Certain medications can have the unintended side effect of affecting thyroid function. While some medications can lead to significant hypothyroidism or hyperthyroidism and those at risk will need to be carefully monitored, some medications may affect thyroid hormone lab tests without causing any symptoms or clinical changes, and may not require treatment. The following medications have been linked to various forms of thyroid disease:

- Amiodarone (more commonly can lead to hypothyroidism, but can be associated with some types of hyperthyroidism)

- Lithium salts (hypothyroidism)

- Some types of interferon and IL-2 (thyroiditis)

- Glucocorticoids, dopamine agonists, and somatostatin analogs (block TSH, which can lead to hypothyroidism)

Hyperthyroidism is a state in which the body is producing too much thyroid hormone. The main hyperthyroid conditions are:

- Graves' disease

- Toxic thyroid nodule

- Thyroid storm

- Toxic nodular struma (Plummer's disease)

- Hashitoxicosis: "transient" hyperthyroidism that can occur in Hashimoto's thyroiditis

Thyroid hormone resistance syndrome is rare, incidence is variously quoted as 1 in 50,000 or 1 in 40,000 live births. More than 1000 individuals have been identified with thyroid hormone resistance, of which 85% had thyroid hormone beta receptor mutation.

Worldwide about one billion people are estimated to be iodine deficient; however, it is unknown how often this results in hypothyroidism. In large population-based studies in Western countries with sufficient dietary iodine, 0.3–0.4% of the population have overt hypothyroidism. A larger proportion, 4.3–8.5%, have subclinical hypothyroidism. Of people with subclinical hypothyroidism, 80% have a TSH level below the 10 mIU/l mark regarded as the threshold for treatment. Children with subclinical hypothyroidism often return to normal thyroid function, and a small proportion develops overt hypothyroidism (as predicted by evolving antibody and TSH levels, the presence of celiac disease, and the presence of a goiter).

Women are more likely to develop hypothyroidism than men. In population-based studies, women were seven times more likely than men to have TSH levels above 10 mU/l. 2–4% of people with subclinical hypothyroidism will progress to overt hypothyroidism each year. The risk is higher in those with antibodies against thyroid peroxidase. Subclinical hypothyroidism is estimated to affect approximately 2% of children; in adults, subclinical hypothyroidism is more common in the elderly, and in Caucasians. There is a much higher rate of thyroid disorders, the most common of which is hypothyroidism, in individuals with Down syndrome and Turner syndrome.

Very severe hypothyroidism and myxedema coma are rare, with it estimated to occur in 0.22 per million people a year. The majority of cases occur in women over 60 years of age, although it may happen in all age groups.

Most hypothyroidism is primary in nature. Central/secondary hypothyroidism affects 1:20,000 to 1:80,000 of the population, or about one out of every thousand people with hypothyroidism.

Screening for hypothyroidism is performed in the newborn period in many countries, generally using TSH. This has led to the early identification of many cases and thus the prevention of developmental delay. It is the most widely used newborn screening test worldwide. While TSH-based screening will identify the most common causes, the addition of T testing is required to pick up the rarer central causes of neonatal hypothyroidism. If T determination is included in the screening done at birth, this will identify cases of congenital hypothyroidism of central origin in 1:16,000 to 1:160,000 children. Considering that these children usually have other pituitary hormone deficiencies, early identification of these cases may prevent complications.

In adults, widespread screening of the general population is a matter of debate. Some organizations (such as the United States Preventive Services Task Force) state that evidence is insufficient to support routine screening, while others (such as the American Thyroid Association) recommend either intermittent testing above a certain age in both sexes or only in women. Targeted screening may be appropriate in a number of situations where hypothyroidism is common: other autoimmune diseases, a strong family history of thyroid disease, those who have received radioiodine or other radiation therapy to the neck, those who have previously undergone thyroid surgery, those with an abnormal thyroid examination, those with psychiatric disorders, people taking amiodarone or lithium, and those with a number of health conditions (such as certain heart and skin conditions). Yearly thyroid function tests are recommended in people with Down syndrome, as they are at higher risk of thyroid disease.

Sequence of events:

1. Iodine deficiency leading to decreased T4 production.

2. Induction of thyroid cell hyperplasia due to low levels of T4. This accounts for the multinodular goitre appearance.

3. Increased replication predisposes to a risk of mutation in the TSH receptor.

4. If the mutated TSH receptor is constitutively active, it would then become 'toxic' and produces excess T3/T4 leading to hyperthyroidism.

There are several causes of hyperthyroidism. Most often, the entire gland is overproducing thyroid hormone. Less commonly, a single nodule is responsible for the excess hormone secretion, called a "hot" nodule. Thyroiditis (inflammation of the thyroid) can also cause hyperthyroidism. Functional thyroid tissue producing an excess of thyroid hormone occurs in a number of clinical conditions.

The major causes in humans are:

- Graves' disease. An autoimmune disease (usually, the most common etiology with 50-80% worldwide, although this varies substantially with location- i.e., 47% in Switzerland (Horst et al., 1987) to 90% in the USA (Hamburger et al. 1981)). Thought to be due to varying levels of iodine in the diet. It is eight times more common in females than males and often occurs in young females, around 20 – 40 years of age.

- Toxic thyroid adenoma (the most common etiology in Switzerland, 53%, thought to be atypical due to a low level of dietary iodine in this country)

- Toxic multinodular goiter

High blood levels of thyroid hormones (most accurately termed hyperthyroxinemia) can occur for a number of other reasons:

- Inflammation of the thyroid is called thyroiditis. There are several different kinds of thyroiditis including Hashimoto's thyroiditis (Hypothyroidism immune-mediated), and subacute thyroiditis (de Quervain's). These may be "initially" associated with secretion of excess thyroid hormone but usually progress to gland dysfunction and, thus, to hormone deficiency and hypothyroidism.

- Oral consumption of excess thyroid hormone tablets is possible (surreptitious use of thyroid hormone), as is the rare event of consumption of ground beef contaminated with thyroid tissue, and thus thyroid hormone (termed "hamburger hyperthyroidism").

- Amiodarone, an antiarrhythmic drug, is structurally similar to thyroxine and may cause either under- or overactivity of the thyroid.

- Postpartum thyroiditis (PPT) occurs in about 7% of women during the year after they give birth. PPT typically has several phases, the first of which is hyperthyroidism. This form of hyperthyroidism usually corrects itself within weeks or months without the need for treatment.

- A struma ovarii is a rare form of monodermal teratoma that contains mostly thyroid tissue, which leads to hyperthyroidism.

- Excess iodine consumption notably from algae such as kelp.

Thyrotoxicosis can also occur after taking too much thyroid hormone in the form of supplements, such as levothyroxine (a phenomenon known as exogenous thyrotoxicosis, alimentary thyrotoxicosis, or occult factitial thyrotoxicosis).

Hypersecretion of thyroid stimulating hormone (TSH), which in turn is almost always caused by a pituitary adenoma, accounts for much less than 1 percent of hyperthyroidism cases.

Normal thyroid hormone function requires normal thyroid hormone transport across cell membrane, appropriate deiodination, thyroid hormone nuclear receptor, thyroid hormone response elements, co-activators, co-repressors, and normal histone acetylation. Any abnormalities in this chain can result in thyroid hormone resistance.

The most common cause of the syndrome are mutations of the β (beta) form ("THRB" gene) of the thyroid hormone receptor, of which over 100 different mutations have been documented.

Mutations in "MCT8" and "SECISBP2" have also been associated with this condition.

Hyperthyroidism is very rare in dogs, occurring in less than 1% of dogs. Hyperthyroidism may be caused by a thyroid tumor. This may be a thyroid carcinoma. About 90% of carcinomas are a very aggressive; they invade the surrounding tissues and metastasize (spread), to other tissues, particularly the lungs. This has a poor prognosis. Surgery to remove the tumor a carcinoma is often very difficult, due to the spread of the tumor to the surrounding tissue, for example, into arteries, the esophagus, or the windpipe. It may be possible to reduce the size of the tumor, thus relieving symptoms and allowing time for other treatments to work. About 10% of thyroid tumors are benign; these often cause few symptoms.

In dogs treated for hypothyroidism (lack of thyroid hormone), hyperthyroidism may occur as a result of an overdose of the thyroid hormone replacement medication, levothyroxine; in this case treatment involves reducing the dose of levothyroxine. Dogs which display coprophagy, that is, which often eat feces, and which live in a household with a dog receiving levothyroxine treatment, may develop hyperthryoidism if they frequently eat the feces from the dog receiving levothyroxine treatment.

Hyperthyroidism may occur if a dog eats an excessive amount of thyroid gland tissue. This has occurred in dogs fed commercial dog food.

Pregnant women who are positive for Hashimoto's thyroiditis may have decreased thyroid function or the gland may fail entirely. If a woman is TPOAb-positive, clinicians can inform her of the risks for themselves and their infants if they go untreated. "Thyroid peroxidase antibodies (TPOAb) are detected in 10% of pregnant women," which presents risks to those pregnancies. Women who have low thyroid function that has not been stabilized are at greater risk of having an infant with: low birth weight, neonatal respiratory distress, hydrocephalus, hypospadias, miscarriage, and preterm delivery. The embryo transplantion rate and successful pregnancy outcomes are improved when Hashimoto's is treated. Recommendations are to only treat pregnant women who are TPOAb-positive throughout the entirety of their pregnancies and to screen all pregnant women for thyroid levels. Close cooperation between the endocrinologist and obstetrician benefits the woman and the infant. The Endocrine Society recommends screening in pregnant women who are considered high-risk for thyroid autoimmune disease.

Thyroid peroxides antibodies testing is recommended for women who have ever been pregnant regardless of pregnancy outcome. "...[P]revious pregnancy plays a major role in development of autoimmune overt hypothyroidism in premenopausal women, and the number of previous pregnancies should be taken into account when evaluating the risk of hypothyroidism in a young women ["sic"]."

One particular familial form is associated with sensorineural deafness (Pendred's syndrome).

OMIM includes the following:

Thyroid dyshormonogenesis (or dyshormogenetic goiter) is a rare condition due to genetic defects in the synthesis of thyroid hormones.

Patients develop hypothyroidism with a goitre.either deficiency of thyroid enzymes or inability to concentrate or ineffective binding

Toxic multinodular goiter (also known as toxic nodular goiter, or Plummer's disease) is a multinodular goiter associated with hyperthyroidism.

It is a common cause of hyperthyroidism in which there is excess production of thyroid hormones from functionally autonomous thyroid nodules, which do not require stimulation from thyroid stimulating hormone (TSH).

Toxic multinodular goiter is the second most common cause of hyperthyroidism (after Graves' disease) in the developed world, whereas iodine deficiency is the most common cause of hypothyroidism in developing-world countries where the population is iodine-deficient. (Decreased iodine leads to decreased thyroid hormone.) However, iodine deficiency can cause goitre (thyroid enlargement); within a goitre, nodules can develop. Risk factors for toxic multinodular goiter include individuals over 60 years of age and being female.

The exact cause is unclear; however, it is believed to involve a combination of genetic and environmental factors. While a theoretical mechanism occurs by which stress could cause an aggravation of the autoimmune response that leads to Graves' disease, more robust clinical data are needed for a firm conclusion.

A genetic predisposition for Graves' disease is seen, with some people more prone to develop TSH receptor activating antibodies due to a genetic cause. Human leukocyte antigen DR (especially DR3) appears to play a role. To date, no clear genetic defect has been found to point to a single gene cause.

Genes believed to be involved include those for thyroglobulin, thyrotropin receptor, protein tyrosine phosphatase nonreceptor type 22, and cytotoxic T-lymphocyte–associated antigen 4, among others.

It has been shown that “the prevalence of positive tests for thyroid antibodies increases with age, with a frequency as high as 33 percent in women 70 years old or older.” The mean age of prevalence in women is higher than in men by one year, (58 and 59 years old respectively).

Autoimmune thyroiditis can affect children. It is very rare in children under the age of five, but can occur;it accounts for around 40 percent of cases in adolescents with goiters.

People with hypothyroidism over the age of 40 have an increased chance of developing autoimmune thyroiditis.

Autoimmune thyroiditis has a higher prevalence in societies that have a higher intake of iodine in their diet, such as the United States and Japan. Also, the rate of lymphocytic infiltration increased in areas where the iodine intake was once low, but increased due to iodine supplementation. “The prevalence of positive serum tests in such areas rises to over 40 percent within 0.5 to 5 years.”

Worldwide, the most common cause for goitre is iodine deficiency, usually seen in countries that do not use iodized salt. Selenium deficiency is also considered a contributing factor. In countries that use iodized salt, Hashimoto's thyroiditis is the most common cause. Goitre can also result from cyanide poisoning; this is particularly common in tropical countries where people eat the cyanide-rich cassava root as the staple food.

- Sarcoidosis

- Amyloidosis

- Hydatidiform mole

- Cysts

- Acromegaly

- Pendred syndrome

Goitre is more common among women, but this includes the many types of goitre caused by autoimmune problems, and not only those caused by simple lack of iodine.

Toxic nodular goiter (TNG) (or toxic multinodular goiter, or Plummer's disease) is a condition that can occur when a hyper-functioning nodule develops within a longstanding goiter. This results in hyperthyroidism, without the eye bulging effects seen in Grave's disease. These toxic nodular goiters are most common in women over the age of 60.

It was named by Henry Stanley Plummer.

Toxic nodular goiter is the presence of thyrotoxicosis and thyroid nodules. It is prevalent in people older than 40 years old who have an iodine deficiency. There is a much higher incidence of TNG in European countries in comparison to the United States. This condition is not common in the United States and Canada due to the iodine addition in table salt. Americans consume much higher dosages of iodine compared to the 25–100 ug/day that Europeans consume.

TNG is caused by a toxic multinodular goiter. Autonomous thyroid nodules become hyper-functional from mutations in the follicular cell. The mutation activates cAMP (cyclic adenosine monophosphate), causing an increase in the cells' function and growth. This is different from the thyroid condition called Grave’s disease, as Grave’s disease causes a hyper-function from external factors such as immunoglobulin that activate the TSH receptors. Hyper-function of TSH, thyroid stimulating hormone, activates the thyroid, which in excess can cause a condition known as goiter. The nodules that form could be driven by a loss of inhibition or gain of function mutations; however, this is purely speculation as the cause is still unknown. These nodules are assumed to be irreversible and when functional can lead to thyrotoxicosis (another name for hyperthyroidism).

Thyrotoxicosis has been documented to have some cases of spontaneous remission without treatment as seen in the study done by Siegel and Lee. It is possible that the remission of thyrotoxicosis is a result of spontaneous hemorrhage and cystic degeneration. This situation means that bleeding would occur in the thyroid, which could cause the nodules to break down, reversing the symptoms. These results of spontaneous remission were contrary to the study’s previous results showing that the nodules were irreversible. Patients presenting symptoms of toxic nodular goiter can also be treated using the same procedures as hyperthyroidism.

The transition from hyperthyroidism to thyroid storm is typically triggered by a non-thyroidal insult including, but not limited to fever, sepsis, dehydration, myocardial infarction, and psychiatric diseases. Individuals are at higher risk of thyroid storm if their hyperthyroidism is incompletely treated or if their anti-thyroid drugs are discontinued. Many of these individuals have underlying primary causes of hyperthyroidism (Graves disease, toxic multi-nodular goiter, solitary toxic adenoma). However, thyroid storm can occur in individuals with unrecognized thyrotoxicosis experiencing non-thyroid surgery, labor, infection, or exposure to certain medications and radiocontrast dyes.

Thyroid cancers are thought to be related to a number of environmental and genetic predisposing factors, but significant uncertainty remains regarding their causes.

Environmental exposure to ionizing radiation from both natural background sources and artificial sources is suspected to play a significant role, and there are significant increased rates of thyroid cancer in those exposed to mantlefield radiation for lymphoma, and those exposed to iodine-131 following the Chernobyl, Fukushima, Kyshtym, and Windscale nuclear disasters. Thyroiditis and other thyroid diseases also predispose to thyroid cancer.

Genetic causes include multiple endocrine neoplasia type 2 which markedly increases rates, particularly of the rarer medullary form of the disease.

A decrease in thyroid hormone binding protein in the setting of various stressors or medications may also cause a rise in free thyroid hormone.

Following is a list of potential risk factors that may lead to iodine deficiency:

1. Low dietary iodine

2. Selenium deficiency

3. Pregnancy

4. Exposure to radiation

5. Increased intake/plasma levels of goitrogens, such as calcium

6. Gender (higher occurrence in women)

7. Smoking tobacco

8. Alcohol (reduced prevalence in users)

9. Oral contraceptives (reduced prevalence in users)

10. Perchlorates

11. Thiocyanates

12. Age (for different types of iodine deficiency at different ages)

In the U.S., the use of iodine has decreased over concerns of overdoses since mid-20th century, and the iodine antagonists bromine, perchlorate and fluoride have become more ubiquitous. In particular, around 1980 the practice of using potassium iodate as dough conditioner in bread and baked goods was gradually replaced by the use of other conditioning agents such as bromide.

Thyroid cancer, in 2010, resulted in 36,000 deaths globally up from 24,000 in 1990. Obesity may be associated with a higher incidence of thyroid cancer, but this relationship remains the subject of much debate.

Thyroid cancer accounts for less than 1% of cancer cases and deaths in the UK. Around 2,700 people were diagnosed with thyroid cancer in the UK in 2011, and around 370 people died from the disease in 2012.