Causes of Hyperthyroidism
Broadly speaking, there are four causes of hyperthyroidism—thyroid overstimulation, thyroid nodules, thyroid disruption, and miscellaneous causes.
Diseases Associated with Thyroid Overstimulation : Graves’ Disease
The most common cause of hyperthyroidism in the United States is Graves’ disease, an autoimmune disease characterized by some or all of the following: hyperthyroidism, goiter, eye changes, and skin changes. Autoimmune diseases are characterized by the presence of autoantibodies circulating in the bloodstream. Antibodies are proteins formed by the immune system to protect the body against foreign chemicals, bacteria, and viruses. In an autoimmune disease, antibodies are formed against the body’s own chemicals. Antibodies may be formed against a receptor, the specific site on a cell that captures a chemical such as a hormone. In Graves’ disease, antibodies are formed against the receptors on thyroid follicular cells that capture thyroid-stimulating hormone (TSH). Remarkably, some of these antibodies duplicate the function of TSH and stimulate the thyroid gland to produce and secrete more thyroid hormone than normal. Autoimmune thyroid diseases, such as Graves’ disease and Hashimoto’s thyroiditis,tend to run in families and are more common in women.
It is not unusual for several generations of women to have either Graves’ disease and hyperthyroidism or Hashimoto’s thyroiditis and hypothyroidism. Patients who have Graves’ disease should tell members of their families—especially their mothers, daughters, sisters, aunts, and nieces—about their condition so that they are aware that there is a hereditary thyroid disease in the family. At least 50% of patients with Graves’ disease will have the antibodies found in Graves’ disease as well as the antibodies characteristic of Hashimoto’s thyroiditis.
A disrupted thyroid gland releases stored thyroid hormone into the bloodstream. Disruption of the thyroid gland is seen in certain types of thyroiditis, which are transient or temporary, including: subacute thyroiditis, postpartum thyroiditis, painless thyroiditis, radiation-induced thyroiditis, and acute suppurative thyroiditi.
Toxic Thyroid Nodules and Toxic Multinodular Goiters
Autonomous function describes the function of a part of the thyroid gland that acts independently of normal control mechanisms. If a thyroid nodule fails to turn off its production of thyroid hormone, it is referred to as an autonomously functioning thyroid nodule or toxic autonomously functioning nodule. An autonomously functioning thyroid nodule is indicated by an increased uptake of radioactive iodine by the nodule. Since uptake of radioactive iodine is greater in the autonomously functioning thyroid nodule than in the surrounding tissue, it is referred to as a hot nodule.
When a thyroid gland containing more than one nodule has one or more autonomously functioning nodules producing sufficient thyroid hormone to cause hyperthyroidism, it is referred to as a toxic multinodular goiter.
Thyroid Overstimulation: Iodine-Induced Hyperthyroidism
Ingestion of excessive iodine can occasionally induce hyperthyroidism in susceptible patients, particularly ones with long-standing multinodular goiters. Iodine-induced hyperthyroidism may also occur weeks to months after exposure to x-ray dyes with iodine, such as those used in CT scans and heart catheterizations.
Symptoms of Hyperthyroidism
There are numerous signs and symptoms of hyperthyroidism. Hyperthyroid patients may have none, some, or many of these signs and symptoms, depending upon the severity of their disease. Patients may also have many of these signs and symptoms and not be hyperthyroid. Therefore, hyperthyroidism cannot be diagnosed by signs and symptoms alone. The diagnosis can only be confirmed after a thorough medical history, physical examination, and the appropriate laboratory tests.
Some Common Signs and Symptoms of Hyperthyroidism
- hair loss
- shortness of breath
- heart murmur
- smooth skin
- generalized itching
- muscle weakness
- feeling hot
- increased perspiration
- moist, wet, red palms
- difficulty sleeping
- fast, strong, or irregular heartbeat
- poor memory
- inability to concentrate
- sudden mood swings
- “racing heart”
- delusions of grandeur
- increased number of bowel movements
- weight loss, in spite of increased appetite
- swollen fingertips
- swollen lymph glands
- retracted eyelids
- menstrual problems
- decreased or increased sexual interest
- fingernails separating from nail beds
Hyperthyroid patients most commonly voice complaints of fatigue, nervousness, irritability, increased sweating, feeling hot all the time (heat intolerance), insomnia, racing heart, hair loss, and poor memory. Many times patients do not realize that they have a poor memory or an inability to concentrate, or that they have become very difficult to live with. Some patients experience a change in libido (interest in sex); it is usually decreased but, in unusual cases, a patient’s appetite for sex may increase tremendously.
Another common symptom in hyperthyroid patients is weight loss in spite of an increased appetite. Overweight patients who lose weight effortlessly from hyperthyroidism are often overjoyed. However, the weight lost is primarily from muscle as opposed to fat, and is frequently accompanied by muscle weakness. Muscle weakness from hyperthyroidism is characterized by an inability to climb stairs or to get up from a deep couch. Other patients may experience difficulty in holding their arms up while brushing their hair or teeth.
When hair loss (alopecia) occurs, patients may also become very frustrated. Stress, hypothyroidism, and, in women, too much male hormone may also cause hair loss. Hair loss due to hyperthyroidism is temporary; the hair will grow back within three to six months after the patients have been successfully treated. Hyperthyroid patients who develop either shortness of breath from muscle weakness or palpitations (a racing and pounding heart) may think that they have developed a heart condition. In hyperthyroid patients with otherwise healthy hearts, palpitations and shortness of breath neither signify the presence of heart disease nor pose a danger to the heart.
The symptoms of hyperthyroidism in older patients may be somewhat different than those in younger patients. For example, apathy may be the only symptom of hyperthyroidism in patients over sixty years of age. This situation occurs often enough that it has been given its own name, apathetic hyperthyroidism.
Testing for Hyperthyroidism
Diagnosis of Hyperthyroidism
Ordinarily, the diagnosis of hyperthyroidism is confirmed by the presence of the typical signs and symptoms, a low TSH level, and elevated thyroid hormone levels. A low TSH level with normal thyroid hormone levels is diagnostic of subclinical hyperthyroidism. A radioactive iodine uptake and thyroid imaging are instrumental in distinguishing among the different causes of hyperthyroidism. This distinction is critical since some types of hyperthyroidism, such as Graves’ disease, are permanent and require definitive therapy, while other types are temporary and respond to symptomatic treatment and the passage of time.
Some Common Testing for Hyperthyroidism
Thyroid-Stimulating Hormone (TSH) is usually low in hyperthyroid patients. There are exceptions such as patients with TSH-producing tumors of the pituitary gland who can be hyperthyroid with a normal or high TSH. Some older patients will have low TSH levels without being hyperthyroid, and many critically ill patients with non-thyroid illnesses will also have low TSH levels. A thyrotropin-releasing hormone (TRH) test is sometimes necessary to confirm that the TSH is truly suppressed.
Most hyperthyroid patients will have high free T4 and high free T3. Ordinarily, only free T4 is measured because this test is more readily available. On the other hand, in some hyperthyroid patients, only free T3—and not free T4—is elevated. It is particularly important to measure free T3 before making the diagnosis of subclinical hyperthyroidism.
Autoantibodies to the TSH receptor (TRAb) are usually found in patients with Graves’ disease. These antibodies are measured by different methods and, therefore, may go by different names such as thyroid stimulating immunoglobulins (TSI).
Radioactive Iodine Uptake and Thyroid Imaging
The radioactive iodine uptake (RAIU) is essential in distinguishing among different causes of hyperthyroidism. The amount of radioactive iodine taken up by the thyroid gland is suppressed in some forms of hyperthyroidism, whereas it is elevated in Graves’ disease. Thyroid imaging may also be very useful in distinguishing Graves’ disease from a toxic autonomously functioning thyroid nodule or a toxic multinodular goiter.
Sedimentation rate testing helps to distinguish subacute thyroiditis from other causes of hyperthyroidism.
Thyroglobulin (Tg) levels will be elevated in all patients with hyperthyroidism except in patients who have taken too much thyroid hormone.
Treatment for Hyperthyroidism
The treatment of patients with hyperthyroidism depends upon both the cause and the severity of the disease. Patients with temporary forms of hyperthyroidism due to disruption of the thyroid gland require only symptomatic treatment and the passage of time.
Almost all patients with permanent forms of hyperthyroidism, such as Graves’ disease, toxic autonomously functioning thyroid nodules, and toxic multinodular goiters, require definitive treatment. Infrequently, Graves’ hyperthyroidism disappears without any treatment (spontaneous remission). There is no way of predicting which patients will have spontaneous remissions or how long the remissions will last. Unfortunately, spontaneous remissions of Graves’ hyperthyroidism do not occur often enough to warrant delaying treatment.
Certain drugs are used to treat only the symptoms of hyperthyroidism without having a significant effect upon the function of the thyroid gland; they simply make patients feel better. For example, some patients with hyperthyroidism experience insomnia and severe anxiety. Sleeping medications and drugs for anxiety may be prescribed to relieve these symptoms until the hyperthyroidism is controlled. Similarly, some beta-blockers will slow down the heart rate and reduce the tremor seen in hyperthyroid patients.
Further reading: Hyperthyroidism Treatments and drugs – Mayo Clinic
Treatment for Graves’ Hyperthyroidism
In considering treatment options for patients with Graves’ hyperthyroidism, it is helpful to bear in mind the following:
- Symptoms of untreated hyperthyroidism from Graves’ disease may wax and wane over a period of months or years.
- Often, the end result of untreated Graves’ hyperthyroidism is hypothyroidism—the thyroid gland “burns out” after ten to twenty years.
- The course of Graves’ eye disease and the course of Graves’ hyperthyroidism are independent of one another. The eye disease charts its own course, even with successful treatment of the hyperthyroidism.
The three basic treatment options for patients with Graves’ hyperthyroidism are:
- radioactive iodine
- antithyroid drugs – propylthiouracil (PTU) or Tapazole (methimazole)
- surgery (thyroidectomy)
The majority of endocrinologists in the United States prefer radioactive iodine to treat patients with Graves’ hyperthyroidism. The treatment is simple, effective, relatively inexpensive, and safe. Many patients ask how it is possible to ablate (destroy) the thyroid gland with the radioactive material without harming any other part of the body. The thyroid gland actively takes up significantly more iodine than any other part of the body; the salivary glands are the only other glands that take up any iodine at all. Therefore, administered radioactive iodine is taken up almost exclusively by the thyroid gland. The overactive thyroid gland gets the full impact of the radiation, while the rest of the body is unaffected.
The following statements are intended to clarify some of the fears about radioactive iodine treatments:
- Radioactive iodine is usually given in liquid or capsule form.
- It is tasteless.
- Side effects are rare.
- Because radioactive iodine passes into breast milk, breastfeeding mothers are asked to wean their babies before treatment.
- It typically takes six weeks after treatment before thyroid hormone production is noticeably reduced.
- In most cases, patients become hypothyroid within three to six months after treatment.
- In more than 90% of patients, only one treatment is required. If patients are still hyperthyroid six months later, they may need a second dose of radioactive iodine.
- Radioactive iodine will not make patients glow in the dark!
It may seem radical to destroy the thyroid gland with radioactive iodine. However, even when patients do not receive treatment, hypothyroidism usually occurs within one or two decades after the onset of Graves’ hyperthyroidism because the thyroid gland eventually “burns out”. With this realization in mind, ablation of the thyroid gland with radioactive iodine does not seem nearly as radical. After a thyroid ablation, patients will require monitoring by a physician for a response to the therapy and testing for hypothyroidism. Once the diagnosis of hypothyroidism is confirmed, levothyroxine therapy is started.