Living Well with Graves' Disease and Hyperthyroidism: What Your Doctor Doesn't Tell You...That You Need to Know

INTRODUCTION

I’ve been a thyroid patient advocate for nearly 10 years, and I’ve received many e-mails from patients throughout this time. Sometimes the notes are despondent. Sometimes they are adamant. But almost always they tell a story like Audrey’s:

I was very tired. As time passed, I got more and more tired, where I couldn’t keep my eyes open. First, the muscles in my legs and then the muscles in my arms became very painful. I couldn’t raise my legs 2 inches off the floor or raise my arms straight up! My eyes bulged; I lost hair; I lost weight; I had jaundice; I had tremors. Finally, a lump appeared on my throat. Writing this out for you, I have tears in my eyes. Through all this, not one doctor picked up on the problem. I was told I was a hypochondriac. Finally, after seeing the lump, my doctor sent me for an ultrasound test and then nuclear testing. Finally, I was diagnosed with Graves’ disease. Imagine the shock on my doctor’s face and his embarrassment.

Lorrie’s experience is also quite common:

I felt kind of off. Nothing so serious that I was suffering terribly, but just not feeling myself. I started a job and soon was plagued by anxiety, stomach problems, heart palpitations, mood swings, and hot flashes. The doctors—I was sent to a gastroenterologist, a psychologist, a general practitioner, a gynecologist, and an allergist—did not have a clue what was wrong with me. They wrote it off to stress and having a sensitive stomach. I continued enduring the symptoms and hoping that they would go away.

I tried to change things about my life in hopes that it would help. But five years after making dietary changes, lifestyle changes, changing my career, and moving cross-country, things were worse. I had even worse heart palpitations, achy joints, breathing problems, and I could not keep weight on. I ate enormous amounts of food that barely allowed me to maintain my weight. So I started the doctor circuit again. The allergist claimed I had asthma and gave me an inhaler. That inhaler nearly killed me one day while exercising because it sent my already skyrocketing heart rate into the stratosphere. Finally, all my symptoms and the fact that my hands were shaking violently clicked with my general practitioner and she gave me a thyroid blood test. I was suffering with severe hyperthyroidism that had gone undetected for years.

Unfortunately, Audrey and Lorrie are not alone. Millions of people in the United States, the majority of whom are women, are suffering from Graves’ disease and hyperthyroidism—conditions that seriously disrupt quality of life and can be fatal if left untreated over time.

I wrote this book to help you determine if you have the symptoms of Graves’ disease and hyperthyroidism. Then you’ll find information to help you get the proper diagnosis, and perhaps most importantly, how to navigate the confusion of treatment options that range from antithyroid drugs to permanent, irreversible treatment such as radioactive iodine to the thyroid or surgery. Finally, the end result for most people treated for Graves’ disease and hyperthyroidism is the opposite condition, hypothyroidism, which means living with an underactive thyroid. You’ll learn how to manage that part of the disease as well, along with common and persistent symptoms such as weight gain, fatigue, depression, and hair loss. You’ll also learn how to have a healthy pregnancy.

This book is for you if

You strongly suspect you have Graves’ disease and/or hyperthyroidism but are having difficulty getting a diagnosis by conventional means.

You aren’t sure if your various symptoms point to hyperthyroidism and you need to find out.

You’ve been diagnosed with Graves’ disease and/or hypothyroidism and have been told that you need to have a particular treatment right away. You want more information before you commit to decisions that may affect your health for the rest of your life.

You have in the past or are currently being treated for Graves’ disease or hyperthyroidism and are still struggling to feel well.

You are receiving what your doctor feels is sufficient treatment, yet you still don’t feel well.

You’re an open-minded health practitioner looking for innovative ways to understand and help your patients with Graves’ disease and hyperthyroidism.

You want to learn about living well with Graves’ disease and hyperthyroidism from the perspective of empowered patients and caring practitioners.

Before I go any further, I think it might be useful to explain my own background. I’m not a doctor. I’m not a health professional. I have a degree in international studies from Georgetown University. In 1997, my battle with my own health led me to start and manage a popular patient-oriented Web site on thyroid disease as well as launch the only monthly report on conventional and alternative thyroid-related health news and treatments. Ultimately, this has turned into my mission as a patient advocate and health writer for books, Web sites, newsletters, and magazines.

As a Hashimoto’s thyroiditis patient myself, I’ve had periods of Hashitoxicosis, or Hashimoto’s-induced hyperthyroidism. Truly, I thought I was going mad. I felt agitated; my skin felt hot; my eyes were spasming, jumpy, and twitching. My eyes got so dry that everything was blurry and I couldn’t drive at night. I could barely concentrate or focus on anything. I was exhausted, but I was restless and anxious when I tried to sleep. Everything I ate went right through me. And I consider myself fortunate because these miserable periods of hyperthyroidism—among the worst times in my life healthwise—were temporary flares in a disease that otherwise has caused me to have an underactive, underfunctioning thyroid.

I have written this book for the millions for whom Graves’ disease and hyperthyroidism is not a temporary flare—it’s a permanent, debilitating condition that can force you to live in a chronic state of poor health if untreated. If you have yet to be diagnosed, you may be mistakenly told that you have panic disorder or bipolar disease. Your friends and family may even accuse you of being anorexic. And you may be going from doctor to doctor looking for answers. I hope you’ll find the answers you need here.

I’ve also written this book for those who have been diagnosed and are looking for ways to understand the various treatments. It’s not enough that radioactive iodine is the standard of care in the United States. You want to know whether there are options that are less drastic and less permanent, or even natural/alternative medicine options. Again, I hope you’ll find the answers and support you need here. Finally, by bringing you the stories of the gracious patients who have shared their own experiences, as well as the innovative and compassionate doctors who have taken the time to provide input on their treatment approaches, I want you to have hope—hope in the realization that you are not alone and hope in a future of living well with Graves’ disease and hyperthyroidism.

PART ONE

Understanding Graves’ Disease and Hyperthyroidism

1

Your Thyroid, Graves’ Disease, and Hyperthyroidism

What Is the Thyroid?

The word thyroid comes from the Greek word thyreoeides, meaning shield-shaped. The two lobes of the thyroid are known as the wings of the butterfly and the area connecting the two lobes is known as the isthmus. Generally speaking, a gland is a discrete and separate soft body made up of a large number of vessels that produce, store, and release—or secrete—some substance. The thyroid is a small gland normally weighing only about an ounce. It is located in the lower part of the neck in front of the windpipe. You’ll know where the thyroid is if you think of it as sitting behind your Adam’s apple.

Glands that secrete their products inside the body, and more specifically those that secrete hormonal and metabolic substances, are known as endocrine glands. This makes your thyroid an endocrine gland, along with the parathyroids, the adrenal gland, the pancreas, and the pituitary gland. Diabetes, like thyroid disease, is considered an endocrine disorder. A doctor who specializes in treating patients with endocrine problems is called an endocrinologist.

Hormones are internal secretions carried in the blood to various organs. Your thyroid’s main purpose is to produce, store, and release two key thyroid hormones: triiodothyronine (T3) and thyroxine (T4). The numbers refer to the amount of iodine molecules attached to each hormone. Thyroid cells absorb iodine. The thyroid obtains iodine through food, iodized salt, and supplements, then combines it with the amino acid tyrosine, converting the iodine/ tyrosine combination into T4 and T3.

A healthy, functioning gland produces about 80 percent T4 and 20 percent T3. T3 is, however, the biologically active hormone that is used by the cells and is several times stronger than T4. The body converts the inactive T4 it produces to active T3 by removing one iodine molecule. This process is sometimes referred to as T4 to T3 conversion, or by the more scientific term monodeiodination. This conversion can take place in organs other than the thyroid, including the hypothalamus, a part of your brain.

T4 and T3 exist in two forms: free/unbound and bound. Free or unbound T4 or T3 is biologically active, and the bound part is bound to the thyroxine-binding globulin (TBG) protein. When measured in the blood, the free or unbound T4 and T3 levels tend to be most representative of the actual hormone available for use by the body.

The role of thyroid hormones is to control your metabolism—the process by which oxygen and calories are converted to energy for use by your cells and organs. There’s not a single cell in your body that doesn’t depend on thyroid hormones for regulation and for energy in some form. Thyroid hormones have a number of functions as they travel through the bloodstream:

Thyroid hormones help cells convert oxygen and calories into energy.

Thyroid hormones help you properly process carbohydrates.

Thyroid hormones aid in the proper functioning of your muscles.

Thyroid hormones help your heart pump properly and effectively.

Thyroid hormones help you breathe normally.

Thyroid hormones help your intestinal system properly digest and eliminate food.

Thyroid hormones help strengthen your hair, nails, and skin.

Thyroid hormones help your brain function properly.

Thyroid hormones help with proper sexual development and functioning.

Thyroid hormones help with normal bone growth.

Now that you have some idea of what the thyroid is and its location and function, let’s look in more detail at how it fits into the overall functioning of the body.

The Thyroid Gland: Setting the Pace

When your thyroid works normally, it produces and secretes the amount of T4 and T3 necessary to keep various bodily functions moving at their proper pace. However, the thyroid does not do this alone. It works as part of a bigger system that includes the pituitary gland—an endocrine gland located at the base of your brain—and the hypothalamus.

Here’s how the system works. The hypothalamus constantly monitors the pace of many of the body’s functions. It also observes and reacts to a number of other factors, including environmental conditions such as heat, cold, and stress. If the hypothalamus senses that certain adjustments are needed to react to any of these factors, it produces thyrotropin-releasing hormone (TRH).

TRH is sent from the hypothalamus to the pituitary gland. The pituitary gland then produces a substance called thyrotropin, better known as thyroid-stimulating hormone (TSH). The pituitary gland also monitors the body and can release TSH based on the thyroid hormones circulating in your blood. TSH is sent to the thyroid gland, where it causes your gland to produce, store, and release more T3 and T4.

Released thyroid hormones are carried through the bloodstream by a plasma protein known as thyroxine-binding globulin (TBG). Now in the bloodstream, the thyroid hormone travels throughout the body, carrying orders to various organs. Upon arriving at a particular tissue in the body, thyroid hormones interact with receptors located inside the nucleus of your cells. Interaction of the hormone and the receptor will trigger a certain function, giving directions to that tissue regarding the rate at which it should operate.

When the hypothalamus senses that the need for increased thyroid hormone production has ended, it reduces production of TRH, which causes the pituitary to decrease production of TSH, which then slows production of thyroid hormone. This system keeps many of the body’s organs working at the proper pace.

Think of the entire feedback loop as resembling the thermostat in your house. It’s set to maintain a particular temperature, and when it detects that your house has become too hot, it signals the heating system to stop blowing heat. Similarly, when the house becomes too cold, the heat will kick on (or the air conditioning will turn off). Like a thermostat set to a particular temperature, your body is wired to maintain a certain level of circulating thyroid hormone function. When thyroid disease or conditions interfere with the system and the feedback process doesn’t work, thyroid problems can develop.

The Prevalence of Thyroid Problems

Thyroid problems are widespread. It’s estimated that more than 200 million people worldwide have thyroid disease. Thyroid problems are particularly common in areas covered at one time by glaciers, where iodine is not present in the soil and in foods. In many of these countries, an enlarged thyroid known as goiter is seen in as many as one in five people, and it is usually due to iodine deficiency. An estimated 8 percent of the world population has goiter, mostly women. Thyroid problems, including autoimmune thyroid disease and thyroid cancer, are also more common in the areas around and downwind of the 1986 Chernobyl nuclear accident.

There are a minimum of 25 million people in the United States with thyroid disease, and as many as half of them are undiagnosed. In the United States, thyroid disease prevalence increases with age: one in five women may develop a thyroid problem. Generally, women are seven times more likely than men to develop thyroid conditions.

It’s thought that Graves’ disease and hyperthyroidism affect slightly less than 1 percent of the U.S. population, or slightly less than 2.9 million people. Some experts believe, however, that as many as 4 percent of Americans, or 11.8 million people, may have mild, subclinical Graves’ disease, with little or no symptoms but with blood test evidence of slight hyperthyroidism.

The prevalence of Graves’ disease is similar among Caucasians and Asians, and it is slightly lower among African-Americans. Graves’ disease and hyperthyroidism affect women eight times more often than men. Graves’ disease accounts for more than 95 percent of childhood hyperthyroidism, so it’s thought that the prevalence of Graves’/hyperthyroidism in children is approximately 0.02 percent. Children make up only 5 percent of all Graves’ and hyperthyroidism patients.

The mortality rate for untreated Graves’ disease and hyperthyroidism is as high as 11 percent. In the United States, however, going without treatment is extremely rare, and when death is associated with these conditions, it’s primarily in the elderly and is typically due to related heart problems.

Thyroid Conditions

There are a number of conditions that can affect the function and structure of the thyroid.

Hypothyroidism/Underactive Thyroid

Hypothyroidism means there is too little thyroid hormone. This can be due to a thyroid that is not producing enough hormone, treatment with radioactive iodine, drugs or nutritional deficiencies, or dysfunction due to nodules, infection, or atrophy. When the thyroid is partially or totally removed as a treatment for cancer, nodules, goiter, Graves’ disease, or hyperthyroidism, the vast majority of patients become permanently hypothyroid. A small number of infants are born with congenital hypothyroidism—that is, either without a thyroid or with a nonfunctioning thyroid. Hypothyroidism is treated with thyroid hormone replacement drugs to provide the body with the thyroid hormone that the gland isn’t able to produce.

Hyperthyroidism/Overactive Thyroid (Thyrotoxicosis)

Thyrotoxicosis refers to the various effects of exposure to too much thyroid hormone. Hyperthyroidism implies that this excess of hormones originated in the thyroid gland itself and not, for example, by taking too many thyroid hormone drugs. Hyperthyroidism can be caused by a number of thyroid problems, including autoimmune thyroid disease, nodules that produce thyroid hormone, overdosage of thyroid hormone replacement drugs, infection, and other causes. Hyperthyroidism is typically treated with drugs to reduce the thyroid’s ability to produce hormones, by radioactive iodine treatment to chemically deactivate the thyroid (a treatment known as ablation), or by surgery.

Goiter/Enlargement

Goiter refers to an enlargement of the thyroid gland. The gland can grow as a response to deficiencies of iodine, thyroid inflammation or infection, or autoimmune disease. Particularly large goiters may be cosmetically unattractive and can compromise breathing and swallowing, so they are often surgically removed. Smaller goiters may respond to drug treatment.

Nodules/Lumps

Many people have nodules in the thyroid, but few are palpable (capable of being felt externally). In some cases, nodules on the thyroid exist without any disease and cause no symptoms. A very small percentage of nodules are cancerous, in which case the entire thyroid is usually surgically removed. The vast majority of nodules are benign; however, they may impair the thyroid’s ability to function properly and may cause hypothyroidism, or they may themselves emit excess thyroid hormone and cause hyperthyroidism. Particularly large nodules that compromise breathing or swallowing are usually surgically removed. Smaller nodules frequently respond to drug treatment.

Thyroid Diseases

A variety of diseases affect the thyroid and trigger thyroid conditions.

Autoimmune Thyroid Disease

There are two different autoimmune diseases in which an immune system dysfunction targets the thyroid: Graves’ disease and Hashimoto’s disease. In the United States, the vast majority of thyroid patients are either hypothyroid or hyperthyroid due to an autoimmune disease. Graves’ disease—sometimes referred to as diffuse toxic goiter because of the usual presence of a goiter—typically causes hyperthyroidism. In Graves’ disease, autoantibodies bind to the gland, which causes hyperthyroidism. Treatment usually involves antithyroid drugs, radioactive iodine ablation, or surgical removal of the thyroid, with the goal being euthyroidism—normal thyroid function—or hypothyroidism. Most Graves’ disease patients end up hypothyroid over time, requiring lifelong thyroid hormone replacement.

Hashimoto’s disease is the most common form of thyroiditis—an inflammation of the thyroid—so the condition is often referred to as Hashimoto’s thyroiditis. It is far more common than Graves’ disease and is the cause of most hypothyroidism in the United States. In Hashimoto’s, antibodies react against proteins in the thyroid, causing gradual destruction of the gland itself. Before the thyroid is destroyed, it has occasional thyrotoxic periods known as Hashitoxicosis during which the thyroid overproduces thyroid hormone. Eventually, however, the gland’s attack on itself destroys the ability to produce thyroid hormones. Typically, treatment involves lifelong thyroid hormone replacement.

Toxic Multinodular Goiter/Toxic Adenoma/Plummer’s Disease

Toxic multinodular goiter, also known as toxic adenoma or Plummer’s disease, describes a condition where the thyroid is enlarged and contains nodules that produce thyroid hormone, causing hyperthyroidism. Treatment usually involves antithyroid drugs, radioactive iodine ablation, or surgical removal of the thyroid. Most patients end up hypothyroid, requiring lifelong thyroid hormone replacement.

Thyroid Cancer

Thyroid cancer is one of the least common cancers in the United States. It is characterized by malignant nodules of the thyroid. Most cases are treatable with surgical removal of the gland, and patients have excellent long-term survival rates. Because the entire thyroid is usually removed, almost all thyroid cancer patients end up hypothyroid and need thyroid hormone replacement for the rest of their life.

Thyroiditis

While Hashimoto’s disease is by far the most common form of thyroiditis, there are other forms that also involve inflammation of the thyroid gland:

De Quervain’s thyroiditis, granulomatous thyroiditis, painful thyroiditis, subacute thyroiditis: a viral-induced thyroiditis that can have a thyrotoxic phase

Painless thyroiditis, silent thyroiditis, lymphocytic thyroiditis: a temporary thyroid condition that may involve mild hyperthyroidism during its thyrotoxic phase followed by a period of hypothyroidism before returning to normal

Postpartum thyroiditis: a form of painless or silent thyroiditis that affects as many as 5 to 9 percent of women within a year of giving birth and typically starts with a thyrotoxic period of hyperthyroidism

Acute suppurative thyroiditis: a rare situation where the thyroid is infected with bacteria and abscessed

Thyrotoxicosis and Hyperthyroidism

Most doctors, except perhaps endocrinologists who specialize in thyroid treatment, tend to use the terms hyperthyroidism and thyrotoxicosis interchangeably, but this is not technically correct. Thyrotoxicosis refers to the various symptomatic and biochemical effects of exposure to too much thyroid hormone. In thyrotoxicosis, it doesn’t matter whether the thyroid gland is the main source of that excess hormone or not.

In contrast, hyperthyroidism—which is a type of thyrotoxicosis—implies that the excess of thyroid hormone comes from overactivity of the thyroid gland itself. In hyperthyroidism, the thyroid synthesizes and releases thyroid hormone more quickly than normal. Dr. Glenn Rothfeld describes the idea of hyperthyroidism well in his book, Thyroid Balance, when he says that it’s like having a stuck accelerator in your car, continually flooding the engine with gasoline.

Causes of Thyrotoxicosis

Hyperthyroidism causes 85 to 90 percent of all thyrotoxicosis cases. Subsequently, almost all hyperthyroidism is caused by Graves’ disease (also known as diffuse toxic goiter). The causes of hyperthyroidism and thyrotoxicosis are listed in the following table, and are explained in this chapter.

CAUSES OF THYROTOXICOSIS

Hyperthyroidism (causes 85–90% of all thyrotoxicosis)

Graves’ Disease (the primary cause of most hyperthyroidism)

Toxic Multinodular Goiter/Toxic Adenoma/Plummer’s Disease

Toxic Adenoma/Autonomous Nodule

De Quervain’s Thyroiditis/Granulomatous Thyroiditis/Painful Thyroiditis/Subacute Thyroiditis

Painless Thyroiditis/Silent Thyroiditis/Lymphocytic Thyroiditis

Postpartum Thyroiditis

Hashimoto’s Disease/Hashitoxicosis

Transient Hyperthyroidism of Hyperemesis Gravidarum (THHG)

Trauma to the Thyroid

Thyrotoxicosis Causes Not Induced by Gland Overproduction (cause 10–15% of all thyrotoxicosis)

Factitious Thyrotoxicosis/Thyrotoxicosis Factitia/Iatrogenic Thyrotoxicosis

Iodide-Induced Thyrotoxicosis/Jod-Basedow Syndrome

Drugs

Organ Donations

Struma Ovarii

Follicular Thyroid Cancer

Pituitary Adenoma

Molar Pregnancy/Choriocarcinoma/Human Chorionic Gonadotropin Elevation

Graves’ Disease and Other Causes of Hyperthyroidism

Graves’ Disease/Diffuse Toxic Goiter

Graves’ disease goes by a variety of names. In addition to diffuse toxic goiter, because goiter is almost always present in the condition, it’s also known as toxic diffuse goiter and as exophthalmic goiter, in recognition of exophthalmos, an eye condition characterized by protrusion of the eyeballs and a characteristic staring expression, which is sometimes seen in Graves’ disease patients.

Graves’ disease was first identified by the British Dr. Caleb Parry in the 1780s, but it was named after the Irish doctor Robert Graves in the 1830s. Occasionally, however, you may see the condition referred to as Parry’s disease in recognition of the earlier doctor’s work. Dr. Baron Carl Adolph von Basedow studied the condition at length in the 1840s. Thus, in the non-English-speaking world, the names von Basedow’s disease, Basedow’s disease, or Graves-Basedow disease are more common, particularly in Germany as well as some other European and African countries.

Graves’ disease is an autoimmune disease in which hyperthyroidism—an excess of thyroid hormone—is triggered by the presence of antibodies known as thyroid-stimulating immunoglobulins (TSIs). TSIs are sometimes called thyrotropin receptor antibodies (TRAb). These TSIs attach or bind themselves to and activate the gland’s receptors for thyroid-stimulating hormone (TSH). In essence, they mimic the effects of TSH and cause the entire thyroid gland to enlarge (diffuse goiter). The thyroid follicles themselves increase their ability to synthesize and release thyroid hormone, so too much thyroid hormone is produced and circulates in the bloodstream.

TSH levels drop to low or undetectable levels because the pituitary and the hypothalamus sense that there is enough thyroid hormone circulating. But because TSI production is not part of the overall feedback loop, the thyroid is continually stimulated to produce more hormone. Therefore, T4 and T3 levels become extremely high and lead to thyrotoxicosis.

The antibodies seen in Graves’ disease can also attack the eyes and the skin, causing two related conditions:

Infiltrative ophthalmopathy, also known as Graves’ ophthalmopathy or thyroid eye disease, which can cause a protrusion or bulging of the eyeball, discomfort in the eyes, and severe vision disturbances in the most serious cases

Infiltrative dermopathy (also known as Graves’ dermopathy or pretibial myxedema), the primary symptom being a thickened patch of skin on the shins

The typical treatments for Graves’ disease can include drugs such as antithyroid drugs, beta blockers, corticosteroids, blockade drugs, and in some cases, an antithyroid/thyroid hormone combination known as block replace therapy. Another treatment frequently used in the United States is thyroid ablation with radioactive iodine 131, a procedure known as RAI. Partial or complete surgical removal of the thyroid is also a treatment for Graves’ disease that resolves the condition quickly. Ultimately, though, there is no cure. Like other autoimmune diseases, the exact cause is still being researched, so treatments focus on eliminating the symptoms, including hyperthyroidism.

Toxic Multinodular Goiter/Plummer’s Disease

In the United States, toxic multinodular goiter (or multinodular toxic goiter) is the second most common cause of hyperthyroidism after Graves’ disease. In areas where iodine deficiency is a problem, it is often the primary cause of hyperthyroidism. Because the condition was initially described by Henry Plummer in 1913, it is also referred to as Plummer’s disease. Toxic multinodular goiter involves multiple nodules that have usually developed over many years, and once the nodules reach a certain size, the follicles begin to produce thyroid hormone on their own. The condition is more common in older people, particularly those with a longstanding goiter. Because of the slow onset of symptoms, it may be harder to diagnose, and subtle development of symptoms may be overlooked or attributed to other causes.

Toxic multinodular goiter can be treated with antithyroid drug therapy, but lifelong treatment may be required. Surgery can be immediately effective in resolving the condition. Some doctors also recommend RAI, but a higher dose than is typically given for Graves’ disease patients may be needed.

Toxic Adenoma/Autonomous Nodule

A toxic adenoma is also known as an autonomously functioning thyroid nodule (AFTN). It is typically a single palpable nodule that gets to a point where it produces thyroid hormone on its own separate from the thyroid’s own production. When the nodule produces enough thyroid hormone to suppress TSH levels, it is labeled toxic. Nodules that are toxic are rarely cancerous; rather, they are almost always benign adenomas.

Toxic nodules rarely go away on their own. Antithyroid drugs can be used as a treatment, but they may have to be taken for the rest of the patient’s life. Surgery can be immediately effective in resolving the condition. Some doctors also recommend RAI. Finally, ablation of the nodule with percutaneous ethanol injection (PEI) is a safe and effective treatment, although it is not widely used. One or two injections of alcohol are given per week for a total of three to six injections per nodule. Many doctors in the United States are not familiar with this easy-to-perform technique. Research has shown that PEI is an appropriate therapy for most toxic adenomas less than 13 milliliters in volume. The size of the nodule is the primary determinant of PEI’s success.

De Quervain’s Thyroiditis/Granulomatous

Thyroiditis/Painful Thyroiditis/Subacute Thyroiditis—

Thyrotoxic Phase

De Quervain’s thyroiditis, also known as granulomatous thyroiditis or painful thyroiditis, results from a viral infection of the thyroid gland. Sometimes also called subacute thyroiditis, this condition was first reported in 1825, but it was recorded in detail by De Quervain in the early 1900s. De Quervain’s thyroiditis usually starts out as a flu, cold, or upper respiratory infection, which then shifts to pain, tenderness, and swelling in the neck, jaw, and thyroid area, along with fever. Initially, it often triggers a 4- to 10-week period of hyperthyroidism as excess thyroid hormone is released into the bloodstream after the virus attacks the thyroid. Later, the thyroid may return to normal or shift into another 4- to 10-week period of hyperthyroidism.

De Quervain’s thyroiditis is most common in temperate climates and occurs more often during the summer and fall. The condition tends to follow viral epidemics, including mumps, measles, influenza, adenovirus, mononucleosis, myocarditis, cat scratch fever, and Coxsackie virus.

Some patients with mild pain and few symptoms do not require any treatment. Those with some hyperthyroid-related symptoms are usually treated with beta blockers, nonsteroidal antiinflammatory drugs (NSAIDs) such as aspirin or ibuprofen, and in severe cases, a short course of corticosteroids to reduce inflammation may be given. Thyroid hormone may be prescribed to help the gland rest.

Painless Thyroiditis/Silent Thyroiditis/Lymphocytic

Thyroiditis—Thyrotoxic Phase

Painless thyroiditis, also known as silent thyroiditis or lymphocytic thyroiditis, is fairly rare and involves a slight enlargement of the thyroid gland. The symptoms are similar to Graves’ disease, but they do not involve any eye symptoms and the thyroid is usually only slightly enlarged. The thyroid is not tender to the touch or painful. Periods of slight hyperthyroidism may be followed by hypothyroidism, but usually the thyroid returns to normal function within 3 months.

Painless thyroiditis usually needs no treatment. It is estimated that 80 percent of patients return to normal thyroid function fairly quickly. During the hyperthyroid phase, however, beta blockers may be given to help alleviate heart rate and anxiety-like symptoms. The second phase is typically a hypothyroid phase that may last several months. Treatment for this stage is with thyroid hormone replacement drugs. Typically, patients are taken off the drugs after a few months to see if thyroid function has returned to normal, which it will for most patients. A small percentage of patients become permanently hypothyroid and need to be on lifelong thyroid hormone replacement.

Postpartum Thyroiditis—Thyrotoxic Phase

Postpartum thyroiditis is a form of silent thyroiditis that develops in 5 to 9 percent of women within a year of having given birth. The condition usually follows a pattern similar to painless thyroiditis, with a period of hypothyroidism followed by hyperthyroidism, followed by a return to normal function within 6 months. This condition is often mistaken for postpartum anxiety or depression.

As with painless thyroiditis, postpartum thyroiditis doesn’t typically require treatment unless symptoms are particularly problematic. In that case, beta blockers may be given during the thyrotoxic phase and thyroid hormone replacement may be