Thyrotoxicosis: Characteristics, Diagnosis, Treatment and Causes

Also called “Basedow’s disease,” it is a syndrome characterized by excessive circulating thyroid hormones in the blood plasma.

Technically, Thyrotoxicosis refers to too much thyroid hormone in the body. Hypothyroidism is when Thyrotoxicosis is due to the overproduction of thyroid hormone by the thyroid gland.

Graves disease

Grave’s disease is the most common cause of hyperthyroidism in Canada. Graves’ disease owes its name to the Irish doctor (Robert Graves). It is sometimes referred to as Basedow’s disease by the German doctor (Karl von Basedow), who also described cases.

Graves’ disease affects approximately one in 100 people. The disease has a genetic component, although not all members of affected families will suffer from this condition. It is more common in women than in men and in smokers compared to non-smokers.

Thyroid Stimulating Immunoglobulin / Antibodies Thyroid Stimulating Hormone Receptors (TSH)

Graves disease is an autoimmune disorder. It is caused by an abnormal protein known as thyroid-stimulating immunoglobulins or TSH receptor antibodies. These antibodies stimulate the thyroid gland to produce large amounts of thyroid hormone (T4 and T3) uncontrolled.

Antibodies are part of the immune system, generally essential to fight infections. Under autoimmune conditions, such as Graves’ disease, the immune system of a susceptible person is activated to produce antibodies that bind to the tissues themselves and can cause health problems.

The trigger for TSH antibody production in Graves is often unclear.


Clinical characteristics of Thyrotoxicosis

The symptoms and signs of Graves’ hyperthyroidism are due to the effects of excess thyroid hormone on the function and metabolism of the body. Common symptoms include weight loss, nervousness, irritability, heat intolerance, excessive sweating, tremors, palpitations, increased bowel movements, and muscle weakness.

Other signs include a rapid pulse, loss of body fat and muscle mass, enlargement of the thyroid (goiter), fine tremors of the fingers, and warm, moist and velvety skin.

Clinically evident ocular signs ( ophthalmopathy ) can occur in patients with Graves’ disease. Fortunately, only about 5% are severe. The eyes protrude from their sockets, can be red and watery, and have swollen eyelids.

The eyes often do not move normally because the swollen eye muscles can not work accurately, and patients can experience double vision. Smokers with Graves’ disease have an increased risk of eye disease; This risk can be reduced by quitting smoking.

Some patients with hyperthyroidism but without Graves’ eye disease may have the appearance of slightly bulging eyes due to spasms of the eyelid muscle, resulting in a fixed formation.

Thyroid hormones have a wide variety of effects on the body, and the symptoms and signs of hyperthyroidism and Thyrotoxicosis reflect this. In simple terms, all metabolic processes are “accelerated.”

For example, the pulse rate may be rapid and occasionally irregular (atrial fibrillation), bowel function may increase, and sweat glands may function excessively. The patient may become more irritable or anxious.

Despite the increase in appetite, the patient can lose weight because food intake can not keep pace with the increase in metabolism. Some patients may gain weight if the appetite increase is more profound than the increase in metabolism.


Thyrotoxicosis is suspected based on the symptoms and signs described above and is confirmed by measuring the stimulating thyroid hormone (TSH) level in the blood.

If TSH is suppressed, it indicates too much thyroid hormone and that blood levels of thyroid hormones (free T4 and T3) are measured to confirm the diagnosis.

Occasionally, the clinical presentation is sufficiently suggestive of Graves, so it is unnecessary to perform more tests.

Suppose there are doubts about the cause of the Thyrotoxicosis and radioactive iodine scintigraphy. In that case, the measurement of antibodies against the TSH receptor or thyroid ultrasound can help distinguish serious from other conditions. It can be ordered according to the specific situation.

Treatment of Thyrotoxicosis

Currently, there is no specific treatment for the underlying abnormality (TSH receptor antibodies) that causes hyperthyroidism in Graves’ disease.

Since the result of this problem is an overstimulation of the thyroid function, the treatment requires blocking the production of thyroid hormone with antithyroid drugs, destroying the thyroid cells with radioactive iodine, or surgically removing the thyroid gland (thyroidectomy).

Some patients will be prescribed a beta-blocker medication until the thyroid hormone levels can be normalized. The beta-blocker can help with some symptoms of Thyrotoxicosis, especially rapid heart rate and tremor, but do not decrease thyroid hormone levels.

Antithyroid drugs

Antithyroid drugs (Propylthiouracil (PTU) and Methimazole are the only ones available in Canada) are often the first treatment given for Graves’ disease.

These drugs partially block the production of thyroid hormone by the thyroid. Therefore, thyroid hormone levels decrease, but they will not return to normal immediately; It often takes weeks.

These medications can be used as initial treatment for patients with Graves’ disease since there is a 50% chance that hyperthyroidism will go into remission. Antithyroid drugs can also be used to reduce thyroid hormone levels while planning for ablation or radioactive iodine surgery.

Often, if a patient does not go into remission after 1-2 years of treatment with antithyroid drugs, or if after antithyroid medications are stopped, hyperthyroidism recurs, then ablation or radioactive iodine surgery can be recommended for definitive treatment.

A small percentage of patients suffer side effects that can rarely be serious (liver problems, low white blood cell count).

Due to recent evidence of an increased risk of side effects of Propylthiouracil on liver function, especially in children, the Food and Drug Administration (FDA) of the United States has issued a warning for its use.

These drugs can sometimes be used to control hyperthyroidism during pregnancy. However, there are rare risks for mothers and fetuses with both drugs and the decision on which medicine to use in each trimester of pregnancy is controversial. It is preferable to treat hyperthyroidism before considering pregnancy.

Radioactive iodine

Radioactive iodine is a safe and effective treatment for Graves’ hyperthyroidism. However, it occasionally aggravates eyesight in patients with Graves’ eye disease, especially if they are also smokers. Preventive therapy with corticosteroids is sometimes justified.

In patients with severe active eye disease, radioactive iodine can be prevented or delayed until the eye disease improves. Radioactive iodine is usually administered in the form of a capsule or clear liquid. Because radioactive iodine takes several weeks or months to full effect, antithyroid tablets are sometimes given until the full impact occurs.

Occasionally (10-20% of patients), hyperthyroidism persists or recurs after treatment with radioactive iodine, but if so, a second dose almost always resolves hyperthyroidism. Most patients develop an underactive thyroid (hypothyroidism) after treatment with radioactive iodine and require lifelong thyroid hormone replacement therapy.

It is essential to control the blood tests of the thyroid in patients who follow radioactive iodine to evaluate the effectiveness of the treatment and control both hyperthyroidism and hypothyroidism.

Thyroidectomy (thyroid surgery)

Surgery may be recommended for patients in whom the goiter is so large that it causes discomfort or significant blockage of the trachea or passage of food (esophagus) or in cases where rapid hyperthyroidism is necessary (for example, cardiac arrhythmia is challenging to manage ).

Thyroidectomy is the treatment of choice if a patient has known or suspected thyroid cancer in addition to Graves’ disease. Thyroidectomy may be considered in patients with severe Graves’ eye disease who desire definitive treatment.

Thyroidectomy is an acceptable treatment for Graves’ disease, but it is not used as frequently as antithyroid drugs or radioactive iodine due to its invasiveness. Thyroidectomy requires admission to the hospital for approximately two days and removal of the gland (by an experienced surgeon).

After the thyroid gland is removed, patients should take thyroid hormone replacement for the rest of their lives to avoid hypothyroidism.

Other causes of hyperthyroidism

In Canada, Graves’ disease represents at least 90% of all patients with hyperthyroidism. Hyperthyroidism can also occur in patients with nodular goiter or due to a benign thyroid nodule that produces an excess of thyroid hormone.

Thyrotoxicosis can also be caused by thyroiditis (inflammation of the thyroid), where the thyroid is damaged, and the thyroid hormone is filtered into the circulation, temporarily increasing the levels of thyroid hormone until this excess thyroid hormone is metabolized or excreted.

The most common thyroiditis (subacute thyroiditis) is caused by a viral infection and is painful. Silent thyroiditis is a similar condition, but without the painful swelling of the thyroid (see Health Guide 6: Thyroiditis).

Silent thyroiditis is due to destructive antibodies and often occurs in the postpartum period (a couple of months after delivery). Some other rare causes of hyperthyroidism do not need to be discussed here.