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Thyroid Gland

Health topicsThyroid Gland

Hashimoto’s disease

by Health Jade Team 3 on
Hashimoto’s disease

Hashimoto’s disease

Hashimoto’s disease also called Hashimoto’s thyroidits, chronic lymphocytic thyroiditis, autoimmune thyroiditis or chronic thyroiditis, is an autoimmune disease that causes chronic inflammation of your thyroid gland or thyroidits. The term “thyroiditis” refers to “inflammation of the thyroid gland”. Hashimoto’s thyroiditis or Hashimoto’s disease was first described by Hashimoto as Struma lymphomatosa in 1912 1. At present, Hashimoto’s disease or Hashimoto’s thyroidits is the most common type of autoimmune endocrine disorder and underactive thyroid (hypothyroidism) in the United States 2, 3, 4. Approximately 2% of the general population are affected by Hashimoto’s disease or Hashimoto’s thyroiditis with a high prevalence in middle-aged individuals and in women, but can be seen at any age, and can also affect men and children 5, 6, 7. Hashimoto’s disease also called Hashimoto’s thyroidits tends to run in families. Over time, the ability of the thyroid gland to produce thyroid hormones often becomes impaired and leads to a gradual decline in function and eventually hypothyroidism (an underactive thyroid).

Hashimoto’s thyroiditis is an autoimmune disorder in which antibodies attacks your thyroid gland, preventing it from producing enough thyroid hormones (tri-iodothyronine [T3] and thyroxine [T4]). Hashimoto’s thyroiditis is distinguished by the presence of autoantibodies against thyroid peroxidase (anti-TPO or antibody to thyroid peroxidase) and thyroglobulin (anti-Tg or thyroglobulin antibody) 8. Low thyroid hormone levels may cause hypothyroidism with a range of symptoms, such as tiredness or fatigue, weight gain, intolerance to cold temperatures, dry skin or dry thinning hair, slowed heart rate, heavy or irregular menstrual periods or fertility problems. Rarely, early in the course of the disease, thyroid gland damage may lead to the release of too much thyroid hormone into your blood, causing symptoms of hyperthyroidism called Hashitoxicosis 9, 10. Hashitoxicosis occurs as a result of the biochemical release of preformed thyroid hormone due to autoimmune destruction of the thyroid. Too much thyroid hormone (hyperthyroidism) can cause weight loss, despite an increased appetite. You might also feel anxious and find it difficult to relax. Hashitoxicosis precedes the signs and symptoms of the hypothyroid state associated with Hashimoto’s thyroiditis and lasts a few weeks to months 9.

Your thyroid gland is a butterfly-shaped gland with 2 lobes (the right lobe and the left lobe — joined by a narrow piece of the thyroid gland called the isthmus) that is located in front of your neck near the base of your throat, beneath the larynx (voice box or Adam’s apple) (Figure 1). In most people, the thyroid gland cannot be seen or felt. Your thyroid gland produces thyroid hormones, tri-iodothyronine (T3) and thyroxine (T4) (the main hormones that your thyroid gland makes) and calcitonin. The thyroid hormones, T3 (tri-iodothyronine) and T4 (thyroxine) influence important body processes such as body temperature, energy levels, growth, your digestion, muscles and heart. Thyroid hormones are important for how your body uses energy, your metabolism, so thyroid hormones affect nearly every organ in your body even the way your heart beats. You might put on weight and feel very tired and lacking in energy if your thyroid gland doesn’t make enough T3 (tri-iodothyronine) and T4 (thyroxine).

In people with Hashimoto’s disease:

  • the immune system makes antibodies that attack the thyroid gland (autoimmune disorder). Usually in Hashimoto’s disease, the immune system produces an antibody to thyroid peroxidase (TPO), a protein that plays an important part in thyroid hormone production. Most people with Hashimoto’s disease will have TPO (thyroid peroxidase) antibodies in their blood. Lab tests for other antibodies associated with Hashimoto’s disease may need to be done.
  • large numbers of white blood cells, which are part of the immune system, build up in the thyroid gland
  • the thyroid gland becomes damaged and can’t make enough thyroid hormones (hypothyroidism)

Many people who have Hashimoto’s disease have no symptoms at all. If the disease does enough damage to the thyroid, it can cause hypothyroidism (underactive thyroid disease). This is because the attack on the thyroid causes the gland to produce fewer hormones. Symptoms of Hashimoto’s disease include:

  • Fatigue.
  • Weight gain.
  • Increased sensitivity to cold.
  • Joint and muscle pain or stiffness.
  • Pale, dry skin.
  • Dry skin, thin hair and / or brittle nails.
  • Puffy face.
  • Hoarse voice.
  • Constipation.
  • Heavier than normal periods in women.
  • Elevated cholesterol.
  • Depression.
  • Visibly enlarged thyroid.
  • Forgetfulness or memory problems.
  • Low sex drive (libido)

Hashimoto’s disease can also cause cognitive symptoms including:

  • depression or low mood
  • an inability to concentrate
  • poor memory

In some cases, your thyroid gland may become noticeably larger (called a goiter) or it may shrink. Lumps or nodules may also develop in your thyroid gland.

Although Hashimoto’s disease can affect people of all ages, it’s most common in women in their 30s and 40s 11. The female-to-male ratio is at least 10:1 10. If someone in your family has had thyroid disease, you may have an increased risk for Hashimoto’s disease. No one is sure why people get Hashimoto’s disease.

Calcitonin is another hormone produced by the thyroid gland. Calcitonin helps to control the amount of calcium circulating in your blood. Calcitonin works with a hormone called parathyroid hormone (PTH) to do this. Parathyroid hormone is made by parathyroid glands. These sit behind and are attached to the thyroid gland (see Figure 1).

If you have symptoms of hypothyroidism, see your doctor. Your doctor will examine you and may run blood tests, including testing your thyroid hormone levels.

If left untreated, hypothyroidism can lead to problems including goiter (an increase in the size of the thyroid gland), heart problems or mental health problems. Occasionally, it can lead to a potentially life-threatening disorder called myxedema coma.

While there is no cure for Hashimoto’s disease, hypothyroidism can be treated. The primary treatment of Hashimoto’s disease is thyroid hormone replacement. Most people with Hashimoto’s disease take a synthetic thyroid hormone medication called levothyroxine (Levoxyl, Synthroid, others) to treat hypothyroidism. The synthetic thyroid hormone works like the T4 hormone naturally produced by the thyroid. Your hypothyroidism can be well-controlled with thyroid hormone medicine, as long as you take the medicine as instructed by your doctor and have regular follow-up blood tests.

If you have mild hypothyroidism, you may not need to have treatment but get regular thyroid stimulating hormone (TSH) tests to monitor thyroid hormone levels.

How common is Hashimoto’s disease?

The number of people who have Hashimoto’s disease in the United States is unknown. However, Hashimoto’s disease is the most common cause of hypothyroidism the United States, which affects about 5 in 100 Americans 12.

Hashimoto is also the most common cause of hypothyroidism in those areas of the world where iodine intake is adequate. The incidence is estimated to be 0.8 per 1000 per year in men and 3.5 per 1000 per year in women 10. The prevalence of thyroid disease, in general, increases with age.

How does eating, diet, and nutrition affect Hashimoto’s disease?

The thyroid gland uses iodine, a mineral in some foods, to make thyroid hormones. However, if you have Hashimoto’s disease or other types of autoimmune thyroid disorders, you may be sensitive to harmful side effects from iodine. Eating foods that have large amounts of iodine—such as kelp, dulse, or other kinds of seaweed, and certain iodine-rich medicines—may cause hypothyroidism or make it worse. Taking iodine supplements can have the same effect.

Talk with members of your health care team about:

  • what foods and beverages to limit or avoid
  • whether you take iodine supplements
  • any cough syrups you take that may contain iodine

However, if you are pregnant, you need to take enough iodine because the baby gets iodine from your diet. Too much iodine can cause problems as well, such as a goiter in the baby. If you are pregnant, talk with your doctor about how much iodine you need.

Researchers are looking at other ways in which diet and supplements such as vitamin D and selenium may affect Hashimoto’s disease 13. However, no specific guidance is currently available 10.

How much iodine do I need?

The amount of iodine you need each day depends on your age. Average daily recommended amounts are listed below in micrograms (mcg).

Table 1 lists the current Recommended Dietary Allowances (RDA – the average daily level of intake sufficient to meet the nutrient requirements of nearly all [97%–98%] healthy individuals; often used to plan nutritionally adequate diets for individuals) for iodine 14. For infants from birth to 12 months, the Food and Nutrition Board at the Institute of Medicine of the National Academies established an Adequate Intake (AI) for iodine that is equivalent to the mean intake of iodine in healthy, breastfed infants in the United States.

The World Health Organization (WHO), United Nations Children’s Fund (UNICEF), and the International Council for the Control of Iodine Deficiency Disorders (ICCIDD) recommend a slightly higher iodine intake for pregnant women of 250 mcg per day 15, 16.

Table 1. Recommended Dietary Allowances (RDAs) for Iodine

AgeMaleFemalePregnancyLactation
Birth to 6 months110 mcg*110 mcg*
7–12 months130 mcg*130 mcg*
1–3 years90 mcg90 mcg
4–8 years90 mcg90 mcg
9–13 years120 mcg120 mcg
14–18 years150 mcg150 mcg220 mcg290 mcg
19+ years150 mcg150 mcg220 mcg290 mcg

Footnote: * Adequate Intake (AI)

What foods are good source for iodine?

Seaweed (such as kelp, nori, kombu, and wakame) is one of the best food sources of iodine 17. Other good sources include fish and other seafood, as well as eggs (see Table 2). Iodine is also present in human breast milk 14 and infant formulas 18. The U.S. Department of Agriculture (USDA) lists the iodine content of numerous foods and beverages 18.

Dairy products contain iodine. However, the amount of iodine in dairy products varies by whether the cows received iodine feed supplements and whether iodophor sanitizing agents were used to clean the cows and milk-processing equipment 19. For example, an analysis of 44 samples of nonfat milk found a range of 38 to 159 mcg per cup (with an average of 85 mcg/cup used for Table 2) 18. Plant-based beverages used as milk substitutes, such as soy and almond beverages, contain relatively small amounts of iodine.

Most commercially prepared bread contains very little iodine unless the manufacturer has used potassium iodate or calcium iodate as a dough conditioner 20. Manufacturers list dough conditioners as an ingredient on product labels but are not required to include iodine on the Nutrition Facts label 21, even though these conditioners provide a substantial amount of iodine. According to 2019 data from the USDA Branded Food Products Database, approximately 20% of ingredient labels for white bread, whole-wheat bread, hamburger buns, and hot dog buns listed iodate. Pasta is not a source of iodine unless it is prepared in water containing iodized salt because it absorbs some of the iodine 22.

Most fruits and vegetables are poor sources of iodine, and the amounts they contain are affected by the iodine content of the soil, fertilizer use, and irrigation practices 20. This variability affects the iodine content of meat and animal products because of its impact on the iodine content of foods that the animals consume 23. The iodine amounts in different seaweed species also vary greatly. For example, commercially available seaweeds in whole or sheet form have iodine concentrations ranging from 16 mcg/g to 2,984 mcg/g 24. For these reasons, the values for the foods listed in Table 2 are approximate but can be used as a guide for estimating iodine intakes.

Table 2. Iodine Content of Selected Foods

FoodMicrograms (mcg)
per serving		Percent DV*
Seaweed, nori, dried, 10 g232155
Bread, whole-wheat, made with iodate dough conditioner, 1 slice198132
Bread, white, enriched, made with iodate dough conditioner, 1 slice185123
Cod, baked, 3 ounces158106
Yogurt, Greek, plain, nonfat, 1 cup11677
Oysters, cooked, 3 ounces9362
Milk, nonfat, 1 cup8557
Iodized table salt, 1.5 g (approx. ¼ teaspoon)7651
Fish sticks, cooked, 3 ounces5839
Pasta, enriched, boiled in water with iodized salt, 1 cup3624
Egg, hard boiled, 1 large2617
Ice cream, chocolate, ½ cup2114
Liver, beef, cooked, 3 ounces149
Cheese, cheddar, 1 ounce149
Shrimp, cooked, 3 ounces139
Tuna, canned in water, drained, 3 ounces75
Soy beverage, 1 cup75
Fruit cocktail in light syrup, canned, ½ cup64
Beef, chuck, roasted, 3 ounces32
Chicken breast, roasted, 3 ounces21
Almond beverage, 1 cup21
Apple juice, 1 cup11
Bread, whole-wheat, made without iodate dough conditioner, 1 slice11
Bread, white, enriched, made without iodate dough conditioner, 1 slice11
Raisin bran cereal, 1 cup11
Rice, brown, cooked, ½ cup11
Corn, canned, ½ cup11
Sea salt, non-iodized, 1.5 g (approx. ¼ teaspoon)<1<1
Broccoli, boiled, ½ cup00
Banana, 1 medium00
Lima beans, mature, boiled, ½ cup00
Green peas, frozen, boiled, ½ cup00
Pasta, enriched, boiled in water without iodized salt, 1 cup00

Footnotes: *DV = Daily Value. The U.S. Food and Drug Administration (FDA) developed DVs to help consumers compare the nutrient contents of foods and dietary supplements within the context of a total diet. The DV for iodine is 150 mcg for adults and children aged 4 years and older. FDA does not require food labels to list iodine content unless iodine has been added to the food. Foods providing 20% or more of the DV are considered to be high sources of a nutrient, but foods providing lower percentages of the DV also contribute to a healthful diet.

[Source 18 ]

Thyroid gland

The thyroid gland is the largest adult gland to have a purely endocrine function, weighing about 25-30 g. The thyroid gland is a small butterfly shaped gland with 2 lobes, the right lobe and the left lobe joined by a narrow piece of the thyroid gland called the isthmus, that is located in front of your neck near the base of your throat, beneath the larynx (voice box or Adam’s apple). About 50% of thyroid glands have a small third lobe, called the pyramidal lobe. It extends superiorly from the isthmus. The thyroid gland makes and releases hormones. You can’t usually feel a thyroid gland that is normal.

The thyroid gland has 2 main types of cells:

  • Follicular cells use iodine from the blood to make thyroid hormones, which help regulate a person’s metabolism. Having too much thyroid hormone (hyperthyroidism) can cause a fast or irregular heartbeat, trouble sleeping, nervousness, hunger, weight loss, and a feeling of being too warm. Having too little thyroid hormone (hypothyroidism) causes a person to slow down, feel tired, and gain weight. The amount of thyroid hormone released by the thyroid gland is regulated by the pituitary gland at the base of the brain, which makes a substance called thyroid-stimulating hormone (TSH) (see Figure 5).
  • C cells also called parafollicular cells at the periphery of the follicles that make calcitonin, a hormone that helps control how your body uses calcium. The parafollicular cells (C cells) respond to rising levels of blood calcium by secreting the hormone calcitonin. Calcitonin antagonizes (blocks) parathyroid hormone (PTH) and stimulates osteoblast activity, thus promoting calcium deposition and bone formation. It is important mainly in children, having relatively little effect in adults.

Other, less common cells in the thyroid gland include immune system cells (lymphocytes) and supportive (stromal) cells.

Thyroid hormone is secreted or inhibited in response to fluctuations in metabolic rate. The brain monitors the body’s metabolic rate and stimulates thyroid hormone secretion through the action of thyrotropin-releasing hormone (TRH) and thyroid stimulating hormone (TSH) as depicted in figure 5.

The primary effect of thyroid hormone (TH) is to increase one’s metabolic rate. As a result, it raises oxygen consumption and has a calorigenic effect—it increases heat production. To ensure an adequate blood and oxygen supply to meet this increased metabolic demand, thyroid hormone also raises the breathing (respiratory) rate, heart rate, and strength of the heartbeat. It stimulates the appetite and accelerates the breakdown of carbohydrates, fats, and protein for fuel. Thyroid hormone also promotes alertness and quicker reflexes; growth hormone secretion; growth of the bones, skin, hair, nails, and teeth; and development of the fetal nervous system.

Figure 1. Thyroid gland and parathyroid gland

Thyroid gland and parathyroid gland

Thyroid gland

Footnotes: Anatomy of the thyroid and parathyroid glands. The thyroid gland lies at the base of the throat near the trachea. It is shaped like a butterfly, with the right lobe and left lobe connected by a thin piece of tissue called the isthmus. The parathyroid glands are four pea-sized organs found in the neck near the thyroid. The thyroid and parathyroid glands make hormones.

Figure 2. Thyroid gland location

Thyroid gland location

Figure 3. Thyroid gland anatomy

Thyroid gland anatomy

Footnote: (a) Gross anatomy, anterior view. (b) Histology, showing the saccular thyroid follicles (the source of thyroid hormone) and nests of C cells (the source of calcitonin).

What does the thyroid gland do?

Formation, storage, and release of thyroid hormones

The thyroid gland is the only endocrine gland that stores its secretory product in large quantities—normally about a 100-day supply. Synthesis and secretion of triiodothyronine (T3) and thyroxine or tetraiodothyronine (T4) occurs as follows:

  1. Iodide trapping. Thyroid follicular cells trap iodide ions (I −) by actively transporting them from the blood into the cytosol. As a result, the thyroid gland normally contains most of the iodide in the body.
  2. Synthesis of thyroglobulin. While the follicular cells are trapping I −, they are also synthesizing thyroglobulin (TGB), a large glycoprotein that is produced in the rough endoplasmic reticulum, modified in the Golgi complex, and packaged into secretory vesicles. The vesicles then undergo exocytosis, which releases thyroglobulin into the lumen of the follicle.
  3. Oxidation of iodide. Some of the amino acids in thyroglobulin are tyrosines that will become iodinated. However, negatively charged iodide  (I −) ions cannot bind to tyrosine until they undergo oxidation (removal of electrons) to iodine: I −→ I. As the iodide ions are being oxidized, they pass through the membrane into the lumen of the follicle.
  4. Iodination of tyrosine. As iodine atoms (I) form, they react with tyrosines that are part of thyroglobulin molecules. Binding of one iodine atom yields monoiodotyrosine (T1), and a second iodination produces diiodotyrosine (T2). The thyroglobulin with attached iodine atoms, a sticky material that accumulates and is stored in the lumen of the thyroid follicle, is termed colloid.
  5. Coupling of monoiodotyrosine (T1) and diiodotyrosine (T2). During the last step in the synthesis of thyroid hormone, two diiodotyrosine (T2) molecules join to form thyroxine (T4) or one T1 and one T2 join to form triiodothyronine (T3).
  6. Pinocytosis and digestion of colloid. Droplets of colloid reenter follicular cells by pinocytosis and merge with lysosomes. Digestive enzymes in the lysosomes break down thyroglobulin, cleaving off molecules of triiodothyronine (T3) and thyroxine (T4).
  7. Secretion of thyroid hormones. Because T3 and T4 are lipid soluble, they diffuse through the plasma membrane into interstitial fluid and then into the blood. T4 normally is secreted in greater quantity than T3, but T3 is several times more potent. Moreover, after T4 enters a body cell, most of it is converted to T3 by removal of one iodine.
  8. Transport thyroid hormones in the blood. More than 99% of both the T3 and the T4 combine with transport proteins in the blood, mainly thyroxine binding globulin (TBG).

Figure 4. Thyroid hormones

Thyroid hormones

Actions of thyroid hormones

Because most body cells have receptors for thyroid hormones, triiodothyronine (T3) and thyroxine (T4) affect tissues throughout the body. Thyroid hormones act on their target cells mainly by inducing gene transcription and protein synthesis. The newly formed proteins in turn carry out the cellular response.

Functions of thyroid hormones include the following:

  1. Increase basal metabolic rate. Thyroid hormones raise the basal metabolic rate (BMR), the rate of energy expenditure under standard or basal conditions (awake, at rest, and fasting). When basal metabolic rate increases, cellular metabolism of carbohydrates, lipids, and proteins increases. Thyroid hormones increase BMR in several ways: (1) They stimulate synthesis of additional Na+/K+ ATPases, which use large amounts of ATP to continually eject sodium ions (Na+) from cytosol into extracellular fluid and potassium ions (K+) from extracellular fluid into cytosol; (2) they increase the concentrations of enzymes involved in cellular respiration, which increases the breakdown of organic fuels and ATP production; and (3) they increase the number and activity of mitochondria in cells, which also increases ATP production. As cells produce and use more ATP, basal metabolic rate increases, more heat is given off and body temperature rises, a phenomenon called the calorigenic effect. In this way, thyroid hormones play an important role in the maintenance of normal body temperature. Normal mammals can survive in freezing temperatures, but those whose thyroid glands have been removed cannot.
  2. Enhance actions of catechlolamines. Thyroid hormones have permissive effects on the catecholamines (epinephrine and norepinephrine) because they up-regulate β-adrenergic receptors. Catecholamines bind to β-adrenergic receptors, promoting sympathetic responses. Therefore, symptoms of excess levels of thyroid hormone include increased heart rate, more forceful heartbeats, and increased blood pressure.
  3. Regulate development and growth of nervous tissue and bones. Thyroid hormones are necessary for the development of the nervous system: They promote synapse formation, myelin production, and growth of dendrites. Thyroid hormones are also required for growth of the skeletal system: They promote formation of ossification centers in developing bones, synthesis of many bone proteins, and secretion of growth hormone (GH) and insulin-like growth factors (IGFs). Deficiency of thyroid hormones during fetal development, infancy, or childhood causes severe mental retardation and stunted bone growth.

Control of thyroid hormone secretion

Thyrotropin-releasing hormone (TRH) from the hypothalamus and thyroid-stimulating hormone (TSH) from the anterior pituitary stimulate secretion of thyroid hormones, as shown in Figure 5:

  1. Low blood levels of T3 and T4 or low metabolic rate stimulate the hypothalamus to secrete thyrotropin-releasing hormone (TRH).
  2. Thyrotropin-releasing hormone (TRH) enters the hypothalamic–hypophyseal portal system and flows to the anterior pituitary, where it stimulates thyrotrophs to secrete thyroid stimulating hormone (TSH).
  3. Thyroid stimulating hormone (TSH) stimulates virtually all aspects of thyroid follicular cell activity, including iodide trapping, hormone synthesis and secretion, and growth of the follicular cells.
  4. The thyroid follicular cells release T3 and T4 into the blood until the metabolic rate returns to normal.
  5. An elevated level of T3 inhibits release of TRH and TSH (negative feedback inhibition).

Conditions that increase ATP demand—a cold environment, hypoglycemia, high altitude, and pregnancy—increase the secretion of the thyroid hormones.

Figure 5. Control of thyroid hormone secretion

Control of thyroid hormone secretion

Footnote: Negative Feedback Inhibition of the Anterior Pituitary Gland by the Thyroid Gland

Control of calcium balance

The hormone produced by the parafollicular cells of the thyroid gland is calcitonin. Calcitonin can decrease the level of calcium in the blood by inhibiting the action of osteoclasts, the cells that break down bone extracellular matrix. The secretion of calcitonin is controlled by a negative feedback system (see Figure 7).

Calcitonin is produced by C cells (clear cells) of the thyroid gland. It is secreted when the blood calcium concentration rises too high, and it lowers the concentration by two principal mechanisms:

  1. Osteoclast inhibition. Within 15 minutes after it is secreted, calcitonin reduces osteoclast activity by as much as 70%, so osteoclasts liberate less calcium from the skeleton.
  2. Osteoblast stimulation. Within an hour, calcitonin increases the number and activity of osteoblasts, which deposit calcium into the skeleton.

Calcitonin plays an important role in children but has only a weak effect in most adults. The osteoclasts of children are highly active in skeletal remodeling and release 5 g or more of calcium into the blood each day. By inhibiting this activity, calcitonin can significantly lower the blood calcium level in children. In adults, however, the osteoclasts release only about 0.8 g of calcium per day. Calcitonin cannot change adult blood calcium very much by suppressing this lesser contribution. Calcitonin deficiency is not known to cause any adult disease. Calcitonin may, however, inhibit bone loss in pregnant and lactating women. Miacalcin, a calcitonin extract derived from salmon that is 10 times more potent than human calcitonin, is prescribed to treat osteoporosis.

Figure 6. Hormonal control of calcium balance

Hormonal control of calcium balance

Footnote: The central panel represents the blood reservoir of calcium and shows its normal (safe) range. Calcitriol and Parathyroid Hormone (PTH) regulate calcium exchanges between the blood and the small intestine and kidneys (left). Calcitonin, calcitriol, and Parathyroid Hormone (PTH) regulate calcium exchanges between blood and bone (right).

Hashimoto’s disease causes

The cause of Hashimoto’s disease or Hashimoto’s thyroidits is poorly understood 25. Hashimoto’s thyroiditis is an autoimmune disease that destroys thyroid cells by cell and antibody-mediated immune processes. Your immune system creates antibodies that attack thyroid cells as if they were bacteria, viruses or some other foreign body. Your immune system wrongly enlists disease-fighting agents that damage cells and lead to cell death. Most Hashimoto’s disease patients develop antibodies to a variety of thyroid antigens, the most common of which is anti-thyroid peroxidase (anti-TPO or antibody to thyroid peroxidase). Many also form antithyroglobulin (anti-Tg or thyroglobulin antibody) and TSH receptor-blocking antibodies (TBII) 25. These antibodies attack your thyroid tissue, eventually leading to inadequate production of thyroid hormone. There is a small subset of the population, no more than 10-15% with the clinically evident disease, that are serum antibody-negative. Positive anti-thyroid peroxidase (anti-TPO) antibodies point to the clinical syndrome 26, 27.

What causes your immune system to attack thyroid cells is not clear. Multiple factors from the external environment and the genetic background contribute to the pathogenesis of Hashimoto’s disease 28. These genetic, environmental, and existential factors provoke the immune system to produce antibodies to thyroid antigens 29, 30, 31, 32, 33, 34, 35, 36. The most important factors associated with Hashimoto’s thyroiditis are summarized in Table 3 below.

Hashimoto’s disease or Hashimoto’s thyroidits can also be part of the Polyglandular Autoimmune Syndrome type 2 with autoimmune adrenal deficiency and type-1 diabetes 37. Hashimoto thyroiditis is also related to several other autoimmune diseases such as pernicious anemia, adrenal insufficiency, and celiac disease. Ruggeri et al. 38 found that Hashimoto disease is associated with a variety of different non-thyroidal autoimmune diseases (NTADs) and diagnosis in adulthood made these even more prevalent.

The onset of Hashimoto’s disease may be related to 26, 27, 39, 40:

  • Genetic factors. Twin studies have shown an increased concordance of autoimmune thyroiditis in monozygotic twins as compared with dizygotic twins. Danish studies have demonstrated concordance rates of 55% in monozygotic twins, compared with only 3% in dizygotic twins 41. This data suggests that 79% of predisposition is due to genetic factors, allotting 21% for environmental and sex hormone influences. 
  • Environmental triggers, such as infection, stress or radiation exposure
  • Interactions between environmental and genetic factors.

Hypothyroidism can also be caused by:

  • some medicines used to treat bipolar disorder or other mental health problems
  • iodine-containing medicines used to treat abnormal heart rhythm
  • exposure to toxins, such as nuclear radiation
  • viruses, such as hepatitis C

Several genes have been involved in Hashimoto’s disease pathogenesis, including genes of the immune response (coded in the Human Leukocyte Antigen (HLA) complex) and thyroid function 28. Other immunoregulatory genes are involved in the development of Hashimoto’s disease, including the single nucleotide polymorphisms (SNPs) in cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), protein tyrosine phosphatase non-receptor type 22 (PTPN22), and CD40 42, 29, 34, 43.

Among the environmental factors are inadequate or excessive iodine intake, infections, or the intake of certain medications 29, 34, 33, 35, 44. Several of the currently used anticancer drugs, such as interferon-alpha, may cause autoimmune thyroid dysfunction 45, 36. The role of smoking and alcohol consumption in the etiopathogenesis of Hashimoto’s disease is still not clear 28. The data suggest that moderate alcohol consumption may protect against Hashimoto’s disease and the development of overt hypothyroidism 36, 46, 47. Furthermore, some studies indicate that smoking decreases the levels of thyroid autoantibodies and the risk of hypothyroidism. However, the mechanism for these protective effects of smoking and drinking remains unclear and must be clarified with future studies 36, 46, 47. In recent years, the influence of stress on the development and course of Hashimoto’s disease has also been investigated. Some studies suggest that stress is involved in the pathogenesis of Hashimoto’s disease, while other evidence indicates that it has no effect 36, 48. A randomized controlled trial by Markomanolaki et al. 49 showed that managing stress is also important in treating Hashimoto’s disease patients. After eight weeks of stress management intervention, patients demonstrated a reduction in antithyroglobulin (anti-Tg) titers, decreased levels of stress, depression, anxiety and improved lifestyle 49. Additionally, the adequate levels of vitamin D and selenium may help prevent or delay the onset of Hashimoto’s disease 33, 35, 50, 51. Moreover, the risk of Hashimoto’s disease is increased in other autoimmune diseases 52, 36.

Most Hashimoto’s disease patients develop antibodies to a variety of thyroid antigens, the most common of which is anti-thyroid peroxidase (anti-TPO). Many also form antithyroglobulin (anti-Tg) and TSH receptor-blocking antibodies (TBII) 10. These antibodies attack the thyroid tissue, eventually leading to inadequate production of thyroid hormone. There is a small subset of the population, no more than 10-15% with the clinically evident disease, that are serum antibody-negative 10.

Table 3. Genetic, environmental and existential factors associated with Hashimoto’s thyroiditis

Genetic FactorsEnvironmental FactorsExistential Factors
Histocompatibility genes
(HLA class I and II)		IodineSex
Immunoregulatory genes (SNPs in HLA, CTLA-4, PTPN22, CD40 genes)Medications (e.g., interferon-α, lithium, amiodarone)Associated diseases
(e.g., type 1 diabetes mellitus, pernicious anaemia, coeliac disease, myasthenia gravis)
Thyroid-specific genesInfections
(e.g., hepatitis C virus)		Age
Genes associated with thyroid peroxidase antibody synthesisSmokingPregnancy
SeleniumDown’s syndrome
Vitamin DMicrobiome composition
AlcoholFamilial aggregation
Radiation Exposure
[Source 28 ]

Risk factors for Hashimoto’s disease

The following factors are associated with an increased risk of Hashimoto’s disease 13:

  • Sex. Women are much more likely to get Hashimoto’s disease.
  • Age. Hashimoto’s disease can occur at any age but more commonly occurs during middle age.
  • Other autoimmune disease. Having another autoimmune disease — such as rheumatoid arthritis, type 1 diabetes or lupus — increases your risk of developing Hashimoto’s disease.
  • Genetics and family history. You’re at higher risk for Hashimoto’s disease if others in your family have thyroid disorders or other autoimmune diseases.
  • Pregnancy. Typical changes in immune function during pregnancy may be a factor in Hashimoto’s disease that begins after pregnancy.
  • Excessive iodine intake. Too much iodine in the diet may function as a trigger among people already at risk for Hashimoto’s disease.
  • Radiation exposure. People exposed to excessive levels of environmental radiation are more prone to Hashimoto’s disease.

Hashimoto’s disease symptoms

Signs and symptoms of Hashimoto’s disease vary widely and are not specific to the disorder. Hashimoto’s disease progresses slowly over the years. Many people with Hashimoto’s disease may not notice signs or symptoms of the disease at first. An ordinary blood test may just show a thyroid hormone imbalance. Because the thyroid gland may grow and get larger, you may have a feeling of fullness or tightness in your throat, though it is usually not painful. You may have trouble swallowing food or liquids. You might have a swelling (a bump) in the front of your neck, the enlarged thyroid is called a goiter. After many years, or even decades, damage to the thyroid may cause the gland to shrink and the goiter to disappear.

Some people with Hashimoto’s disease have symptoms such as tiredness, forgetfulness, depression, coarse dry skin, slow heartbeat, weight gain, constipation and intolerance to cold. A blood test can tell if your thyroid gland is underactive. Other blood tests can be done to look for Hashimoto’s disease.

Eventually, the decline in thyroid hormone production can result in hypothyroidism with any of the following:

  • Fatigue and sluggishness
  • Increased sensitivity to cold
  • Increased sleepiness
  • Dry skin
  • Constipation
  • Muscle weakness
  • Muscle aches, tenderness and stiffness
  • Joint pain and stiffness
  • Irregular or excessive menstrual bleeding
  • Depression
  • Problems with memory or concentration
  • Swelling of the thyroid (goiter)
  • A puffy face
  • Brittle nails
  • Hair loss
  • Enlargement of the tongue

Because these symptoms could result from any number of disorders, it’s important to see your doctor as soon as possible for a timely and accurate diagnosis.

When to see a doctor

See your doctor if you develop these signs and symptoms:

  • Tiredness for no apparent reason
  • Dry skin
  • Pale, puffy face
  • Constipation

You’ll also need to see your doctor for periodic testing of your thyroid function if:

  • You’ve had thyroid surgery
  • You’ve had treatment with radioactive iodine or anti-thyroid medications
  • You’ve had radiation therapy to your head, neck or upper chest

If you have high blood cholesterol, talk to your doctor about whether hypothyroidism may be a cause.

And if you’re receiving hormone therapy for hypothyroidism caused by Hashimoto’s thyroiditis, schedule follow-up visits as often as your doctor recommends. It’s important to make sure you’re receiving the correct dose of medicine. Over time, the dose you need to adequately replace your thyroid function may change.

Hashimoto’s disease complications

Thyroid hormones are essential for the healthy function of many body systems. Therefore, when Hashimoto’s disease and hypothyroidism are left untreated, many complications can occur. These include:

  • Goiter. A goiter is enlargement of the thyroid. As thyroid hormone production declines due to Hashimoto’s disease, the thyroid receives signals from the pituitary gland to make more. This cycle may result in a goiter. It’s generally not uncomfortable, but a large goiter can affect your appearance and may interfere with swallowing or breathing.
  • Heart problems. Hypothyroidism can result in poor heart function, an enlarged heart and irregular heartbeats. It can also result in high levels of low-density lipoprotein (LDL) cholesterol — the “bad” cholesterol — that is a risk factor for cardiovascular disease and heart failure.
  • Peripheral neuropathy. Hypothyroidism that goes without treatment for a long time can damage the peripheral nerves. These are the nerves that carry information from the brain and spinal cord to the rest of the body. Peripheral neuropathy may cause pain, numbness and tingling in the arms and legs.
  • Infertility. Low levels of thyroid hormone can interfere with ovulation, which can limit fertility. Some of the causes of hypothyroidism, such as autoimmune disorders, also can harm fertility.
  • Mental health issues. Depression or other mental health disorders may occur early in Hashimoto’s disease and may become more severe over time.
  • Sexual and reproductive dysfunction. In women, hypothyroidism can result in a reduced sexual desire (libido), an inability to ovulate, and irregular and excessive menstrual bleeding. Men with hypothyroidism may have a reduced libido, erectile dysfunction and a lowered sperm count.
  • Poor pregnancy outcomes. Hypothyroidism during pregnancy may increase the risk of a miscarriage or preterm birth. Babies born to women with untreated hypothyroidism are at risk for decreased intellectual abilities, autism, speech delays and other developmental disorders.
  • Birth defects. Babies born to people with untreated thyroid disease may have a higher risk of birth defects compared with babies born to mothers who do not have thyroid disease. Infants with hypothyroidism present at birth that goes untreated are at risk of serious physical and mental development problems. But if the condition is diagnosed within the first few months of life, the chances of typical development are excellent.
  • Myxedema coma. This rare, life-threatening condition can develop due to long-term, severe, untreated hypothyroidism. Its signs and symptoms include drowsiness followed by profound lethargy and unconsciousness. A myxedema coma may be triggered by exposure to cold, sedatives, infection or other stress on your body. Myxedema requires immediate emergency medical treatment.

Hashimoto’s disease diagnosis

In general, your doctor may test for Hashimoto’s thyroiditis if you’re feeling increasingly tired or sluggish, have dry skin, constipation, and a hoarse voice, or have had previous thyroid problems or goiter.

Diagnosis of Hashimoto’s thyroiditis is based on your signs and symptoms and the results of blood tests that measure levels of thyroid hormone and thyroid-stimulating hormone (TSH) produced in the pituitary gland. These may include:

  • A hormone test. Blood tests can determine the amount of hormones produced by your thyroid and pituitary glands. If your thyroid is underactive, the level of thyroid hormone is low. At the same time, the level of TSH is elevated because your pituitary gland tries to stimulate your thyroid gland to produce more thyroid hormone.
  • An antibody test. Because Hashimoto’s thyroiditis is an autoimmune disorder, the cause involves production of abnormal antibodies. A blood test may confirm the presence of antibodies against thyroid peroxidase (TPO antibodies), an enzyme normally found in the thyroid gland that plays an important role in the production of thyroid hormones.

In the past, doctors weren’t able to detect an underactive thyroid (hypothyroidism), the main indicator of Hashimoto’s thyroiditis, until symptoms were fairly advanced. But by using the sensitive TSH test, doctors can diagnose thyroid disorders much earlier, often before you experience symptoms.

Because the TSH test is the best screening test, your doctor will likely check TSH first and follow with a thyroid hormone test if needed. TSH tests also play an important role in managing hypothyroidism. These tests also help your doctor determine the right dosage of medication, both initially and over time.

Testing thyroid function

To determine if hypothyroidism is the cause of your symptoms, your doctor will order blood tests that may include the following:

  • Thyroid stimulating hormone (TSH) test. Thyroid stimulating hormone (TSH) is produced by the pituitary gland. When the pituitary detects low thyroid hormones in the blood, it sends TSH to the thyroid to prompt an increase in thyroid hormone production. High TSH levels in the blood indicates hypothyroidism.
  • Thyroxine (T4) tests. The main thyroid hormone is thyroxine (T4). A low blood level of T4 confirms the findings of a TSH (thyroid stimulating hormone) test and indicates the problem is within the thyroid itself.

Antibody tests

More than one disease process can lead to hypothyroidism. To determine if Hashimoto’s disease is the cause of hypothyroidism, your doctor will order an antibody test.

The intended purpose of an antibody is to flag disease-causing foreign agents that need to be destroyed by other actors in the immune system. In an autoimmune disorder, the immune system produces rogue antibodies that target healthy cells or proteins in the body.

Usually in Hashimoto’s disease, the immune system produces an antibody to thyroid peroxidase (anti-TPO), a protein that plays an important part in thyroid hormone production. Most people with Hashimoto’s disease will have TPO antibodies (anti-TPO) in their blood. Lab tests for other antibodies associated with Hashimoto’s disease may also need to be done.

Thyroglobulin antibodies (anti-Tg) can also be a sign of Hashimoto disease. Most people with Hashimoto disease have high levels of both thyroglobulin antibodies (anti-Tg) and TPO antibodies (anti-TPO).

Circulating antibody to thyroid peroxidase (anti-TPO) are found in about 90% of Hashimoto’s disease patients. Anti-thyroglobulin antibodies (anti-Tg) are less sensitive (positive in about 60–80% of patients) and less specific than antibody to thyroid peroxidase (anti-TPO) 53, 29, 54.

You probably won’t need other tests to confirm you have Hashimoto’s disease. However, if your doctor suspects Hashimoto’s disease but you don’t have antithyroid antibodies in your blood, you may have an ultrasound of your thyroid. The ultrasound images can show the size of your thyroid and other features of Hashimoto’s disease. The ultrasound also can rule out other causes of an enlarged thyroid, such as thyroid nodules—small lumps in the thyroid gland.

Hashimoto’s disease treatment

How your doctors treat Hashimoto’s disease usually depends on whether your thyroid is damaged enough to cause hypothyroidism. If you don’t have hypothyroidism or you have mild hypothyroidism, your doctor may choose to simply check your symptoms and do regular thyroid stimulating hormone (TSH) tests to monitor your thyroid hormone levels.

Most people with Hashimoto’s disease need take a synthetic thyroid hormone medication called levothyroxine (Levoxyl, Synthroid, others) to treat hypothyroidism. The synthetic thyroid hormone works like the thyroxine (T4) hormone naturally produced by your thyroid. Prescribed in pill form for many years, this medicine is now also available as a liquid and in a soft gel capsule 13. These newer formulas may be helpful to people with digestive problems that affect how the thyroid hormone pill is absorbed.

Some foods and supplements can affect how well your body absorbs levothyroxine. Examples include grapefruit juice, espresso coffee, soy, and multivitamins that contain iron or calcium 12, 55. Taking levothyroxine on an empty stomach can prevent this from happening. Your doctor may ask you to take the levothyroxine in the morning, 30 to 60 minutes before you eat your first meal.

Your doctor will give you a blood test about 6 to 8 weeks after you begin taking levothyroxine and adjust your dose if needed. Each time you change your dose, you’ll have another blood test. Once you’ve reached a dose that’s working for you, your doctor will likely repeat the blood test in 6 months and then once a year.

Never stop taking your levothyroxine or take a higher dose without talking with your doctor first. Taking too much thyroid hormone medicine can cause serious problems, such as atrial fibrillation or osteoporosis 39.

Thyroxine (T4) hormone replacement therapy

Hypothyroidism associated with Hashimoto’s disease is treated with a synthetic hormone called levothyroxine (Levoxyl, Synthroid, others). The recommended dose of levothyroxine is 1.6 to 1.8 mcg/kg/day 10. The synthetic hormone works like the thyroxine (T4) hormone naturally produced by the thyroid. The treatment goal is to restore and maintain adequate thyroxine (T4) hormone levels and improve symptoms of hypothyroidism. You will need this treatment for the rest of your life.

Monitoring the dosage

Your doctor will determine a dosage of levothyroxine that’s appropriate for your age, weight, current thyroid production, other medical conditions and other factors. Your doctor will retest your TSH (thyroid stimulating hormone) levels about 6 to 10 weeks later and adjust the dosage as necessary.

Once the best dosage is determined, you will continue to take the medication once a day. You’ll need follow-up tests once a year to monitor TSH (thyroid stimulating hormone) levels or any time after your doctor changes your dosage.

A levothyroxine pill is usually taken in the morning before you eat. Talk to your doctor if you have any questions about when or how to take the pill. Also, ask what to do if you accidentally skip a dose. If your health insurance requires you to switch to a generic drug or a different brand, talk to your doctor.

Precautions

Because levothyroxine acts like natural thyroxine (T4) in your body, there are generally no side effects as long as the treatment is resulting in “natural” levels of thyroxine (T4) for your body.

Too much thyroid hormone can worsen bone loss that causes weak, brittle bones (osteoporosis) or cause irregular heartbeats (arrhythmias) the most common being atrial fibrillation.

Effects of other substances

Certain medications, supplements and foods may affect your ability to absorb levothyroxine. It may be necessary to take levothyroxine at least four hours before these substances. Talk to your doctor about any of the following:

  • Soy products
  • High-fiber foods
  • Iron supplements, including multivitamins that contain iron
  • Cholestyramine (Prevalite), a medication used to lower blood cholesterol levels
  • Aluminum hydroxide, which is found in some antacids
  • Sucralfate, an ulcer medication
  • Calcium supplements

Triiodothyronine (T3) hormone replacement therapy

Naturally produced thyroxine (T4) is converted into another thyroid hormone called triiodothyronine (T3). The thyroxine (T4) replacement hormone is also converted into triiodothyronine (T3), and for most people the thyroxine (T4) replacement therapy results in an adequate supply of triiodothyronine (T3) for the body.

For people who need better symptom control, a doctor also may prescribe a synthetic triiodothyronine (T3) (Cytomel) or a synthetic T4 and T3 combination. Side effects of triiodothyronine (T3) hormone replacement include rapid heartbeat, insomnia and anxiety. These treatments may be tested with a trial period of 3 to 6 months.

Is a combination of hormones needed?

Levothyroxine is the synthetic form of the natural thyroxine (T4). Thyroxine (T4) is converted into Triiodothyronine (T3) in the body. While most people are treated successfully with levothyroxine alone, some people don’t feel completely normal on levothyroxine.

Researchers have investigated whether adjusting standard hypothyroidism treatment to replace some thyroxine (T4) with small amounts of triiodothyronine (T3) may offer benefit. But, the majority of studies have determined that the addition of triiodothyronine (T3) does not offer any advantage over treatment with thyroxine (T4) alone.

There is some evidence that triiodothyronine (T3) may offer benefit to certain subsets of people, such as people who have had their thyroid surgically removed (thyroidectomy). Research is ongoing.

Triiodothyronine (T3) can be given alone as liothyronine (Cytomel) or in combination with thyroxine (T4) as liotrix (Thyrolar). Taking a combination T4 and T3 ends up producing higher than normal levels of triiodothyronine (T3), especially soon after the medication is taken. This can cause a fast heart rate, anxiety and trouble sleeping.

But, for those who haven’t gotten enough relief from thyroxine (T4) alone, adding Cytomel to standard levothyroxine treatment for a three- to six-month trial is a long enough period to see if the combination helps you.

Alternative medicine

Products with triiodothyronine (T3) and thyroxine (T4) hormones derived from pigs or other animals are available as prescriptions or as dietary supplements, such as Armour Thyroid, in the United States. Concerns about these products include the following:

  • The balance of thyroxine (T4) and triiodothyronine (T3) in animals isn’t the same as in humans.
  • The exact amount of thyroxine (T4) and triiodothyronine (T3) in each batch of a natural extract product can vary, leading to unpredictable levels of these hormones in your blood.

Anti-inflammatory diet

An anti-inflammatory diet rich in vitamins, minerals and polyphenols is recommended as diet therapy for Hashimoto’s disease 56, 44, 57. The theory behind the inflammation has to do with the leaky gut syndrome, where there is an insult to the gut mucosa, which allows the penetrance of proteins that do not typically enter the bloodstream via transporters in the gut mucosa. It is theorized that a response similar to molecular mimicry occurs, and antibodies are produced against the antigens. Unfortunately, the antigen may be very structurally similar to thyroid peroxidase, leading to antibody formation against this enzyme. The concept of an autoimmune diet is based on healing the gut and decreasing the severity of the autoimmune response.

Natural antioxidants like vitamin A, vitamin C and vitamin E are found in products of plant origin, including a wide variety of vegetables and fruits. Sources of vitamin C include broccoli, peppers, black currant, strawberries, lemons, spinach, kiwifruit, oranges, grapefruit, limes, tomatoes, raspberries, asparagus, pineapples, fennel and parsley. The best source of vitamin E is avocado, nuts, seeds, egg, milk and whole grains. In addition, vitamin A is present in foods such as liver, carrot, broccoli, butter, pumpkin, cheese, egg, mango and milk 58. According to the current findings, the Mediterranean diet may show the most benefits for Hashimoto’s disease patients with its antioxidant properties 59.

One study by Ostrowska et al. 60 assessed the effectiveness of two “reducing diets” and their effect on thyroid parameters in female obese patients with Hashimoto’s disease. All women who received levothyroxine, selenium and zinc were randomly assigned to the study group following individually balanced elimination/reducing diets, in accordance with the previously performer food sensitivity tests, and the control group following reducing diets with the same caloric content, but without product elimination. The anthropometric and thyroid parameters have changed in both groups during the nutritional intervention. This research showed that weight reduction may improve thyroid function in patients suffering from obesity and Hashimoto’s disease 60. Moreover, an individually selected elimination reducing diet was more effective than classic reducing diets with the same energy intake and macronutrient content and can lead to better therapeutic outcomes, which may cause an anti-inflammatory effect 60.

One case report 61 showed a novel approach that led to the improvement of symptoms and a reduction of thyroid antibodies in a 23-year-old woman with Hashimoto’s disease. The woman presented with symptoms of fatigue, hair loss, energy and mood disturbance, problems with insomnia and daytime napping. The thyroid antibodies were strongly positive, with a normal TSH level. Integrative treatment was started, which involved nutritional changes and micronutrient supplementation 61. This supplementation supported the methylation cycle, anti-oxidant capacity and stress management, and included vitamin C, vitamin B1, vitamin B2, vitamin B5, vitamin B6, Pyridoxal-5 Phosphate, zinc picolonate, L-5 methyltetrahydrofolate, magnesium glycinate, selenomethionine, N- Acetyl Cysteine and methylcobalamin (vitamin B12). The patient followed a paleo-style diet without grains and dairy products and increased consumption of bone broth and fermented foods as well as organic animal protein as tolerated. In addition, daily meditation and mindfulness techniques were recommended, and gentle exercise three times a week was added. After 15 months of treatment, there was a reduction in antithyroid antibodies and a significant relief of symptoms. This case demonstrated the potential benefits of an integrative approach to autoimmunity and oxidative stress in Hashimoto’s disease 61.

In a pilot study by Abbott et al. 62, women participated in a 10-week online health coaching program focused on implementing an “autoimmune protocol diet”. They applied a modified paleolithic diet. In the referred study, there were no significant changes in thyroid function markers, as well as serum antithyroid antibody concentrations, although the number of immune cells and an inflammatory processes marker (high sensitivity CRP) were decreased. These results suggest that an “autoimmune protocol” may decrease inflammation and modulate the immune system. Moreover, the therapy improves health-related quality of life (measured by 36-Item Short-Form Health Survey) and reduces symptoms of the diseases (measured by the Medical Symptoms Questionnaire) 62. A case study with a 49-year-old obese Hashimoto’s disease woman indicated that a modified autoimmune paleo low-calorie diet might improve TSH, anti-TPO antibody, body composition and lipid profile 63.

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  48. Effraimidis G., Tijssen J.G.P., Brosschot J.F., Wiersinga W.M. Involvement of Stress in the Pathogenesis of Autoimmune Thyroid Disease: A Prospective Study. Psychoneuroendocrinology. 2012;37:1191–1198. doi: 10.1016/j.psyneuen.2011.12.009
  49. Markomanolaki ZS, Tigani X, Siamatras T, Bacopoulou F, Tsartsalis A, Artemiadis A, Megalooikonomou V, Vlachakis D, Chrousos GP, Darviri C. Stress Management in Women with Hashimoto’s thyroiditis: A Randomized Controlled Trial. J Mol Biochem. 2019;8(1):3-12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6688766
  50. Rostami R., Nourooz-Zadeh S., Mohammadi A., Khalkhali H.R., Ferns G., Nourooz-Zadeh J. Serum Selenium Status and Its Interrelationship with Serum Biomarkers of Thyroid Function and Antioxidant Defense in Hashimoto’s Thyroiditis. Antioxidants. 2020;9:1070. doi: 10.3390/antiox9111070
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Health topicsThyroid Gland

Hashimoto’s thyroidits

by Health Jade Team 3 on
Hashimoto’s disease

Hashimoto’s thyroidits

Hashimoto’s thyroiditis also known as Hashimoto’s disease, chronic lymphocytic thyroiditis, autoimmune thyroiditis or chronic thyroiditis, is the most common cause of hypothyroidism (underactive thyroid gland) in the United States. Hashimoto’s thyroiditis is an autoimmune disorder in which antibodies attacks your thyroid gland, preventing it from producing enough thyroid hormones (tri-iodothyronine [T3] and thyroxine [T4]). Hashimoto’s thyroiditis is distinguished by the presence of autoantibodies against thyroid peroxidase (anti-TPO or antibody to thyroid peroxidase) and thyroglobulin (anti-Tg or thyroglobulin antibody) 1. Low thyroid hormone levels may cause hypothyroidism with a range of symptoms, such as tiredness or fatigue, weight gain, intolerance to cold temperatures, dry skin or dry thinning hair, slowed heart rate, heavy or irregular menstrual periods or fertility problems. Rarely, early in the course of the disease, thyroid gland damage may lead to the release of too much thyroid hormone into your blood, causing symptoms of hyperthyroidism called Hashitoxicosis 2, 3. Hashitoxicosis occurs as a result of the biochemical release of preformed thyroid hormone due to autoimmune destruction of the thyroid. Too much thyroid hormone (hyperthyroidism) can cause weight loss, despite an increased appetite. You might also feel anxious and find it difficult to relax. Hashitoxicosis precedes the signs and symptoms of the hypothyroid state associated with Hashimoto’s thyroiditis and lasts a few weeks to months 2.

Your thyroid gland is a butterfly-shaped gland with 2 lobes (the right lobe and the left lobe — joined by a narrow piece of the thyroid gland called the isthmus) that is located in front of your neck near the base of your throat, beneath the larynx (voice box or Adam’s apple) (Figure 1). In most people, the thyroid gland cannot be seen or felt. Your thyroid gland produces thyroid hormones, tri-iodothyronine (T3) and thyroxine (T4) (the main hormones that your thyroid gland makes) and calcitonin. The thyroid hormones, T3 (tri-iodothyronine) and T4 (thyroxine) influence important body processes such as body temperature, energy levels, growth, your digestion, muscles and heart. Thyroid hormones are important for how your body uses energy, your metabolism, so thyroid hormones affect nearly every organ in your body even the way your heart beats. You might put on weight and feel very tired and lacking in energy if your thyroid gland doesn’t make enough T3 (tri-iodothyronine) and T4 (thyroxine).

Calcitonin is another hormone produced by the thyroid gland. Calcitonin helps to control the amount of calcium circulating in your blood. Calcitonin works with a hormone called parathyroid hormone (PTH) to do this. Parathyroid hormone is made by parathyroid glands. These sit behind and are attached to the thyroid gland (see Figure 1).

In people with Hashimoto’s disease:

  • the immune system makes antibodies that attack the thyroid gland (autoimmune disorder). Usually in Hashimoto’s disease, the immune system produces an antibody to thyroid peroxidase (TPO), a protein that plays an important part in thyroid hormone production. Most people with Hashimoto’s disease will have TPO (thyroid peroxidase) antibodies in their blood. Lab tests for other antibodies associated with Hashimoto’s disease may need to be done.
  • large numbers of white blood cells, which are part of the immune system, build up in the thyroid gland
  • the thyroid gland becomes damaged and can’t make enough thyroid hormones

Hashimoto’s disease is an autoimmune disorder affecting the thyroid gland. In Hashimoto’s thyroiditis, the immune-system cells lead to the death of the thyroid’s hormone-producing cells. Hashimoto’s disease usually results in a decline in thyroid hormones production (hypothyroidism).

The symptoms of hypothyroidism might be mild, or they might be severe. They include:

  • fatigue
  • being unable to stand the cold
  • weight gain
  • constipation
  • muscle pain
  • dry skin, thin hair and / or brittle nails
  • low sex drive (libido)

Hashimoto’s disease can also cause cognitive symptoms including:

  • depression or low mood
  • an inability to concentrate
  • poor memory

In some cases, your thyroid gland may become noticeably larger (called a goiter) or it may shrink. Lumps or nodules may also develop in your thyroid gland.

Although Hashimoto’s disease can affect people of all ages, it’s most common in women in their 30s and 40s 4. The female-to-male ratio is at least 10:1 3. If someone in your family has had thyroid disease, you may have an increased risk for Hashimoto’s disease. No one is sure why people get Hashimoto’s disease.

If you have symptoms of hypothyroidism, see your doctor. Your doctor will examine you and may run blood tests, including testing your thyroid hormone levels.

If left untreated, hypothyroidism can lead to problems including goiter (an increase in the size of the thyroid gland), heart problems or mental health problems. Occasionally, it can lead to a potentially life-threatening disorder called myxedema coma.

While there is no cure for Hashimoto’s disease, hypothyroidism can be treated. The primary treatment of Hashimoto’s disease is thyroid hormone replacement. Most people with Hashimoto’s disease take a synthetic thyroid hormone medication called levothyroxine (Levoxyl, Synthroid, others) to treat hypothyroidism. The synthetic thyroid hormone works like the T4 hormone naturally produced by the thyroid. Your hypothyroidism can be well-controlled with thyroid hormone medicine, as long as you take the medicine as instructed by your doctor and have regular follow-up blood tests.

If you have mild hypothyroidism, you may not need to have treatment but get regular thyroid stimulating hormone (TSH) tests to monitor thyroid hormone levels.

How common is Hashimoto’s disease?

The number of people who have Hashimoto’s disease in the United States is unknown. However, Hashimoto’s disease is the most common cause of hypothyroidism the United States, which affects about 5 in 100 Americans 5.

Hashimoto is also the most common cause of hypothyroidism in those areas of the world where iodine intake is adequate. The incidence is estimated to be 0.8 per 1000 per year in men and 3.5 per 1000 per year in women 3. The prevalence of thyroid disease, in general, increases with age.

How does eating, diet, and nutrition affect Hashimoto’s disease?

The thyroid gland uses iodine, a mineral in some foods, to make thyroid hormones. However, if you have Hashimoto’s disease or other types of autoimmune thyroid disorders, you may be sensitive to harmful side effects from iodine. Eating foods that have large amounts of iodine—such as kelp, dulse, or other kinds of seaweed, and certain iodine-rich medicines—may cause hypothyroidism or make it worse. Taking iodine supplements can have the same effect.

Talk with members of your health care team about:

  • what foods and beverages to limit or avoid
  • whether you take iodine supplements
  • any cough syrups you take that may contain iodine

However, if you are pregnant, you need to take enough iodine because the baby gets iodine from your diet. Too much iodine can cause problems as well, such as a goiter in the baby. If you are pregnant, talk with your doctor about how much iodine you need.

Researchers are looking at other ways in which diet and supplements such as vitamin D and selenium may affect Hashimoto’s disease 6. However, no specific guidance is currently available 3.

How much iodine do I need?

The amount of iodine you need each day depends on your age. Average daily recommended amounts are listed below in micrograms (mcg).

Table 1 lists the current Recommended Dietary Allowances (RDA – the average daily level of intake sufficient to meet the nutrient requirements of nearly all [97%–98%] healthy individuals; often used to plan nutritionally adequate diets for individuals) for iodine 7. For infants from birth to 12 months, the Food and Nutrition Board at the Institute of Medicine of the National Academies established an Adequate Intake (AI) for iodine that is equivalent to the mean intake of iodine in healthy, breastfed infants in the United States.

The World Health Organization (WHO), United Nations Children’s Fund (UNICEF), and the International Council for the Control of Iodine Deficiency Disorders (ICCIDD) recommend a slightly higher iodine intake for pregnant women of 250 mcg per day 8, 9.

Table 1. Recommended Dietary Allowances (RDAs) for Iodine

AgeMaleFemalePregnancyLactation
Birth to 6 months110 mcg*110 mcg*
7–12 months130 mcg*130 mcg*
1–3 years90 mcg90 mcg
4–8 years90 mcg90 mcg
9–13 years120 mcg120 mcg
14–18 years150 mcg150 mcg220 mcg290 mcg
19+ years150 mcg150 mcg220 mcg290 mcg

Footnote: * Adequate Intake (AI)

What foods are good source for iodine?

Seaweed (such as kelp, nori, kombu, and wakame) is one of the best food sources of iodine 10. Other good sources include fish and other seafood, as well as eggs (see Table 2). Iodine is also present in human breast milk 7 and infant formulas 11. The U.S. Department of Agriculture (USDA) lists the iodine content of numerous foods and beverages 11.

Dairy products contain iodine. However, the amount of iodine in dairy products varies by whether the cows received iodine feed supplements and whether iodophor sanitizing agents were used to clean the cows and milk-processing equipment 12. For example, an analysis of 44 samples of nonfat milk found a range of 38 to 159 mcg per cup (with an average of 85 mcg/cup used for Table 2) 11. Plant-based beverages used as milk substitutes, such as soy and almond beverages, contain relatively small amounts of iodine.

Most commercially prepared bread contains very little iodine unless the manufacturer has used potassium iodate or calcium iodate as a dough conditioner 13. Manufacturers list dough conditioners as an ingredient on product labels but are not required to include iodine on the Nutrition Facts label 14, even though these conditioners provide a substantial amount of iodine. According to 2019 data from the USDA Branded Food Products Database, approximately 20% of ingredient labels for white bread, whole-wheat bread, hamburger buns, and hot dog buns listed iodate. Pasta is not a source of iodine unless it is prepared in water containing iodized salt because it absorbs some of the iodine 15.

Most fruits and vegetables are poor sources of iodine, and the amounts they contain are affected by the iodine content of the soil, fertilizer use, and irrigation practices 13. This variability affects the iodine content of meat and animal products because of its impact on the iodine content of foods that the animals consume 16. The iodine amounts in different seaweed species also vary greatly. For example, commercially available seaweeds in whole or sheet form have iodine concentrations ranging from 16 mcg/g to 2,984 mcg/g 17. For these reasons, the values for the foods listed in Table 2 are approximate but can be used as a guide for estimating iodine intakes.

Table 2. Iodine Content of Selected Foods

FoodMicrograms (mcg)
per serving		Percent DV*
Seaweed, nori, dried, 10 g232155
Bread, whole-wheat, made with iodate dough conditioner, 1 slice198132
Bread, white, enriched, made with iodate dough conditioner, 1 slice185123
Cod, baked, 3 ounces158106
Yogurt, Greek, plain, nonfat, 1 cup11677
Oysters, cooked, 3 ounces9362
Milk, nonfat, 1 cup8557
Iodized table salt, 1.5 g (approx. ¼ teaspoon)7651
Fish sticks, cooked, 3 ounces5839
Pasta, enriched, boiled in water with iodized salt, 1 cup3624
Egg, hard boiled, 1 large2617
Ice cream, chocolate, ½ cup2114
Liver, beef, cooked, 3 ounces149
Cheese, cheddar, 1 ounce149
Shrimp, cooked, 3 ounces139
Tuna, canned in water, drained, 3 ounces75
Soy beverage, 1 cup75
Fruit cocktail in light syrup, canned, ½ cup64
Beef, chuck, roasted, 3 ounces32
Chicken breast, roasted, 3 ounces21
Almond beverage, 1 cup21
Apple juice, 1 cup11
Bread, whole-wheat, made without iodate dough conditioner, 1 slice11
Bread, white, enriched, made without iodate dough conditioner, 1 slice11
Raisin bran cereal, 1 cup11
Rice, brown, cooked, ½ cup11
Corn, canned, ½ cup11
Sea salt, non-iodized, 1.5 g (approx. ¼ teaspoon)<1<1
Broccoli, boiled, ½ cup00
Banana, 1 medium00
Lima beans, mature, boiled, ½ cup00
Green peas, frozen, boiled, ½ cup00
Pasta, enriched, boiled in water without iodized salt, 1 cup00

Footnotes: *DV = Daily Value. The U.S. Food and Drug Administration (FDA) developed DVs to help consumers compare the nutrient contents of foods and dietary supplements within the context of a total diet. The DV for iodine is 150 mcg for adults and children aged 4 years and older. FDA does not require food labels to list iodine content unless iodine has been added to the food. Foods providing 20% or more of the DV are considered to be high sources of a nutrient, but foods providing lower percentages of the DV also contribute to a healthful diet.

[Source 11 ]

Thyroid gland

The thyroid gland is the largest adult gland to have a purely endocrine function, weighing about 25-30 g. The thyroid gland is a small butterfly shaped gland with 2 lobes, the right lobe and the left lobe joined by a narrow piece of the thyroid gland called the isthmus, that is located in front of your neck near the base of your throat, beneath the larynx (voice box or Adam’s apple). About 50% of thyroid glands have a small third lobe, called the pyramidal lobe. It extends superiorly from the isthmus. The thyroid gland makes and releases hormones. You can’t usually feel a thyroid gland that is normal.

The thyroid gland has 2 main types of cells:

  • Follicular cells use iodine from the blood to make thyroid hormones, which help regulate a person’s metabolism. Having too much thyroid hormone (hyperthyroidism) can cause a fast or irregular heartbeat, trouble sleeping, nervousness, hunger, weight loss, and a feeling of being too warm. Having too little thyroid hormone (hypothyroidism) causes a person to slow down, feel tired, and gain weight. The amount of thyroid hormone released by the thyroid gland is regulated by the pituitary gland at the base of the brain, which makes a substance called thyroid-stimulating hormone (TSH) (see Figure 5).
  • C cells also called parafollicular cells at the periphery of the follicles that make calcitonin, a hormone that helps control how your body uses calcium. The parafollicular cells (C cells) respond to rising levels of blood calcium by secreting the hormone calcitonin. Calcitonin antagonizes (blocks) parathyroid hormone (PTH) and stimulates osteoblast activity, thus promoting calcium deposition and bone formation. It is important mainly in children, having relatively little effect in adults.

Other, less common cells in the thyroid gland include immune system cells (lymphocytes) and supportive (stromal) cells.

Thyroid hormone is secreted or inhibited in response to fluctuations in metabolic rate. The brain monitors the body’s metabolic rate and stimulates thyroid hormone secretion through the action of thyrotropin-releasing hormone (TRH) and thyroid stimulating hormone (TSH) as depicted in figure 5.

The primary effect of thyroid hormone (TH) is to increase one’s metabolic rate. As a result, it raises oxygen consumption and has a calorigenic effect—it increases heat production. To ensure an adequate blood and oxygen supply to meet this increased metabolic demand, thyroid hormone also raises the breathing (respiratory) rate, heart rate, and strength of the heartbeat. It stimulates the appetite and accelerates the breakdown of carbohydrates, fats, and protein for fuel. Thyroid hormone also promotes alertness and quicker reflexes; growth hormone secretion; growth of the bones, skin, hair, nails, and teeth; and development of the fetal nervous system.

Figure 1. Thyroid gland and parathyroid gland

Thyroid gland and parathyroid gland

Thyroid gland

Footnotes: Anatomy of the thyroid and parathyroid glands. The thyroid gland lies at the base of the throat near the trachea. It is shaped like a butterfly, with the right lobe and left lobe connected by a thin piece of tissue called the isthmus. The parathyroid glands are four pea-sized organs found in the neck near the thyroid. The thyroid and parathyroid glands make hormones.

Figure 2. Thyroid gland location

Thyroid gland location

Figure 3. Thyroid gland anatomy

Thyroid gland anatomy

Footnote: (a) Gross anatomy, anterior view. (b) Histology, showing the saccular thyroid follicles (the source of thyroid hormone) and nests of C cells (the source of calcitonin).

What does the thyroid gland do?

Formation, storage, and release of thyroid hormones

The thyroid gland is the only endocrine gland that stores its secretory product in large quantities—normally about a 100-day supply. Synthesis and secretion of triiodothyronine (T3) and thyroxine or tetraiodothyronine (T4) occurs as follows:

  1. Iodide trapping. Thyroid follicular cells trap iodide ions (I −) by actively transporting them from the blood into the cytosol. As a result, the thyroid gland normally contains most of the iodide in the body.
  2. Synthesis of thyroglobulin. While the follicular cells are trapping I −, they are also synthesizing thyroglobulin (TGB), a large glycoprotein that is produced in the rough endoplasmic reticulum, modified in the Golgi complex, and packaged into secretory vesicles. The vesicles then undergo exocytosis, which releases thyroglobulin into the lumen of the follicle.
  3. Oxidation of iodide. Some of the amino acids in thyroglobulin are tyrosines that will become iodinated. However, negatively charged iodide  (I −) ions cannot bind to tyrosine until they undergo oxidation (removal of electrons) to iodine: I −→ I. As the iodide ions are being oxidized, they pass through the membrane into the lumen of the follicle.
  4. Iodination of tyrosine. As iodine atoms (I) form, they react with tyrosines that are part of thyroglobulin molecules. Binding of one iodine atom yields monoiodotyrosine (T1), and a second iodination produces diiodotyrosine (T2). The thyroglobulin with attached iodine atoms, a sticky material that accumulates and is stored in the lumen of the thyroid follicle, is termed colloid.
  5. Coupling of monoiodotyrosine (T1) and diiodotyrosine (T2). During the last step in the synthesis of thyroid hormone, two diiodotyrosine (T2) molecules join to form thyroxine (T4) or one T1 and one T2 join to form triiodothyronine (T3).
  6. Pinocytosis and digestion of colloid. Droplets of colloid reenter follicular cells by pinocytosis and merge with lysosomes. Digestive enzymes in the lysosomes break down thyroglobulin, cleaving off molecules of triiodothyronine (T3) and thyroxine (T4).
  7. Secretion of thyroid hormones. Because T3 and T4 are lipid soluble, they diffuse through the plasma membrane into interstitial fluid and then into the blood. T4 normally is secreted in greater quantity than T3, but T3 is several times more potent. Moreover, after T4 enters a body cell, most of it is converted to T3 by removal of one iodine.
  8. Transport thyroid hormones in the blood. More than 99% of both the T3 and the T4 combine with transport proteins in the blood, mainly thyroxine binding globulin (TBG).

Figure 4. Thyroid hormones

Thyroid hormones

Actions of thyroid hormones

Because most body cells have receptors for thyroid hormones, triiodothyronine (T3) and thyroxine (T4) affect tissues throughout the body. Thyroid hormones act on their target cells mainly by inducing gene transcription and protein synthesis. The newly formed proteins in turn carry out the cellular response.

Functions of thyroid hormones include the following:

  1. Increase basal metabolic rate. Thyroid hormones raise the basal metabolic rate (BMR), the rate of energy expenditure under standard or basal conditions (awake, at rest, and fasting). When basal metabolic rate increases, cellular metabolism of carbohydrates, lipids, and proteins increases. Thyroid hormones increase BMR in several ways: (1) They stimulate synthesis of additional Na+/K+ ATPases, which use large amounts of ATP to continually eject sodium ions (Na+) from cytosol into extracellular fluid and potassium ions (K+) from extracellular fluid into cytosol; (2) they increase the concentrations of enzymes involved in cellular respiration, which increases the breakdown of organic fuels and ATP production; and (3) they increase the number and activity of mitochondria in cells, which also increases ATP production. As cells produce and use more ATP, basal metabolic rate increases, more heat is given off and body temperature rises, a phenomenon called the calorigenic effect. In this way, thyroid hormones play an important role in the maintenance of normal body temperature. Normal mammals can survive in freezing temperatures, but those whose thyroid glands have been removed cannot.
  2. Enhance actions of catechlolamines. Thyroid hormones have permissive effects on the catecholamines (epinephrine and norepinephrine) because they up-regulate β-adrenergic receptors. Catecholamines bind to β-adrenergic receptors, promoting sympathetic responses. Therefore, symptoms of excess levels of thyroid hormone include increased heart rate, more forceful heartbeats, and increased blood pressure.
  3. Regulate development and growth of nervous tissue and bones. Thyroid hormones are necessary for the development of the nervous system: They promote synapse formation, myelin production, and growth of dendrites. Thyroid hormones are also required for growth of the skeletal system: They promote formation of ossification centers in developing bones, synthesis of many bone proteins, and secretion of growth hormone (GH) and insulin-like growth factors (IGFs). Deficiency of thyroid hormones during fetal development, infancy, or childhood causes severe mental retardation and stunted bone growth.

Control of thyroid hormone secretion

Thyrotropin-releasing hormone (TRH) from the hypothalamus and thyroid-stimulating hormone (TSH) from the anterior pituitary stimulate secretion of thyroid hormones, as shown in Figure 5:

  1. Low blood levels of T3 and T4 or low metabolic rate stimulate the hypothalamus to secrete thyrotropin-releasing hormone (TRH).
  2. Thyrotropin-releasing hormone (TRH) enters the hypothalamic–hypophyseal portal system and flows to the anterior pituitary, where it stimulates thyrotrophs to secrete thyroid stimulating hormone (TSH).
  3. Thyroid stimulating hormone (TSH) stimulates virtually all aspects of thyroid follicular cell activity, including iodide trapping, hormone synthesis and secretion, and growth of the follicular cells.
  4. The thyroid follicular cells release T3 and T4 into the blood until the metabolic rate returns to normal.
  5. An elevated level of T3 inhibits release of TRH and TSH (negative feedback inhibition).

Conditions that increase ATP demand—a cold environment, hypoglycemia, high altitude, and pregnancy—increase the secretion of the thyroid hormones.

Figure 5. Control of thyroid hormone secretion

Control of thyroid hormone secretion

Footnote: Negative Feedback Inhibition of the Anterior Pituitary Gland by the Thyroid Gland

Control of calcium balance

The hormone produced by the parafollicular cells of the thyroid gland is calcitonin. Calcitonin can decrease the level of calcium in the blood by inhibiting the action of osteoclasts, the cells that break down bone extracellular matrix. The secretion of calcitonin is controlled by a negative feedback system (see Figure 7).

Calcitonin is produced by C cells (clear cells) of the thyroid gland. It is secreted when the blood calcium concentration rises too high, and it lowers the concentration by two principal mechanisms:

  1. Osteoclast inhibition. Within 15 minutes after it is secreted, calcitonin reduces osteoclast activity by as much as 70%, so osteoclasts liberate less calcium from the skeleton.
  2. Osteoblast stimulation. Within an hour, calcitonin increases the number and activity of osteoblasts, which deposit calcium into the skeleton.

Calcitonin plays an important role in children but has only a weak effect in most adults. The osteoclasts of children are highly active in skeletal remodeling and release 5 g or more of calcium into the blood each day. By inhibiting this activity, calcitonin can significantly lower the blood calcium level in children. In adults, however, the osteoclasts release only about 0.8 g of calcium per day. Calcitonin cannot change adult blood calcium very much by suppressing this lesser contribution. Calcitonin deficiency is not known to cause any adult disease. Calcitonin may, however, inhibit bone loss in pregnant and lactating women. Miacalcin, a calcitonin extract derived from salmon that is 10 times more potent than human calcitonin, is prescribed to treat osteoporosis.

Figure 6. Hormonal control of calcium balance

Hormonal control of calcium balance

Footnote: The central panel represents the blood reservoir of calcium and shows its normal (safe) range. Calcitriol and Parathyroid Hormone (PTH) regulate calcium exchanges between the blood and the small intestine and kidneys (left). Calcitonin, calcitriol, and Parathyroid Hormone (PTH) regulate calcium exchanges between blood and bone (right).

Hashimoto’s thyroiditis causes

The cause of Hashimoto’s disease or Hashimoto’s thyroidits is poorly understood 18. Hashimoto’s thyroiditis is an autoimmune disease that destroys thyroid cells by cell and antibody-mediated immune processes. Your immune system creates antibodies that attack thyroid cells as if they were bacteria, viruses or some other foreign body. Your immune system wrongly enlists disease-fighting agents that damage cells and lead to cell death. Most Hashimoto’s disease patients develop antibodies to a variety of thyroid antigens, the most common of which is anti-thyroid peroxidase (anti-TPO or antibody to thyroid peroxidase). Many also form antithyroglobulin (anti-Tg or thyroglobulin antibody) and TSH receptor-blocking antibodies (TBII) 18. These antibodies attack your thyroid tissue, eventually leading to inadequate production of thyroid hormone. There is a small subset of the population, no more than 10-15% with the clinically evident disease, that are serum antibody-negative. Positive anti-thyroid peroxidase (anti-TPO) antibodies point to the clinical syndrome 19, 20.

What causes your immune system to attack thyroid cells is not clear. Multiple factors from the external environment and the genetic background contribute to the pathogenesis of Hashimoto’s disease 21. These genetic, environmental, and existential factors provoke the immune system to produce antibodies to thyroid antigens 22, 23, 24, 25, 26, 27, 28, 29. The most important factors associated with Hashimoto’s thyroiditis are summarized in Table 3 below.

Hashimoto’s disease or Hashimoto’s thyroidits can also be part of the Polyglandular Autoimmune Syndrome type 2 with autoimmune adrenal deficiency and type-1 diabetes 30. Hashimoto thyroiditis is also related to several other autoimmune diseases such as pernicious anemia, adrenal insufficiency, and celiac disease. Ruggeri et al. 31 found that Hashimoto disease is associated with a variety of different non-thyroidal autoimmune diseases (NTADs) and diagnosis in adulthood made these even more prevalent.

The onset of Hashimoto’s disease may be related to 19, 20, 32, 33:

  • Genetic factors. Twin studies have shown an increased concordance of autoimmune thyroiditis in monozygotic twins as compared with dizygotic twins. Danish studies have demonstrated concordance rates of 55% in monozygotic twins, compared with only 3% in dizygotic twins 34. This data suggests that 79% of predisposition is due to genetic factors, allotting 21% for environmental and sex hormone influences. 
  • Environmental triggers, such as infection, stress or radiation exposure
  • Interactions between environmental and genetic factors.

Hypothyroidism can also be caused by:

  • some medicines used to treat bipolar disorder or other mental health problems
  • iodine-containing medicines used to treat abnormal heart rhythm
  • exposure to toxins, such as nuclear radiation
  • viruses, such as hepatitis C

Several genes have been involved in Hashimoto’s disease pathogenesis, including genes of the immune response (coded in the Human Leukocyte Antigen (HLA) complex) and thyroid function 21. Other immunoregulatory genes are involved in the development of Hashimoto’s disease, including the single nucleotide polymorphisms (SNPs) in cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), protein tyrosine phosphatase non-receptor type 22 (PTPN22), and CD40 35, 22, 27, 36.

Among the environmental factors are inadequate or excessive iodine intake, infections, or the intake of certain medications 22, 27, 26, 28, 37. Several of the currently used anticancer drugs, such as interferon-alpha, may cause autoimmune thyroid dysfunction 38, 29. The role of smoking and alcohol consumption in the etiopathogenesis of Hashimoto’s disease is still not clear 21. The data suggest that moderate alcohol consumption may protect against Hashimoto’s disease and the development of overt hypothyroidism 29, 39, 40. Furthermore, some studies indicate that smoking decreases the levels of thyroid autoantibodies and the risk of hypothyroidism. However, the mechanism for these protective effects of smoking and drinking remains unclear and must be clarified with future studies 29, 39, 40. In recent years, the influence of stress on the development and course of Hashimoto’s disease has also been investigated. Some studies suggest that stress is involved in the pathogenesis of Hashimoto’s disease, while other evidence indicates that it has no effect 29, 41. A randomized controlled trial by Markomanolaki et al. 42 showed that managing stress is also important in treating Hashimoto’s disease patients. After eight weeks of stress management intervention, patients demonstrated a reduction in antithyroglobulin (anti-Tg) titers, decreased levels of stress, depression, anxiety and improved lifestyle 42. Additionally, the adequate levels of vitamin D and selenium may help prevent or delay the onset of Hashimoto’s disease 26, 28, 43, 44. Moreover, the risk of Hashimoto’s disease is increased in other autoimmune diseases 45, 29.

Most Hashimoto’s disease patients develop antibodies to a variety of thyroid antigens, the most common of which is anti-thyroid peroxidase (anti-TPO). Many also form antithyroglobulin (anti-Tg) and TSH receptor-blocking antibodies (TBII) 3. These antibodies attack the thyroid tissue, eventually leading to inadequate production of thyroid hormone. There is a small subset of the population, no more than 10-15% with the clinically evident disease, that are serum antibody-negative 3.

Table 3. Genetic, environmental and existential factors associated with Hashimoto’s thyroiditis

Genetic FactorsEnvironmental FactorsExistential Factors
Histocompatibility genes
(HLA class I and II)		IodineSex
Immunoregulatory genes (SNPs in HLA, CTLA-4, PTPN22, CD40 genes)Medications (e.g., interferon-α, lithium, amiodarone)Associated diseases
(e.g., type 1 diabetes mellitus, pernicious anaemia, coeliac disease, myasthenia gravis)
Thyroid-specific genesInfections
(e.g., hepatitis C virus)		Age
Genes associated with thyroid peroxidase antibody synthesisSmokingPregnancy
SeleniumDown’s syndrome
Vitamin DMicrobiome composition
AlcoholFamilial aggregation
Radiation Exposure
[Source 21 ]

Risk factors for Hashimoto’s thyroiditis

The following factors are associated with an increased risk of Hashimoto’s disease 6:

  • Sex. Women are much more likely to get Hashimoto’s disease.
  • Age. Hashimoto’s disease can occur at any age but more commonly occurs during middle age.
  • Other autoimmune disease. Having another autoimmune disease — such as rheumatoid arthritis, type 1 diabetes or lupus — increases your risk of developing Hashimoto’s disease.
  • Genetics and family history. You’re at higher risk for Hashimoto’s disease if others in your family have thyroid disorders or other autoimmune diseases.
  • Pregnancy. Typical changes in immune function during pregnancy may be a factor in Hashimoto’s disease that begins after pregnancy.
  • Excessive iodine intake. Too much iodine in the diet may function as a trigger among people already at risk for Hashimoto’s disease.
  • Radiation exposure. People exposed to excessive levels of environmental radiation are more prone to Hashimoto’s disease.

Hashimoto’s thyroiditis symptoms

Signs and symptoms of Hashimoto’s disease vary widely and are not specific to the disorder. Hashimoto’s disease progresses slowly over the years. Many people with Hashimoto’s disease may not notice signs or symptoms of the disease at first. An ordinary blood test may just show a thyroid hormone imbalance. Because the thyroid gland may grow and get larger, you may have a feeling of fullness or tightness in your throat, though it is usually not painful. You may have trouble swallowing food or liquids. You might have a swelling (a bump) in the front of your neck, the enlarged thyroid is called a goiter. After many years, or even decades, damage to the thyroid may cause the gland to shrink and the goiter to disappear.

Some people with Hashimoto’s disease have symptoms such as tiredness, forgetfulness, depression, coarse dry skin, slow heartbeat, weight gain, constipation and intolerance to cold. A blood test can tell if your thyroid gland is underactive. Other blood tests can be done to look for Hashimoto’s disease.

Eventually, the decline in thyroid hormone production can result in hypothyroidism with any of the following:

  • Fatigue and sluggishness
  • Increased sensitivity to cold
  • Increased sleepiness
  • Dry skin
  • Constipation
  • Muscle weakness
  • Muscle aches, tenderness and stiffness
  • Joint pain and stiffness
  • Irregular or excessive menstrual bleeding
  • Depression
  • Problems with memory or concentration
  • Swelling of the thyroid (goiter)
  • A puffy face
  • Brittle nails
  • Hair loss
  • Enlargement of the tongue

Because these symptoms could result from any number of disorders, it’s important to see your doctor as soon as possible for a timely and accurate diagnosis.

When to see a doctor

See your doctor if you develop these signs and symptoms:

  • Tiredness for no apparent reason
  • Dry skin
  • Pale, puffy face
  • Constipation

You’ll also need to see your doctor for periodic testing of your thyroid function if:

  • You’ve had thyroid surgery
  • You’ve had treatment with radioactive iodine or anti-thyroid medications
  • You’ve had radiation therapy to your head, neck or upper chest

If you have high blood cholesterol, talk to your doctor about whether hypothyroidism may be a cause.

And if you’re receiving hormone therapy for hypothyroidism caused by Hashimoto’s thyroiditis, schedule follow-up visits as often as your doctor recommends. It’s important to make sure you’re receiving the correct dose of medicine. Over time, the dose you need to adequately replace your thyroid function may change.

Hashimoto’s thyroiditis complications

Thyroid hormones are essential for the healthy function of many body systems. Therefore, when Hashimoto’s disease and hypothyroidism are left untreated, many complications can occur. These include:

  • Goiter. A goiter is enlargement of the thyroid. As thyroid hormone production declines due to Hashimoto’s disease, the thyroid receives signals from the pituitary gland to make more. This cycle may result in a goiter. It’s generally not uncomfortable, but a large goiter can affect your appearance and may interfere with swallowing or breathing.
  • Heart problems. Hypothyroidism can result in poor heart function, an enlarged heart and irregular heartbeats. It can also result in high levels of low-density lipoprotein (LDL) cholesterol — the “bad” cholesterol — that is a risk factor for cardiovascular disease and heart failure.
  • Peripheral neuropathy. Hypothyroidism that goes without treatment for a long time can damage the peripheral nerves. These are the nerves that carry information from the brain and spinal cord to the rest of the body. Peripheral neuropathy may cause pain, numbness and tingling in the arms and legs.
  • Infertility. Low levels of thyroid hormone can interfere with ovulation, which can limit fertility. Some of the causes of hypothyroidism, such as autoimmune disorders, also can harm fertility.
  • Mental health issues. Depression or other mental health disorders may occur early in Hashimoto’s disease and may become more severe over time.
  • Sexual and reproductive dysfunction. In women, hypothyroidism can result in a reduced sexual desire (libido), an inability to ovulate, and irregular and excessive menstrual bleeding. Men with hypothyroidism may have a reduced libido, erectile dysfunction and a lowered sperm count.
  • Poor pregnancy outcomes. Hypothyroidism during pregnancy may increase the risk of a miscarriage or preterm birth. Babies born to women with untreated hypothyroidism are at risk for decreased intellectual abilities, autism, speech delays and other developmental disorders.
  • Birth defects. Babies born to people with untreated thyroid disease may have a higher risk of birth defects compared with babies born to mothers who do not have thyroid disease. Infants with hypothyroidism present at birth that goes untreated are at risk of serious physical and mental development problems. But if the condition is diagnosed within the first few months of life, the chances of typical development are excellent.
  • Myxedema coma. This rare, life-threatening condition can develop due to long-term, severe, untreated hypothyroidism. Its signs and symptoms include drowsiness followed by profound lethargy and unconsciousness. A myxedema coma may be triggered by exposure to cold, sedatives, infection or other stress on your body. Myxedema requires immediate emergency medical treatment.

Hashimoto’s thyroiditis diagnosis

In general, your doctor may test for Hashimoto’s thyroiditis if you’re feeling increasingly tired or sluggish, have dry skin, constipation, and a hoarse voice, or have had previous thyroid problems or goiter.

Diagnosis of Hashimoto’s thyroiditis is based on your signs and symptoms and the results of blood tests that measure levels of thyroid hormone and thyroid-stimulating hormone (TSH) produced in the pituitary gland. These may include:

  • A hormone test. Blood tests can determine the amount of hormones produced by your thyroid and pituitary glands. If your thyroid is underactive, the level of thyroid hormone is low. At the same time, the level of TSH is elevated because your pituitary gland tries to stimulate your thyroid gland to produce more thyroid hormone.
  • An antibody test. Because Hashimoto’s thyroiditis is an autoimmune disorder, the cause involves production of abnormal antibodies. A blood test may confirm the presence of antibodies against thyroid peroxidase (TPO antibodies), an enzyme normally found in the thyroid gland that plays an important role in the production of thyroid hormones.

In the past, doctors weren’t able to detect an underactive thyroid (hypothyroidism), the main indicator of Hashimoto’s thyroiditis, until symptoms were fairly advanced. But by using the sensitive TSH test, doctors can diagnose thyroid disorders much earlier, often before you experience symptoms.

Because the TSH test is the best screening test, your doctor will likely check TSH first and follow with a thyroid hormone test if needed. TSH tests also play an important role in managing hypothyroidism. These tests also help your doctor determine the right dosage of medication, both initially and over time.

Testing thyroid function

To determine if hypothyroidism is the cause of your symptoms, your doctor will order blood tests that may include the following:

  • Thyroid stimulating hormone (TSH) test. Thyroid stimulating hormone (TSH) is produced by the pituitary gland. When the pituitary detects low thyroid hormones in the blood, it sends TSH to the thyroid to prompt an increase in thyroid hormone production. High TSH levels in the blood indicates hypothyroidism.
  • Thyroxine (T4) tests. The main thyroid hormone is thyroxine (T4). A low blood level of T4 confirms the findings of a TSH (thyroid stimulating hormone) test and indicates the problem is within the thyroid itself.

Antibody tests

More than one disease process can lead to hypothyroidism. To determine if Hashimoto’s disease is the cause of hypothyroidism, your doctor will order an antibody test.

The intended purpose of an antibody is to flag disease-causing foreign agents that need to be destroyed by other actors in the immune system. In an autoimmune disorder, the immune system produces rogue antibodies that target healthy cells or proteins in the body.

Usually in Hashimoto’s disease, the immune system produces an antibody to thyroid peroxidase (anti-TPO), a protein that plays an important part in thyroid hormone production. Most people with Hashimoto’s disease will have TPO antibodies (anti-TPO) in their blood. Lab tests for other antibodies associated with Hashimoto’s disease may also need to be done.

Thyroglobulin antibodies (anti-Tg) can also be a sign of Hashimoto disease. Most people with Hashimoto disease have high levels of both thyroglobulin antibodies (anti-Tg) and TPO antibodies (anti-TPO).

Circulating antibody to thyroid peroxidase (anti-TPO) are found in about 90% of Hashimoto’s disease patients. Anti-thyroglobulin antibodies (anti-Tg) are less sensitive (positive in about 60–80% of patients) and less specific than antibody to thyroid peroxidase (anti-TPO) 46, 22, 47.

You probably won’t need other tests to confirm you have Hashimoto’s disease. However, if your doctor suspects Hashimoto’s disease but you don’t have antithyroid antibodies in your blood, you may have an ultrasound of your thyroid. The ultrasound images can show the size of your thyroid and other features of Hashimoto’s disease. The ultrasound also can rule out other causes of an enlarged thyroid, such as thyroid nodules—small lumps in the thyroid gland.

Hashimoto’s thyroiditis treatment

How your doctors treat Hashimoto’s disease usually depends on whether your thyroid is damaged enough to cause hypothyroidism. If you don’t have hypothyroidism or you have mild hypothyroidism, your doctor may choose to simply check your symptoms and do regular thyroid stimulating hormone (TSH) tests to monitor your thyroid hormone levels.

Most people with Hashimoto’s disease need take a synthetic thyroid hormone medication called levothyroxine (Levoxyl, Synthroid, others) to treat hypothyroidism. The synthetic thyroid hormone works like the thyroxine (T4) hormone naturally produced by your thyroid. Prescribed in pill form for many years, this medicine is now also available as a liquid and in a soft gel capsule 6. These newer formulas may be helpful to people with digestive problems that affect how the thyroid hormone pill is absorbed.

Some foods and supplements can affect how well your body absorbs levothyroxine. Examples include grapefruit juice, espresso coffee, soy, and multivitamins that contain iron or calcium 5, 48. Taking levothyroxine on an empty stomach can prevent this from happening. Your doctor may ask you to take the levothyroxine in the morning, 30 to 60 minutes before you eat your first meal.

Your doctor will give you a blood test about 6 to 8 weeks after you begin taking levothyroxine and adjust your dose if needed. Each time you change your dose, you’ll have another blood test. Once you’ve reached a dose that’s working for you, your doctor will likely repeat the blood test in 6 months and then once a year.

Never stop taking your levothyroxine or take a higher dose without talking with your doctor first. Taking too much thyroid hormone medicine can cause serious problems, such as atrial fibrillation or osteoporosis 32.

Thyroxine (T4) hormone replacement therapy

Hypothyroidism associated with Hashimoto’s disease is treated with a synthetic hormone called levothyroxine (Levoxyl, Synthroid, others). The recommended dose of levothyroxine is 1.6 to 1.8 mcg/kg/day 3. The synthetic hormone works like the thyroxine (T4) hormone naturally produced by the thyroid. The treatment goal is to restore and maintain adequate thyroxine (T4) hormone levels and improve symptoms of hypothyroidism. You will need this treatment for the rest of your life.

Monitoring the dosage

Your doctor will determine a dosage of levothyroxine that’s appropriate for your age, weight, current thyroid production, other medical conditions and other factors. Your doctor will retest your TSH (thyroid stimulating hormone) levels about 6 to 10 weeks later and adjust the dosage as necessary.

Once the best dosage is determined, you will continue to take the medication once a day. You’ll need follow-up tests once a year to monitor TSH (thyroid stimulating hormone) levels or any time after your doctor changes your dosage.

A levothyroxine pill is usually taken in the morning before you eat. Talk to your doctor if you have any questions about when or how to take the pill. Also, ask what to do if you accidentally skip a dose. If your health insurance requires you to switch to a generic drug or a different brand, talk to your doctor.

Precautions

Because levothyroxine acts like natural thyroxine (T4) in your body, there are generally no side effects as long as the treatment is resulting in “natural” levels of thyroxine (T4) for your body.

Too much thyroid hormone can worsen bone loss that causes weak, brittle bones (osteoporosis) or cause irregular heartbeats (arrhythmias) the most common being atrial fibrillation.

Effects of other substances

Certain medications, supplements and foods may affect your ability to absorb levothyroxine. It may be necessary to take levothyroxine at least four hours before these substances. Talk to your doctor about any of the following:

  • Soy products
  • High-fiber foods
  • Iron supplements, including multivitamins that contain iron
  • Cholestyramine (Prevalite), a medication used to lower blood cholesterol levels
  • Aluminum hydroxide, which is found in some antacids
  • Sucralfate, an ulcer medication
  • Calcium supplements

Triiodothyronine (T3) hormone replacement therapy

Naturally produced thyroxine (T4) is converted into another thyroid hormone called triiodothyronine (T3). The thyroxine (T4) replacement hormone is also converted into triiodothyronine (T3), and for most people the thyroxine (T4) replacement therapy results in an adequate supply of triiodothyronine (T3) for the body.

For people who need better symptom control, a doctor also may prescribe a synthetic triiodothyronine (T3) (Cytomel) or a synthetic T4 and T3 combination. Side effects of triiodothyronine (T3) hormone replacement include rapid heartbeat, insomnia and anxiety. These treatments may be tested with a trial period of 3 to 6 months.

Is a combination of hormones needed?

Levothyroxine is the synthetic form of the natural thyroxine (T4). Thyroxine (T4) is converted into Triiodothyronine (T3) in the body. While most people are treated successfully with levothyroxine alone, some people don’t feel completely normal on levothyroxine.

Researchers have investigated whether adjusting standard hypothyroidism treatment to replace some thyroxine (T4) with small amounts of triiodothyronine (T3) may offer benefit. But, the majority of studies have determined that the addition of triiodothyronine (T3) does not offer any advantage over treatment with thyroxine (T4) alone.

There is some evidence that triiodothyronine (T3) may offer benefit to certain subsets of people, such as people who have had their thyroid surgically removed (thyroidectomy). Research is ongoing.

Triiodothyronine (T3) can be given alone as liothyronine (Cytomel) or in combination with thyroxine (T4) as liotrix (Thyrolar). Taking a combination T4 and T3 ends up producing higher than normal levels of triiodothyronine (T3), especially soon after the medication is taken. This can cause a fast heart rate, anxiety and trouble sleeping.

But, for those who haven’t gotten enough relief from thyroxine (T4) alone, adding Cytomel to standard levothyroxine treatment for a three- to six-month trial is a long enough period to see if the combination helps you.

Alternative medicine

Products with triiodothyronine (T3) and thyroxine (T4) hormones derived from pigs or other animals are available as prescriptions or as dietary supplements, such as Armour Thyroid, in the United States. Concerns about these products include the following:

  • The balance of thyroxine (T4) and triiodothyronine (T3) in animals isn’t the same as in humans.
  • The exact amount of thyroxine (T4) and triiodothyronine (T3) in each batch of a natural extract product can vary, leading to unpredictable levels of these hormones in your blood.

Anti-inflammatory diet

An anti-inflammatory diet rich in vitamins, minerals and polyphenols is recommended as diet therapy for Hashimoto’s disease 49, 37, 50. The theory behind the inflammation has to do with the leaky gut syndrome, where there is an insult to the gut mucosa, which allows the penetrance of proteins that do not typically enter the bloodstream via transporters in the gut mucosa. It is theorized that a response similar to molecular mimicry occurs, and antibodies are produced against the antigens. Unfortunately, the antigen may be very structurally similar to thyroid peroxidase, leading to antibody formation against this enzyme. The concept of an autoimmune diet is based on healing the gut and decreasing the severity of the autoimmune response.

Natural antioxidants like vitamin A, vitamin C and vitamin E are found in products of plant origin, including a wide variety of vegetables and fruits. Sources of vitamin C include broccoli, peppers, black currant, strawberries, lemons, spinach, kiwifruit, oranges, grapefruit, limes, tomatoes, raspberries, asparagus, pineapples, fennel and parsley. The best source of vitamin E is avocado, nuts, seeds, egg, milk and whole grains. In addition, vitamin A is present in foods such as liver, carrot, broccoli, butter, pumpkin, cheese, egg, mango and milk 51. According to the current findings, the Mediterranean diet may show the most benefits for Hashimoto’s disease patients with its antioxidant properties 52.

One study by Ostrowska et al. 53 assessed the effectiveness of two “reducing diets” and their effect on thyroid parameters in female obese patients with Hashimoto’s disease. All women who received levothyroxine, selenium and zinc were randomly assigned to the study group following individually balanced elimination/reducing diets, in accordance with the previously performer food sensitivity tests, and the control group following reducing diets with the same caloric content, but without product elimination. The anthropometric and thyroid parameters have changed in both groups during the nutritional intervention. This research showed that weight reduction may improve thyroid function in patients suffering from obesity and Hashimoto’s disease 53. Moreover, an individually selected elimination reducing diet was more effective than classic reducing diets with the same energy intake and macronutrient content and can lead to better therapeutic outcomes, which may cause an anti-inflammatory effect 53.

One case report 54 showed a novel approach that led to the improvement of symptoms and a reduction of thyroid antibodies in a 23-year-old woman with Hashimoto’s disease. The woman presented with symptoms of fatigue, hair loss, energy and mood disturbance, problems with insomnia and daytime napping. The thyroid antibodies were strongly positive, with a normal TSH level. Integrative treatment was started, which involved nutritional changes and micronutrient supplementation 54. This supplementation supported the methylation cycle, anti-oxidant capacity and stress management, and included vitamin C, vitamin B1, vitamin B2, vitamin B5, vitamin B6, Pyridoxal-5 Phosphate, zinc picolonate, L-5 methyltetrahydrofolate, magnesium glycinate, selenomethionine, N- Acetyl Cysteine and methylcobalamin (vitamin B12). The patient followed a paleo-style diet without grains and dairy products and increased consumption of bone broth and fermented foods as well as organic animal protein as tolerated. In addition, daily meditation and mindfulness techniques were recommended, and gentle exercise three times a week was added. After 15 months of treatment, there was a reduction in antithyroid antibodies and a significant relief of symptoms. This case demonstrated the potential benefits of an integrative approach to autoimmunity and oxidative stress in Hashimoto’s disease 54.

In a pilot study by Abbott et al. 55, women participated in a 10-week online health coaching program focused on implementing an “autoimmune protocol diet”. They applied a modified paleolithic diet. In the referred study, there were no significant changes in thyroid function markers, as well as serum antithyroid antibody concentrations, although the number of immune cells and an inflammatory processes marker (high sensitivity CRP) were decreased. These results suggest that an “autoimmune protocol” may decrease inflammation and modulate the immune system. Moreover, the therapy improves health-related quality of life (measured by 36-Item Short-Form Health Survey) and reduces symptoms of the diseases (measured by the Medical Symptoms Questionnaire) 55. A case study with a 49-year-old obese Hashimoto’s disease woman indicated that a modified autoimmune paleo low-calorie diet might improve TSH, anti-TPO antibody, body composition and lipid profile 56.

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  32. Chaker L, Bianco AC, Jonklaas J, Peeters RP. Hypothyroidism. Lancet. 2017 Sep 23;390(10101):1550-1562. doi: 10.1016/S0140-6736(17)30703-1
  33. Ott J, Promberger R, Kober F, Neuhold N, Tea M, Huber JC, Hermann M. Hashimoto’s thyroiditis affects symptom load and quality of life unrelated to hypothyroidism: a prospective case-control study in women undergoing thyroidectomy for benign goiter. Thyroid. 2011 Feb;21(2):161-7. doi: 10.1089/thy.2010.0191. Epub 2010 Dec 27. Erratum in: Thyroid. 2011 Apr;21(4):467.
  34. Brix TH, Hegedüs L, Gardas A, Banga JP, Nielsen CH. Monozygotic twin pairs discordant for Hashimoto’s thyroiditis share a high proportion of thyroid peroxidase autoantibodies to the immunodominant region A. Further evidence for genetic transmission of epitopic “fingerprints”. Autoimmunity. 2011 May;44(3):188-94. doi: 10.3109/08916934.2010.518575
  35. Klubo-Gwiezdzinska J., Wartofsky L. Hashimoto Thyroiditis: An Evidence-Based Guide to Etiology, Diagnosis and Treatment. Pol. Arch. Intern. Med. 2022;132:16222. doi: 10.20452/pamw.16222
  36. Kust D., Matesa N. The Impact of Familial Predisposition on the Development of Hashimoto’s Thyroiditis. Acta Clin. Belg. 2020;75:104–108. doi: 10.1080/17843286.2018.1555115
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  38. Torino F., Barnabei A., Paragliola R., Baldelli R., Appetecchia M., Corsello S.M. Thyroid Dysfunction as an Unintended Side Effect of Anticancer Drugs. Thyroid. 2013;23:1345–1366. doi: 10.1089/thy.2013.0241
  39. Carlé A., Pedersen I.B., Knudsen N., Perrild H., Ovesen L., Rasmussen L.B., Jørgensen T., Laurberg P. Moderate Alcohol Consumption May Protect against Overt Autoimmune Hypothyroidism: A Population-Based Case-Control Study. Eur. J. Endocrinol. 2012;167:483–490. doi: 10.1530/EJE-12-0356
  40. Effraimidis G., Tijssen J.G.P., Wiersinga W.M. Alcohol Consumption as a Risk Factor for Autoimmune Thyroid Disease: A Prospective Study. Eur. Thyroid J. 2012;1:99–104. doi: 10.1159/000338920
  41. Effraimidis G., Tijssen J.G.P., Brosschot J.F., Wiersinga W.M. Involvement of Stress in the Pathogenesis of Autoimmune Thyroid Disease: A Prospective Study. Psychoneuroendocrinology. 2012;37:1191–1198. doi: 10.1016/j.psyneuen.2011.12.009
  42. Markomanolaki ZS, Tigani X, Siamatras T, Bacopoulou F, Tsartsalis A, Artemiadis A, Megalooikonomou V, Vlachakis D, Chrousos GP, Darviri C. Stress Management in Women with Hashimoto’s thyroiditis: A Randomized Controlled Trial. J Mol Biochem. 2019;8(1):3-12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6688766
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12 Body SystemsThyroid Gland

Thyroid gland

by Health Jade Team on
thyroid gland

What is the thyroid gland

The thyroid gland is the largest adult gland to have a purely endocrine function, weighing about 25-30 g. The butterfly-shaped thyroid gland is located adjacent to the trachea just inferior to the larynx (voice box) and is named for the nearby shield like thyroid cartilage of the larynx.

The thyroid gland is composed of right and left lateral lobes, one on either side of the trachea, that are connected by an isthmus in front of the trachea. About 50% of thyroid glands have a small third lobe, called the pyramidal lobe. It extends superiorly from the isthmus.

Microscopic spherical sacs called thyroid follicles make up most of the thyroid gland. The wall of each follicle consists primarily of cells called follicular cells, most of which extend to the lumen (internal space) of the follicle. A basement membrane surrounds each follicle. When the follicular cells are inactive, their shape is low cuboidal to squamous, but under the influence of thyroid stimulating hormone (TSH) they become active in secretion and range from cuboidal to low columnar in shape. The follicular cells produce two hormones: thyroxine, which is also called tetraiodothyronine (T4) because it contains four atoms of iodine and triiodothyronine (T3), which contains three atoms of iodine. T3 and T4 together are also known as thyroid hormones.

A few cells called parafollicular cells or C cells lie between follicles. They produce the hormone calcitonin, which helps regulate calcium homeostasis.

Like other endocrine glands, the thyroid releases these hormones directly into the bloodstream. Each follicle is surrounded by a basket like network of capillaries, the globular clusters of blood vessels. These are supplied by the superior and inferior thyroid arteries. The thyroid receives one of the body’s highest rates of blood flow per gram of tissue and consequently has a dark reddish brown color.

Thyroid hormone is secreted or inhibited in response to fluctuations in metabolic rate. The brain monitors the body’s metabolic rate and stimulates thyroid hormone (TH) secretion through the action of thyrotropin-releasing hormone (TRH) and thyroid stimulating hormone (TSH) as depicted in figure 3.

The primary effect of thyroid hormone (TH) is to increase one’s metabolic rate. As a result, it raises oxygen consumption and has a calorigenic effect—it increases heat production. To ensure an adequate blood and oxygen supply to meet this increased metabolic demand, thyroid hormone also raises the respiratory rate, heart rate, and strength of the heartbeat. It stimulates the appetite and accelerates the breakdown of carbohydrates, fats, and protein for fuel. Thyroid hormone also promotes alertness and quicker reflexes; growth hormone secretion; growth of the bones, skin, hair, nails, and teeth; and development of the fetal nervous system.

The thyroid gland also contains nests of parafollicular cells, also called clear (C) cells, at the periphery of the follicles. They respond to rising levels of blood calcium by secreting the hormone calcitonin. Calcitonin antagonizes parathyroid hormone and stimulates osteoblast activity, thus promoting calcium deposition and bone formation. It is important mainly in children, having relatively little effect in adults.

Figure 1. Thyroid gland and parathyroid gland

Thyroid gland

Footnotes: Anatomy of the thyroid and parathyroid glands. The thyroid gland lies at the base of the throat near the trachea. It is shaped like a butterfly, with the right lobe and left lobe connected by a thin piece of tissue called the isthmus. The parathyroid glands are four pea-sized organs found in the neck near the thyroid. The thyroid and parathyroid glands make hormones.

Figure 2. Thyroid gland

Thyroid gland

Figure 3. Thyroid gland location

Thyroid gland location

Thyroid gland function

Formation, Storage, and Release of Thyroid Hormones

The thyroid gland is the only endocrine gland that stores its secretory product in large quantities—normally about a 100-day supply. Synthesis and secretion of triiodothyronine (T3) and tetraiodothyronine (T4) occurs as follows:

  1. Iodide trapping. Thyroid follicular cells trap iodide ions (I −) by actively transporting them from the blood into the cytosol. As a result, the thyroid gland normally contains most of the iodide in the body.
  2. Synthesis of thyroglobulin. While the follicular cells are trapping I −, they are also synthesizing thyroglobulin (TGB), a large glycoprotein that is produced in the rough endoplasmic reticulum, modified in the Golgi complex, and packaged into secretory vesicles. The vesicles then undergo exocytosis, which releases thyroglobulin into the lumen of the follicle.
  3. Oxidation of iodide. Some of the amino acids in thyroglobulin are tyrosines that will become iodinated. However, negatively charged iodide  (I −) ions cannot bind to tyrosine until they undergo oxidation (removal of electrons) to iodine: I −→ I. As the iodide ions are being oxidized, they pass through the membrane into the lumen of the follicle.
  4. Iodination of tyrosine. As iodine atoms (I) form, they react with tyrosines that are part of thyroglobulin molecules. Binding of one iodine atom yields monoiodotyrosine (T1), and a second iodination produces diiodotyrosine (T2). The thyroglobulin with attached iodine atoms, a sticky material that accumulates and is stored in the lumen of the thyroid follicle, is termed colloid.
  5. Coupling of monoiodotyrosine (T1) and diiodotyrosine (T2). During the last step in the synthesis of thyroid hormone, two diiodotyrosine (T2) molecules join to form tetraiodothyronine (T4) or one T1 and one T2 join to form triiodothyronine (T3).
  6. Pinocytosis and digestion of colloid. Droplets of colloid reenter follicular cells by pinocytosis and merge with lysosomes. Digestive enzymes in the lysosomes break down thyroglobulin, cleaving off molecules of T3 and T4.
  7. Secretion of thyroid hormones. Because T3 and T4 are lipid soluble, they diffuse through the plasma membrane into interstitial fluid and then into the blood. T4 normally is secreted in greater quantity than T3, but T3 is several times more potent. Moreover, after T4 enters a body cell, most of it is converted to T3 by removal of one iodine.
  8. Transport in the blood. More than 99% of both the T3 and the T4 combine with transport proteins in the blood, mainly thyroxine binding globulin (TBG).

Figure 4. Thyroid gland anatomy

Thyroid gland anatomy

Footnote: (a) Gross anatomy, anterior view. (b) Histology, showing the saccular thyroid follicles (the source of thyroid hormone) and nests of C cells (the source of calcitonin).

Actions of Thyroid Hormones

Because most body cells have receptors for thyroid hormones, T3 and T4 affect tissues throughout the body. Thyroid hormones act on their target cells mainly by inducing gene transcription and protein synthesis. The newly formed proteins in turn carry out the cellular response.

Functions of thyroid hormones include the following:

  1. Increase basal metabolic rate. Thyroid hormones raise the basal metabolic rate (BMR), the rate of energy expenditure under standard or basal conditions (awake, at rest, and fasting). When basal metabolic rate increases, cellular metabolism of carbohydrates, lipids, and proteins increases. Thyroid hormones increase BMR in several ways: (1) They stimulate synthesis of additional Na+/K+ ATPases, which use large amounts of ATP to continually eject sodium ions (Na+) from cytosol into extracellular fluid and potassium ions (K+) from extracellular fluid into cytosol; (2) they increase the concentrations of enzymes involved in cellular respiration, which increases the breakdown of organic fuels and ATP production; and (3) they increase the number and activity of mitochondria in cells, which also increases ATP production. As cells produce and use more ATP, basal metabolic rate increases, more heat is given off and body temperature rises, a phenomenon called the calorigenic effect. In this way, thyroid hormones play an important role in the maintenance of normal body temperature. Normal mammals can survive in freezing temperatures, but those whose thyroid glands have been removed cannot.
  2. Enhance actions of catechlolamines. Thyroid hormones have permissive effects on the catecholamines (epinephrine and norepinephrine) because they up-regulate β-adrenergic receptors. Catecholamines bind to β-adrenergic receptors, promoting sympathetic responses. Therefore, symptoms of excess levels of thyroid hormone include increased heart rate, more forceful heartbeats, and increased blood pressure.
  3. Regulate development and growth of nervous tissue and bones. Thyroid hormones are necessary for the development of the nervous system: They promote synapse formation, myelin production, and growth of dendrites. Thyroid hormones are also required for growth of the skeletal system: They promote formation of ossification centers in developing bones, synthesis of many bone proteins, and secretion of growth hormone (GH) and insulin-like growth factors (IGFs). Deficiency of thyroid hormones during fetal development, infancy, or childhood causes severe mental retardation and stunted bone growth.

Control of Thyroid Hormone Secretion

Thyrotropin-releasing hormone (TRH) from the hypothalamus and thyroid-stimulating hormone (TSH) from the anterior pituitary stimulate secretion of thyroid hormones, as shown in Figure 5:

  1. Low blood levels of T3 and T4 or low metabolic rate stimulate the hypothalamus to secrete thyrotropin-releasing hormone (TRH).
  2. Thyrotropin-releasing hormone (TRH) enters the hypothalamic–hypophyseal portal system and flows to the anterior pituitary, where it stimulates thyrotrophs to secrete thyroid stimulating hormone (TSH).
  3. Thyroid stimulating hormone (TSH) stimulates virtually all aspects of thyroid follicular cell activity, including iodide trapping, hormone synthesis and secretion, and growth of the follicular cells.
  4. The thyroid follicular cells release T3 and T4 into the blood until the metabolic rate returns to normal.
  5. An elevated level of T3 inhibits release of TRH and TSH (negative feedback inhibition).

Conditions that increase ATP demand—a cold environment, hypoglycemia, high altitude, and pregnancy—increase the secretion of the thyroid hormones.

Figure 5. Control of thyroid hormone secretion

Control of thyroid hormone secretion

Footnote: Negative Feedback Inhibition of the Anterior Pituitary Gland by the Thyroid Gland

Control of calcium balance

The hormone produced by the parafollicular cells of the thyroid gland is calcitonin. Calcitonin can decrease the level of calcium in the blood by inhibiting the action of osteoclasts, the cells that break down bone extracellular matrix. The secretion of calcitonin is controlled by a negative feedback system (see Figure 7).

Calcitonin is produced by C cells (clear cells) of the thyroid gland. It is secreted when the blood calcium concentration rises too high, and it lowers the concentration by two principal mechanisms:

  1. Osteoclast inhibition. Within 15 minutes after it is secreted, calcitonin reduces osteoclast activity by as much as 70%, so osteoclasts liberate less calcium from the skeleton.
  2. Osteoblast stimulation. Within an hour, calcitonin increases the number and activity of osteoblasts, which deposit calcium into the skeleton.

Calcitonin plays an important role in children but has only a weak effect in most adults. The osteoclasts of children are highly active in skeletal remodeling and release 5 g or more of calcium into the blood each day. By inhibiting this activity, calcitonin can significantly lower the blood calcium level in children. In adults, however, the osteoclasts release only about 0.8 g of calcium per day. Calcitonin cannot change adult blood calcium very much by suppressing this lesser contribution. Calcitonin deficiency is not known to cause any adult disease. Calcitonin may, however, inhibit bone loss in pregnant and lactating women. Miacalcin, a calcitonin extract derived from salmon that is 10 times more potent than human calcitonin, is prescribed to treat osteoporosis.

Figure 6. Hormonal control of calcium balance

Hormonal control of calcium balance

Footnote: The central panel represents the blood reservoir of calcium and shows its normal (safe) range. Calcitriol and Parathyroid Hormone (PTH) regulate calcium exchanges between the blood and the small intestine and kidneys (left). Calcitonin, calcitriol, and Parathyroid Hormone (PTH) regulate calcium exchanges between blood and bone (right).

Figure 7. Correction of hypercalcemia (high blood calcium)

correction of high blood calcium

Footnote: Correction of high blood calcium by calcitonin

Thyroid gland problems

Thyroid hormones (T3 and T4) regulate how the body breaks down food and either uses that energy immediately or stores it for the future. In other words, your thyroid hormones regulate your body’s metabolism.

Another gland, called the anterior pituitary gland, actually controls how well the thyroid works. The anterior pituitary gland is located at the base of the brain and produces thyroid-stimulating hormone (TSH). The bloodstream carries TSH to the thyroid gland, where it tells the thyroid to produce more thyroid hormones, as needed.

Thyroid hormones influence virtually every organ system in the body. They tell organs how fast or slow they should work. Thyroid hormones also regulate the consumption of oxygen and the production of heat.

When outside influences such as disease, damage to the thyroid or certain medicines break down communication between your thyroid and the anterior pituitary gland and the hypothalamus, your thyroid might not produce enough hormone. This would slow down all of your body’s functions, a condition known as hypothyroidism or underactive thyroid. Your thyroid could also produce too much hormone sending your systems into overdrive, a condition known as hyperthyroidism or overactive thyroid. These two conditions are most often features of an underlying thyroid disease.

Thyroid problems include:

  • Goiter – enlargement of the thyroid gland
  • Hyperthyroidism – when your thyroid gland makes more thyroid hormones than your body needs
  • Hypothyroidism – when your thyroid gland does not make enough thyroid hormones
  • Thyroid cancer
  • Thyroid nodules – lumps in the thyroid gland
  • Thyroiditis – swelling of the thyroid

To diagnose thyroid diseases, doctors use a medical history, physical exam, and thyroid tests. They sometimes also use a biopsy. Treatment depends on the problem, but may include medicines, radioiodine therapy, or thyroid surgery.

What is Goiter ?

A simple goiter is an enlargement of the thyroid gland 1. It is usually not a tumor or cancer.

Simple goiters are more common in:

  • People over age 40
  • People with a family history of goiter
  • Women

Causes of goiter

The thyroid gland is an important organ of the endocrine system. It is located at the front of the neck just above where your collarbones meet. The gland makes the hormones that control the way every cell in the body uses energy. This process is called metabolism.

Iodine deficiency is the most common cause of goiter. The body needs iodine to produce thyroid hormone. If you do not have enough iodine in your diet, the thyroid gets larger to try and capture all the iodine it can, so it can make the right amount of thyroid hormone. So, a goiter can be a sign the thyroid is not able to make enough thyroid hormone. The use of iodized salt in the United States prevents a lack of iodine in the diet.

Other causes of goiter include:

  • The body’s immune system attacking the thyroid gland (autoimmune problem) e.g. Graves’ disease
  • Certain medicines (lithium, amiodarone)
  • Infections
  • Cigarette smoking
  • Certain foods (soy, peanuts, vegetables in the broccoli and cabbage family)
  • Toxic nodular goiter, an enlarged thyroid gland that has a small, rounded growth or many growths called nodules, which produce too much thyroid hormone.

Symptoms of goiter

The main symptom is an enlarged thyroid gland. The size may range from a single small nodule to a large mass at the front of the neck.

Some people with a simple goiter may have symptoms of an underactive thyroid gland.

In rare cases, an enlarged thyroid can put pressure on the windpipe (trachea) and food tube (esophagus). This can lead to:

  • Breathing difficulties (with very large goiters), especially when lying flat on the back
  • Cough
  • Hoarseness
  • Swallowing difficulties, especially with solid food
  • Pain in the area of the thyroid

How is goiter diagnosed ?

The health care provider will do a physical exam. This involves feeling your neck as you swallow. Swelling in the area of the thyroid may be felt.

If you have a very large goiter, you may have pressure on your neck veins. As a result, when the provider asks you to raise your arms above your head, you may feel dizzy.

Blood tests may be ordered to measure thyroid function:

  • Free thyroxine (T4)
  • Thyroid stimulating hormone (TSH)

Tests to look for abnormal and possibly cancerous areas in the thyroid gland include:

  • Thyroid scan and uptake
  • Ultrasound of the thyroid

If nodules are found on an ultrasound, a biopsy may be needed to check for thyroid cancer.

Treatment of goiter

A goiter only needs to be treated if it is causing symptoms.

Treatments for an enlarged thyroid include:

  • Thyroid hormone replacement pills if the goiter is due to an underactive thyroid
  • Small doses of Lugol’s iodine or potassium iodine solution if the goiter is due to a lack of iodine
  • Radioactive iodine to shrink the gland, especially if the thyroid is producing too much thyroid hormone
  • Surgery (thyroidectomy) to remove all or part of the gland

Outlook (Prognosis) of goiter

A simple goiter may disappear on its own, or may become larger. Over time, the thyroid gland may stop making enough thyroid hormone. This condition is called hypothyroidism.

In some cases, a goiter becomes toxic and produces thyroid hormone on its own. This can cause high levels of thyroid hormone, a condition called hyperthyroidism.

When to see a Medical Professional

Call your provider if you experience any swelling in the front of your neck or any other symptoms of goiter.

Prevention of goiter

Using iodized table salt prevents most simple goiters.

What is Hashimoto’s thyroiditis ?

Hashimoto’s thyroiditis (also called autoimmune or chronic lymphocytic thyroiditis) is the most common thyroid disease in the United States 2. It is an inherited condition that affects over 10 million Americans and is about seven times more common in women than in men.

Hashimoto’s thyroiditis is characterized by the production of immune cells and autoantibodies by the body’s immune system that can damage thyroid cells and compromise their ability to make thyroid hormone. Hypothyroidism occurs if the amount of thyroid hormone which can be produced is not enough for the body’s needs. The thyroid gland may also enlarge, forming a goiter.

Causes of Hashimoto’s thyroiditis

Hashimoto’s thyroiditis results from a malfunction in the immune system. When working properly, the immune system is designed to protect the body against invaders such as bacteria, viruses and other foreign substances. The immune system of someone with Hashimoto’s thyroiditis mistakenly recognizes normal thyroid cells as foreign tissue, and it produces antibodies that may destroy these cells. Although various environmental factors have been studied, none have been positively proven to be the cause of Hashimoto’s thyroiditis.

Signs & Symptoms of Hashimoto’s thyroiditis

Hashimoto’s thyroiditis may not cause symptoms for many years and may remain undiagnosed until an enlarged thyroid gland or abnormal blood tests are discovered as part of a routine examination. When symptoms do develop, they are either related to local pressure in the neck caused by the goiter itself or to the low levels of thyroid hormone.

The first sign of this disease may be painless swelling in the lower front of the neck. This enlargement may eventually become easily visible. It may be associated with an uncomfortable pressure sensation in the lower neck, and this pressure on surrounding structures may cause additional symptoms, including difficulty swallowing.

Although many of the symptoms associated with thyroid hormone deficiency occur commonly in patients without thyroid disease, patients with Hashimoto’s thyroiditis who develop hypothyroidism are more likely to experience the following:

  • Fatigue
  • Drowsiness
  • Forgetfulness
  • Difficulty with learning
  • Dry, brittle hair and nails
  • Dry, itchy skin
  • Puffy face
  • Constipation
  • Sore muscles
  • Weight gain
  • Heavy menstrual flow
  • Increased sensitivity to many medications

The thyroid enlargement and/or hypothyroidism caused by Hashimoto’s thyroiditis progresses in many patients, causing a slow worsening of symptoms. Therefore, patients should be recognized and adequately treated with thyroid hormone. Optimal treatment with thyroid hormone will eliminate any symptoms due to thyroid hormone deficiency, usually prevent further thyroid enlargement, and may sometimes cause shrinkage of an enlarged thyroid gland.

How is Hashimoto’s thyroiditis diagnosed ?

A physician experienced in the diagnosis and treatment of thyroid disease can detect a goiter due to Hashimoto’s thyroiditis by performing a physical examination and can recognize hypothyroidism by identifying characteristic symptoms, finding typical physical signs and performing appropriate laboratory tests.

Tests

THYROID ANTIBODIES: Testing for increased thyroid antibodies provides the most specific laboratory evidence of Hashimoto’s thyroiditis, but the antibodies are not present in all cases.

TSH (THYROID-STIMULATING HORMONE OR THYROTROPIN): Increased TSH level in the blood is the most accurate indicator of hypothyroidism. TSH is produced by another gland, the pituitary, which is located behind the nose at the base of the brain. The level of TSH rises dramatically when the thyroid gland even slightly under produces thyroid hormone. So, in patients with normal pituitary function, a normal level of TSH reliably excludes hypothyroidism.

FREE THYROXINE ESTIMATE: The active portion of all of the thyroxine circulating in the blood. A low level of free thyroxine is consistent with thyroid hormone deficiency. However, free thyroxine values in the “normal range” may actually represent thyroid hormone deficiency in a particular patient, since a high level of TSH stimulation may keep the free thyroxine levels “within normal limits” for many years.

FINE-NEEDLE ASPIRATION OF THE THYROID: Usually not necessary for most patients with Hashimoto’s thyroiditis, but a good way to diagnose difficult cases and a necessary procedure if a thyroid nodule is also present.

How is Hashimoto’s thyroiditis treated ?

For patients with thyroid enlargement (goiter) or hypothyroidism, thyroid hormone therapy is clearly needed, since proper dosage corrects any symptoms due to thyroid hormone deficiency and may decrease the goiter’s size. Treatment generally consists of taking a single daily tablet of levothyroxine. Older patients who may have underlying heart disease are usually started on a low dose and gradually increased, while younger, healthy patients can be started on full replacement doses at once.

While you may improve in many ways within a week, the full impact of thyroid medicine may take quite some time. For example, skin changes may take up to 3-6 months to resolve. Because of the generally permanent and often progressive nature of Hashimoto’s thyroiditis, it is usually necessary to treat it throughout one’s lifetime and to realize that dosage of medicine required may have to be adjusted from time to time.

Optimal adjustment of thyroid hormone dosage, guided by laboratory tests rather than symptoms alone, is critical, since the body is very sensitive to even small changes in thyroid hormone levels. Levothyroxine tablets come in 12 different strengths, and it is essential to take them in a consistent manner every day. If the dose is not adequate, the thyroid gland may continue to enlarge and symptoms of hypothyroidism will persist. This may be associated with increased serum cholesterol levels, possibly increasing the risk for atherosclerosis and heart disease. If the dose is too strong, it can cause symptoms of hyperthyroidism, creating excessive strain on the heart and an increased risk of developing osteoporosis.

What is hyperthyroidism ?

Hyperthyroidism develops when the body is exposed to excessive amounts of thyroid hormone. This disorder occurs in almost one percent of all Americans and affects women five to 10 times more often than men 3. In its mildest form, hyperthyroidism may not cause recognizable symptoms. More often, however, the symptoms are discomforting, disabling or even life-threatening.

What are the causes of hyperthyroidism ?

Graves’ disease: Graves’ disease (named after Irish physician Robert Graves) is an autoimmune disorder that frequently results in thyroid enlargement and hyperthyroidism. In some patients, swelling of the muscles and other tissues around the eyes may develop, causing eye prominence, discomfort or double vision. Like other autoimmune diseases, this condition tends to affect multiple family members. It is much more common in women than in men and tends to occur in younger patients.

Postpartum thyroiditis: Five to 10 percent of women develop mild to moderate hyperthyroidism within several months of giving birth. Hyperthyroidism in this condition usually lasts for approximately one to two months. It is often followed by several months of hypothyroidism, but most women will eventually recover normal thyroid function. In some cases, however, the thyroid gland does not heal, so the hypothyroidism becomes permanent and requires lifelong thyroid hormone replacement. This condition may occur again with subsequent pregnancies.

Silent thyroiditis: Transient (temporary) hyperthyroidism can be caused by silent thyroiditis, a condition which appears to be the same as postpartum thyroiditis, but is not related to pregnancy. It is not accompanied by a painful thyroid gland.

Subacute thyroiditis: This condition may follow a viral infection and is characterized by painful thyroid gland enlargement and inflammation, which results in the release of large amounts of thyroid hormones into the blood. Fortunately, this condition usually resolves spontaneously. The thyroid usually heals itself over several months, but often not before a temporary period of low thyroid hormone production (hypothyroidism) occurs.

Toxic multinodular goiter: Multiple nodules in the thyroid can produce excessive thyroid hormone, causing hyperthyroidism. Typically diagnosed in patients over the age of 50, this disorder is more likely to affect heart rhythm. In many cases, the person has had the goiter for many years before it becomes overactive.

Toxic nodule: A single nodule or lump in the thyroid can also produce more thyroid hormone than the body requires and lead to hyperthyroidism. This disorder is not familial.

Excessive iodine ingestion: Various sources of high iodine concentrations, such as kelp tablets, some expectorants, amiodarone (Cordarone, Pacerone – medications used to treat certain problems with heart rhythms) and x-ray dyes may occasionally cause hyperthyroidism in patients who are prone to it.

Overmedication with thyroid hormone: Patients who receive excessive thyroxine replacement treatment can develop hyperthyroidism. They should have their thyroid hormone dosage evaluated by a physician at least once each year and should NEVER give themselves “extra” doses.

What are the signs and symptoms of hyperthyroidism ?

When hyperthyroidism develops, a goiter (enlargement of the thyroid) is usually present and may be associated with some or many of the following features:

  • Fast heart rate, often more than 100 beats per minute
  • Becoming anxious, irritable, argumentative
  • Trembling hands
  • Weight loss, despite eating the same amount or even more than usual
  • Intolerance of warm temperatures and increased likelihood to perspire
  • Loss of scalp hair
  • Tendency of fingernails to separate from the nail bed
  • Muscle weakness, especially of the upper arms and thighs
  • Loose and frequent bowel movements
  • Smooth skin
  • Change in menstrual pattern
  • Increased likelihood for miscarriage
  • Prominent “stare” of the eyes
  • Protrusion of the eyes, with or without double vision (in patients with Graves’ disease)
  • Irregular heart rhythm, especially in patients older than 60 years of age
  • Accelerated loss of calcium from bones, which increases the risk of osteoporosis and fractures

How is hyperthyroidism diagnosed ?

Sometimes a general physician can diagnose and treat the cause of hyperthyroidism, but assistance is often needed from an endocrinologist, a physician who specializes in managing thyroid disease. Characteristic symptoms and physical signs of the disease can be detected by a trained physician. In addition, tests can be used to confirm the diagnosis and to determine the cause.

Tests

TSH (THYROID-STIMULATING HORMONE OR THYROTROPIN): A low TSH level in the blood is the most accurate indicator of hyperthyroidism. The body shuts off production of this pituitary hormone when the thyroid gland even slightly overproduces thyroid hormone. If the TSH level is low, it is very important to also check thyroid hormone levels to confirm the diagnosis of hyperthyroidism.

ESTIMATES OF FREE THYROXINE AND FREE TRIIODOTHYRONINE: When hyperthyroidism develops, free thyroxine and free triiodothyronine levels rise above previous values in that specific patient (although they may still fall within the normal range for the general population) and are often considerably elevated.

TSI (THYROID-STIMULATING IMMUNOGLOBULIN): A substance often found in the blood when Graves’ disease is the cause of hyperthyroidism.

RADIOACTIVE IODINE UPTAKE (RAIU): The amount of iodine the thyroid gland can collect, and a thyroid scan, which shows how the iodine is distributed throughout the thyroid gland.

THYROID SCAN: This information can be useful in determining the cause of hyperthyroidism and, ultimately, its treatment.

How is hyperthyroidism treated ?

Appropriate management of hyperthyroidism requires careful evaluation and ongoing care by a physician experienced in the treatment of this complex condition.

Before the development of current treatment options, the death rate from severe hyperthyroidism was as high as 50 percent. Now several effective treatments are available and, with proper management, death from hyperthyroidism is rare. Deciding which treatment is best depends on what caused the hyperthyroidism, its severity and other conditions present.

  • Antithyroid Drugs

In the United States, two drugs are available for treating hyperthyroidism: propylthiouracil (PTU) and methimazole (Tapazole). Except for early pregnancy, methimazole is preferred because PTU can cause fatal liver damage, although rarely. These medications control hyperthyroidism by slowing thyroid hormone production. They may take several months to normalize thyroid hormone levels. Some patients with hyperthyroidism caused by Graves’ disease experience a spontaneous or natural remission of hyperthyroidism after a 12- to 18-month course of treatment with these drugs and may sometimes avoid permanent underactivity of the thyroid (hypothyroidism), which often occurs as a result of using the other methods of treating hyperthyroidism. Unfortunately, the remission is frequently only temporary, with the hyperthyroidism recurring after several months or years off medication and requiring additional treatment, so relatively few patients are treated solely with antithyroid medication in the United States.

Antithyroid drugs may cause an allergic reaction in about five percent of patients who use them. This usually occurs during the first six weeks of drug treatment. Such a reaction may include rash or hives; but after discontinuing use of the drug, the symptoms resolve within one to two weeks and there is no permanent damage.

A more serious side effect, but occurring in only about one in 250-500 patients during the first four to eight weeks of treatment, is a rapid decrease of white blood cells in the bloodstream. This could increase susceptibility to serious infection. Symptoms such as a sore throat, infection or fever should be reported promptly to your physician, and a white blood cell count should be done immediately. In nearly every case, when a person stops using the medication, the white blood cell count returns to normal. Very rarely, antithyroid drugs may cause severe liver problems, which can be detected by monitoring blood tests or joint problems characterized by joint pain and/or swelling. Your physician should be contacted if there is yellowing of the skin (jaundice), fever, loss of appetite or abdominal pain.

  • Radioactive Iodine Treatment

Iodine is an essential ingredient in the production of thyroid hormone. Each molecule of thyroid hormone contains either four (T4) or three (T3) molecules of iodine. Since most overactive thyroid glands are quite hungry for iodine, it was discovered in the 1940s that the thyroid could be “tricked” into destroying itself by simply feeding it radioactive iodine. The radioactive iodine is given by mouth, usually in capsule form, and is quickly absorbed from the bowel. It then enters the thyroid cells from the bloodstream and gradually destroys them. Maximal benefit is usually noted within three to six months.

It is not possible to eliminate “just the right amount” of the diseased thyroid gland, since radioiodine eventually damages all thyroid cells. Therefore, most endocrinologists strive to completely destroy the diseased thyroid gland with a single dose of radioiodine. This results in the intentional development of an underactive thyroid state (hypothyroidism), which is easily, predictably and inexpensively corrected by lifelong daily use of oral thyroid hormone replacement therapy. Although every effort is made to calculate the correct dose of radioiodine for each patient, not every treatment will successfully correct the hyperthyroidism, particularly if the goiter is quite large and a second dose of radioactive iodine is occasionally needed.

Thousands of patients have received radioiodine treatment, including former President of the United States George H. W. Bush and his wife, Barbara. The treatment is a very safe, simple and reliably effective one. Because of this, it is considered by most thyroid specialists in the United States to be the treatment of choice for hyperthyroidism cases caused by overproduction of thyroid hormone.

  • Surgical Removal of the Thyroid

Although seldom used now as the preferred treatment for hyperthyroidism, operating to remove most of the thyroid gland may occasionally be recommended in certain situations, such as a pregnant woman with severe uncontrolled disease in whom radioiodine would not be safe for the baby. Surgery usually leads to permanent hypothyroidism and lifelong thyroid hormone replacement therapy.

  • Other Treatments

A drug from the class of beta-adrenergic blocking agents (which decrease the effects of excess thyroid hormone) may be used temporarily to control hyperthyroid symptoms until other therapies take effect. In cases where hyperthyroidism is caused by thyroiditis or excessive ingestion of either iodine or thyroid hormone, this may be the only type of treatment required. Iodine drops are prescribed when hyperthyroidism is severe or prior to undergoing surgery for Graves’ disease.

What is hypothyroidism ?

An underactive thyroid, or hypothyroidism, occurs when the thyroid gland produces less than the normal amount of thyroid hormone. The result is the “slowing down” of many bodily functions. Although hypothyroidism may be temporary, it usually is a permanent condition. Of the nearly 30 million people estimated to be suffering from thyroid dysfunction, most have hypothyroidism.

Causes of hypothyroidism

Autoimmune thyroiditis: The body’s immune system may produce a reaction in the thyroid gland that results in hypothyroidism and, most often, a goiter (enlargement of the thyroid). Other autoimmune diseases may be associated with this disorder, and additional family members may also be affected.

Central or pituitary hypothyroidism: TSH (Thyroid-stimulating hormone) is produced by the pituitary gland, which is located behind the nose at the base of the brain. Any destructive disease of the pituitary gland or hypothalamus, which sits just above the pituitary gland, may cause damage to the cells that secrete TSH, which stimulates the thyroid to produce normal amounts of thyroid hormone. This is a very rare cause of hypothyroidism.

Congenital hypothyroidism: An infant may be born with an inadequate amount of thyroid tissue or an enzyme defect that does not allow normal thyroid hormone production. If this condition is not treated promptly, physical stunting and/or mental damage (cretinism) may develop.

Medications: Lithium, high doses of iodine and amiodarone — an antiarrhythmic agent used for various types of cardiac dysrhythmias — can cause hypothyroidism.

Postpartum thyroiditis: Five percent to 10 percent of women develop mild to moderate hyperthyroidism within several months of giving birth. Hyperthyroidism in this condition usually lasts for approximately one to two months. It is often followed by several months of hypothyroidism, but most women will eventually recover normal thyroid function. In some cases, however, the thyroid gland does not heal, so the hypothyroidism becomes permanent and requires lifelong thyroid hormone replacement. This condition may occur again with subsequent pregnancies.

Radioactive iodine treatment: Hypothyroidism frequently develops as a desired therapeutic goal after the use of radioactive iodine treatment for hyperthyroidism.

Silent Thyroiditis: Transient (temporary) hyperthyroidism can be caused by silent thyroiditis, a condition which appears to be the same as postpartum thyroiditis but not related to pregnancy. It is not accompanied by a painful thyroid gland.

Subacute thyroiditis: This condition may follow a viral infection and is characterized by painful thyroid gland enlargement and inflammation, which results in the release of large amounts of thyroid hormone into the blood. Fortunately, this condition usually resolves spontaneously. The thyroid usually heals itself over several months, but often not before a temporary period of hypothyroidism occurs.

Thyroid surgery: Hypothyroidism may be related to surgery on the thyroid gland, especially if most of the thyroid has been removed.

What are the signs and symptoms of hypothyroidism ?

In its earliest stage, hypothyroidism may cause few symptoms, since the body has the ability to partially compensate for a failing thyroid gland by increasing the stimulation to it, much like pressing down on the accelerator when climbing a hill to keep the car going the same speed. As thyroid hormone production decreases and the body’s metabolism slows, a variety of features may result.

  • Pervasive fatigue
  • Drowsiness
  • Forgetfulness
  • Difficulty with learning
  • Dry, brittle hair and nails
  • Dry, itchy skin
  • Puffy face
  • Constipation
  • Sore muscles
  • Weight gain and fluid retention
  • Heavy and/or irregular menstrual flow
  • Increased frequency of miscarriages
  • Increased sensitivity to many medications

How is hypothyroidism diagnosed ?

Characteristic symptoms and physical signs, which can be detected by a physician, can signal hypothyroidism. However, the condition may develop so slowly that many patients do not realize that their body has changed, so it is critically important to perform diagnostic laboratory tests to confirm the diagnosis and to determine the cause of hypothyroidism. A primary care physician may make the diagnosis of hypothyroidism, but assistance is often needed from an endocrinologist, a physician who is a specialist in thyroid diseases.

Tests

TSH (THYROID-STIMULATING HORMONE OR THYROTROPIN): An increased TSH level in the blood is the most accurate indicator of primary (non-pituitary) hypothyroidism. Production of this pituitary hormone is increased when the thyroid gland even slightly underproduces thyroid hormone.

ESTIMATES OF FREE THYROXINE: The active thyroid hormone in the blood. It is important to note that there is a range of free thyroxine levels in the blood of normal people, similar to the range for height, and that a value of free thyroxine that is “within normal limits” for the general population may not be appropriate for a particular individual.

THYROID ANTIBODIES: Indicates the likelihood of auto-immune thyroiditis being the cause of hypothyroidism.

How is hypothyroidism treated ?

Hypothyroidism is generally treated with a single daily dose of levothyroxine, given as a tablet. An experienced physician can prescribe the correct form and dosage to return the thyroid balance to normal. Older patients who may have underlying heart disease are usually started at a low dose and gradually increased while younger healthy patients can be started on full replacement doses at once. Thyroid hormone acts very slowly in some parts of the body, so it may take several months after treatment for some features to improve.

Levothyroxine tablets come in 12 different strengths, and it is essential to take them in a consistent manner every day. A dose of thyroid hormone that is too low may fail to prevent enlargement of the thyroid gland, allow symptoms of hypothyroidism to persist, and be associated with increased serum cholesterol levels, which may increase the risk for atherosclerosis and heart disease. A dose that is too high can cause symptoms of hyperthyroidism, create excessive strain on the heart, and lead to an increased risk of developing osteoporosis.

It is extremely important that women planning to become pregnant are kept well adjusted, since hypothyroidism can affect the development of the baby. During pregnancy, thyroid hormone replacement requirements often change, so more frequent monitoring is necessary. Various medications and supplements (particularly iron) may affect the absorption of thyroid hormone; therefore, the levels may need more frequent monitoring during illness or change in medication and supplements.

Thyroid hormone is critical for normal brain development in babies. Infants requiring thyroid hormone therapy should NOT be treated with purchased liquid suspensions, since the active hormone may deteriorate once dissolved and the baby could receive less thyroid hormone than necessary. Instead, infants with hypothyroidism should receive their thyroid hormone by crushing a single tablet daily of the correct dose and suspending it in one teaspoon of liquid and administering it properly.

Since most cases of hypothyroidism are permanent and often progressive, it is usually necessary to treat this condition throughout one’s lifetime. Periodic monitoring of TSH levels and clinical status are necessary to ensure that the proper dose is being given, since medication doses may have to be adjusted from time to time. Optimal adjustment of thyroid hormone dosage is critical, since the body is very sensitive to even small changes in thyroid hormone levels.

Appropriate management of hypothyroidism requires continued care by a physician experienced in the treatment of this condition.

Thyroid Cancer

The thyroid gland is located in the lower front of the neck, above the collarbones and below the voice box (larynx). Thyroid cancer (carcinoma) usually appears as a painless lump in this area 4. In most cases, the lump is only on one side, and the results of thyroid function tests (blood tests) are usually normal.

There are four main types of thyroid cancer (papillary, follicular, medullary and anaplastic), but the vast majority of cases are either papillary or follicular 4.

  • Papillary thyroid cancer is the most common type of thyroid cancer, accounting for 70 to 80 percent of all cases. It is most commonly diagnosed in women 30-40 years old and most frequently spreads to cervical (neck) lymph nodes.
  • Follicular thyroid cancer is the second most common type of thyroid cancer, accounting for 10 to 15 percent of cases. Although it usually does not spread, when it does it goes to the lungs and bones through the bloodstream.
  • Most common types of thyroid cancer are “sporadic” or isolated, and not inherited. However, an uncommon type of thyroid cancer, medullary cancer, which makes up about five percent of all thyroid cancers, can be familial, or run in families. When medullary cancer is inherited as a familial disease, it can be detected by a genetic blood test. Unless the disease is inherited, your children will not be affected.
  • Anaplastic thyroid cancer accounts for less than five percent of thyroid cancer patients. It is the most aggressive form of thyroid cancer and treatment is rarely effective.

Because the most common thyroid cancers, papillary and follicular, tend to grow slowly, usually do not spread beyond the neck and respond to treatment, most patients with thyroid cancers have excellent prognoses. For example, the 20-year survival of the most common type, papillary thyroid cancer, is almost 95 percent.

The estimated number of newly diagnosed thyroid cancer patients has continued an upward trend for more than 15 years! This represents an alarming and rapid percentage increase for any form of cancer, especially since most all other cancers are either stable or declining in their incidence rates. Fortunately, virtually the entire rate of increasing thyroid cancer patients annually is due to newly diagnosed papillary cancer, rather than other types of more aggressive thyroid cancer. The exact cause (or causes) is not clear; but, this rise in the incidence of papillary thyroid cancer has been attributed to better and earlier diagnostic imaging with ultrasound. However, other background environmental causes are difficult to exclude and there are continuing efforts to analyze this incidence trend.

What are the causes of thyroid cancer ?

As with many types of cancer, the specific reason for developing thyroid cancer remains a mystery in the vast majority of patients. Some major risk factors are:

  • External radiation to the head or neck, especially during childhood
  • Genetic predisposition (the influence of heredity), particularly for the medullary type of thyroid cancer

What are the signs and symptoms of thyroid cancer ?

Many patients with thyroid cancer have no symptoms and are found by chance to have a lump in the thyroid gland during a routine physical exam, or an imaging study of the neck done for unrelated reasons such as a carotid ultrasound, CT or MRI scan of the spine or chest. Other patients with thyroid cancer become aware of a gradually enlarging lump in the front portion of the neck, which usually moves with swallowing. Occasionally, the lump may cause a feeling of pressure. Obviously, finding a lump in the neck should be brought to the attention of your physician, even in the absence of other symptoms.

How is thyroid cancer diagnosed ?

First, your physician takes a detailed history and performs a careful physical examination, especially of the thyroid gland. The best diagnostic approach for a specific patient will be determined by your physician after careful consideration of all the facts. The tests available to your physician for evaluation of the thyroid lump include, but are not limited to, the following:

  • Fine-needle aspiration biopsy: This is usually done first and, if positive, significantly reduces the need for more elaborate and expensive testing
  • Ultrasonography – this may be required for guidance of the fine needle biopsy if the nodule is difficult to feel
  • Thyroid scan – this can be done to see if the mass is capable of concentrating radioiodine, particularly in those patients with low TSH levels, who are likely to have hot nodules, which are almost always benign.
  • Blood studies.

How is thyroid cancer treated ?

The great majority of patients with thyroid cancer have a disease that can be successfully treated. In order to ensure your chances for a successful outcome, it is important to receive treatment and follow-up care from those with a great deal of experience in the diagnosis and treatment of thyroid cancer. This is usually an endocrinologist, a doctor who specializes in hormone-related disorders.

What treatment will you require ?

Treatment depends on the type and extent of cancer. Treatment options include surgery, radioactive iodine, external radiation (see below), and chemotherapy. All patients require thyroid surgery and many receive radioiodine after surgery (see below).

What kind of surgery ?

Removal of part or all of the thyroid gland (thyroidectomy) is the first step in management. Lymph nodes with cancer in them are also removed. A surgeon who has experience with thyroid cancer is the best choice for performing your surgery.

You may be thinking, “Shouldn’t I be seeing an oncologist?” The answer is usually no. An endocrinologist is the physician who deals primarily with the diagnosis, treatment and follow-up of most patients with thyroid cancer. However, if/when standard therapy fails to control the progression of thyroid cancer and chemotherapy is being considered, then consultation with an oncologist is appropriate.

Will you require radiation ? If so, what at type ?

Conventional radiation therapy, the type that is generally used for cancer, is not used very often to treat thyroid cancer 4. It is reserved to treat thyroid cancer that cannot be removed surgically or eliminated with radioactive iodine. Fortunately, it is only required to treat a small minority of thyroid cancer cases. This type of radiation treatment is often referred to as external radiation therapy because the source of the radiation comes from outside the body.

Most often patients with thyroid cancer who require radiation treatment receive radioactive iodine. This type of radiation works internally once it enters your body. It is administered by either swallowing a capsule or drinking a radioactive liquid containing a radioactive form of iodine.

What are Thyroid Nodules ?

A thyroid nodule is a lump in or on the thyroid gland 5. Thyroid nodules are common, but are usually not diagnosed. They are detected in about six percent of women and one to two percent of men. They are 10 times as common in older individuals than in younger ones. Sometimes several nodules will develop in the same person. Any time a lump is discovered in thyroid tissue, the possibility of malignancy (cancer) must be considered. Fortunately, the vast majority of thyroid nodules are benign (not cancerous) 5.

What causes a thyroid nodule ?

Nodules can be caused by a simple overgrowth of “normal” thyroid tissue, fluid-filled cysts, inflammation (thyroiditis), or a tumor (either benign or cancerous).

What are the signs and symptoms of a thyroid nodule ?

Most patients with thyroid nodules have no symptoms whatsoever. Many are found by chance to have a lump in the thyroid gland on a routine physical exam or an imaging study of the neck done for unrelated reasons (for example, a CT or MRI scan of the spine or chest, a carotid ultrasound, etc.). In addition, a substantial number of nodules are first noticed by patients or those they know who see a lump in the front portion of the neck, which may or may not cause symptoms, such as a vague pressure sensation or discomfort when swallowing.

Obviously, finding a lump in the neck should be brought to the attention of your physician, even in the absence of symptoms.

How is a thyroid nodule diagnosed ?

THYROID SCAN: A thyroid scan is a picture of the thyroid gland taken after a small dose of a radioactive isotope normally concentrated by thyroid cells has been injected or swallowed. The scan tells whether the nodule is hyperfunctioning (a “hot” nodule), or taking up more radioactivity than normal thyroid tissue does; taking up the same amount as normal tissue (a “warm” nodule); or taking up less (a “cold” nodule). Because cancer is rarely found in hot nodules, a scan showing a hot nodule eliminates the need for fine needle biopsy. If a hot nodule causes hyperthyroidism, it can be treated with radioiodine or surgery.

THYROID NEEDLE BIOPSY: A thyroid fine needle biopsy employs a very thin needle, usually smaller than one used to draw blood and is a simple procedure that can be performed in the physician’s office. Many physicians numb the skin over the nodule prior to the biopsy, but it is not necessary to be put to sleep, and patients can usually return to work or home afterward with no ill effects. This test provides specific information about a particular patient’s nodule, information that no other test can offer short of surgery. Although the test is not perfect, a thyroid needle biopsy will provide sufficient information on which to base a treatment decision more than 75 percent of the time, eliminating the need for additional diagnostic studies.

Use of fine needle biopsy has drastically reduced the number of patients who have undergone unnecessary operations for benign nodules. However, about 10 to 20 percent of biopsy specimens are interpreted as inconclusive or inadequate; that is, the pathologist cannot be certain whether the nodule is cancerous or benign. This situation is particularly common with cystic (fluid-filled) nodules, which contain very few thyroid cells to examine, and with those nodules composed of clusters of thyroid or follicular cells that cannot be conclusively determined to be either benign or malignant. In such cases, a physician who is experienced with thyroid disease can use other criteria to make a decision about whether or not to operate. The fine needle biopsy can be repeated in those patients whose initial attempt failed to yield enough material to make a diagnosis. Many physicians use thyroid ultrasonography (ultrasound) to guide the needle’s placement.

THYROID ULTRASONOGRAPHY: Thyroid ultrasonography is a procedure for obtaining pictures of the thyroid gland by using high-frequency sound waves that pass through the skin and are reflected back to the machine to create detailed images of the thyroid. It can visualize nodules as small as two to three millimeters. Ultrasound distinguishes thyroid cysts (fluid-filled nodules) from solid nodules. Many nodules have both solid and cystic components, and very few purely cystic nodules occur. Recent advances in ultrasonography help physicians identify nodules that are more likely to be cancerous.

Thyroid ultrasonography is also utilized for guidance of a fine needle for aspirating thyroid nodules. Ultrasound guidance enables physicians to biopsy the nodule to obtain an adequate amount of material for interpretation. Such guidance allows the biopsy sample to be obtained from the solid portion of those nodules that are both solid and cystic, and it avoids getting a specimen from the surrounding normal thyroid tissue if the nodule is small. Even when a thyroid biopsy sample is reported as benign, the size of the nodule should be monitored. A thyroid ultrasound examination provides an objective and precise method for detection of a change in the size of the nodule. A nodule with a benign biopsy that is stable or decreasing in size is unlikely to be malignant or require surgical treatment.

How is a thyroid nodule treated ?

Your endocrinologist will use the tests mentioned above to arrive at a recommendation for optimal management of your nodule. Most patients who appear to have benign nodules require no specific treatment and can simply be followed by their physician. Some physicians prescribe levothyroxine with hopes of preventing nodule growth or reducing the size of cold nodules, while radioiodine may be used to treat hot nodules.

If cancer is suspected, surgical treatment will be recommended. The primary goal of therapy is to remove all thyroid nodules that are cancerous and, if malignancy is confirmed, remove the rest of the thyroid gland along with any abnormal lymph nodes. If surgery is not recommended, it is important to have regular follow-up of the nodule by a physician experienced in such an evaluation.

References
  1. Goiter – simple. Medline Plus. https://medlineplus.gov/ency/article/001178.htm
  2. What is Hashimoto’s thyroiditis ? American Association of Clinical Endocrinologists. https://www.empoweryourhealth.org/endocrine-conditions/thyroid/about_hashimotos_thyroiditis
  3. What is hyperthyroidism ? American Association of Clinical Endocrinologists. https://www.empoweryourhealth.org/thyroid/about_hyperthyroidism
  4. About Thyroid Cancer. American Association of Clinical Endocrinologists. https://www.empoweryourhealth.org/endocrine-conditions/thyroid/about_thyroid_cancer
  5. About Thyroid Nodules. American Association of Clinical Endocrinologists. https://www.empoweryourhealth.org/endocrine-conditions/thyroid/about_thyroid_nodules
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