves’

disease, about 20 per cent do not. The others may have one of several other conditions that lead to the increased production of free T4 and T3 (thyroid hormones). The treatment of these conditions may differ from treatment of Graves’ disease, so recognising them is important.

Factitious
(false) hyperthyroidism occurs when a person is consuming large amounts of thyroid hormone without a doctor’s knowledge. Usually some kind of psychological disturbance or a misguided attempt to lose weight causes this behaviour. The way to distinguish between this cause and other causes of hyperthyroidism is to check the size of the thyroid gland; someone with factitious hyperthyroidism has a small thyroid gland. The gland is suppressed by the large amount of thyroid hormone. If a radioactive iodine uptake is done (refer to Chapter 4), the person’s thyroid gland won’t absorb a great deal of the iodine.

A large thyroid with many nodules that is exposed to a lot of iodine may trigger hyperthyroidism (see Chapter 9). Sometimes, a single nodule may produce excessive amounts of thyroid hormone and cause the rest of the thyroid to shrink. These conditions are felt by a doctor and confirmed by an ultrasound study or a thyroid scan (refer to Chapter 4).

Occasionally, the thyroid produces large amounts of T3 but normal or even low levels of T4. This condition is called
T3 thyrotoxicosis
. T3 thyrotoxicosis is an autoimmune condition and produces the same signs and symptoms and is treated in exactly the same way as Graves’ disease (which is associated with a high free T4 level). This condition is really just Graves’ disease with a predominance of T3. Doctors don’t yet know why T3 is elevated in these cases rather than T4. If you have the signs and symptoms of hyperthyroidism but your free T4 level is normal or even low, ensure that your doctor measures your T3 level.

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A condition called
subacute thyroiditis
(see Chapter 11) may cause the release of a lot of thyroid hormone from the thyroid and briefly cause hyperthyroidism.

In the condition, the thyroid is usually tender, and the hyperthyroidism does not last.

A certain (not very common) type of tumour called a
choriocarcinoma
, which arises from the placental tissue between a foetus and its mother, produces a lot of a hormone that stimulates the thyroid. This hormone, human chorionic gonadotrophin, can be measured in the blood.

Finally,
central hyperthyroidism
is also possible, although it occurs much less frequently than Graves’ disease. Too much thyrotrophin-releasing hormone from the hypothalamus in the brain, or too much thyroid-stimulating hormone (TSH) from the pituitary gland in the brain (often as a result of a tumour) causes central hyperthyroidism. In this condition, the person’s TSH level is high (whereas with Graves’ disease this level is low). The person may experience symptoms of increased pressure in the brain, such as headache or loss of part of the visual field.

Your doctor shouldn’t have difficulty differentiating Graves’ disease from any of the conditions discussed in this section, especially if the doctor looks for signs that your eyes and skin are changing, and requests tests that check for thyroid autoantibodies.

Choosing the Best Treatment

for Graves’ Disease

The treatment of Graves’ disease has evolved over the years as doctors and researchers have come to understand it better and additional tools have become available. As soon as doctors understood that the thyroid was responsible for the excessive production of thyroid hormones, the obvious response was to cut out the offending tissue. This produced an era of great thyroid surgeons, along with a lot of unexpected problems that are described in the next section. Around 1950, the administration of radioactive iodine (RAI) started to replace surgery and, although it cures many people, the treatment brings its own difficulties. Finally, antithyroid drugs became available.

Each form of treatment has its pros and cons. Interestingly, doctors in Europe generally prefer treating with antithyroid pills, while doctors in the United States are more likely to choose radioactive iodine. The following sections explain the advantages and disadvantages of each form of treatment. As a rule, however, research shows that each form of treatment, whether antithyroid drugs, radioactive iodine, or surgery, is associated with similar improvements in quality of life and similar degrees of patient satisfaction, 11_031727 ch06.qxp 9/6/06 10:43 PM Page 75

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so the choice often comes down to the doctor or patient’s preference. The effectiveness of any treatment is initially monitored by measuring levels of free thyroxine (T4) as low levels of thyroid-stimulating hormone (TSH) often persist for many months despite the proper treatment.

Thyroid surgery

Thyroid surgery involves the removal of all or part of the thyroid gland.

Surgery quickly reduces the symptoms of hyperthyroidism as it removes the source of those symptoms – the thyroid that was producing too much hormone.

With the availability of non-surgical treatments, surgery is rarely done today for hyperthyroidism. Some situations leave surgery as the only choice, such as the following:

ߜ The patient refuses to take radioactive iodine and develops an allergy or a bad reaction to antithyroid pills (or simply fails to take them).

ߜ The thyroid gland is extremely large, which means that radioactive iodine or antithyroid pills are less effective.

ߜ The diagnosis of hyperthyroidism is made during pregnancy and is not properly controlled with antithyroid drugs, causing problems for the mother or the foetus. (Surgery is okay if done between the third and sixth month of pregnancy.)

ߜ The thyroid has nodules that suggest a possible cancer.

One reason why surgery is not often used to treat thyroid conditions these days is that surgery carries certain risks:

ߜ Any operation requiring anaesthesia involves risk.

ߜ Surgery is not safe for someone with severe heart or lung disease.

ߜ Surgery is not advisable during the last three months of pregnancy, because it could induce early labour.

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