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.

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"]."

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.”

The strong genetic component is borne out in studies on monozygotic twins, with a concordance of 38-55%, with an even higher concordance of circulating thyroid antibodies not in relation to clinical presentation (up to 80% in monozygotic twins). Neither result was seen to a similar degree in dizygotic twins, offering strong favour for high genetic aetiology.

Hashimoto's thyroiditis is associated with "CTLA-4" ("Cytotoxic T-lymphocyte Antigen-4") gene polymorphisms. CTLA-4 downregulates., i.e. transmits an inhibitory signal to T cells so reduced functioning is associated with increased T-lymphocyte activity. A family history of thyroid disorders is common, with the "HLA-DR5" gene most strongly implicated conferring a relative risk of 3 in the UK.

Having other autoimmune diseases is a risk factor to develop Hashimoto’s thyroiditis, and the opposite is also true. Autoimmune diseases most commonly associated to Hashimoto’s thyroiditis include celiac disease, type 1 diabetes, vitiligo, and alopecia.

Preventable environmental factors, including high iodine intake, selenium deficiency, as well as infectious diseases and certain drugs, have been implicated in the development of autoimmune thyroid disease in genetically predisposed individuals.

The genes implicated vary in different ethnic groups and the incidence is increased in people with chromosomal disorders, including Turner, Down, and Klinefelter syndromes usually associated with autoantibodies against thyroglobulin and thyroperoxidase. Progressive depletion of these cells as the cytotoxic immune response leads to higher degrees of primary hypothyroidism, presenting with a poverty of T3/T4 levels, and compensatory elevations of TSH.

Most types of thyroiditis are three to five times more likely to be found in women than in men. The average age of onset is between thirty and fifty years of age. This disease tends to be geographical and seasonal, and is most common in summer and fall.

Treatments for this disease depend on the type of thyroiditis that is diagnosed. For the most common type, which is known as Hashimoto's thyroiditis, the treatment is to immediately start hormone replacement. This prevents or corrects the hypothyroidism, and it also generally keeps the gland from getting bigger. However, Hashimoto's thyroiditis can initially present with excessive thyroid hormone being released from the thyroid gland (hyperthyroid). In this case the patient may only need bed rest and non-steroidal anti-inflammatory medications; however, some need steroids to reduce inflammation and to control palpitations. Also, doctors may prescribe beta blockers to lower the heart rate and reduce tremors, until the initial hyperthyroid period has resolved.

Hypothyroidism is a state in which the body is not producing enough thyroid hormones, or is not able to respond to / utilize existing thyroid hormones properly. The main categories are:

- Thyroiditis: an inflammation of the thyroid gland

- Hashimoto's thyroiditis / Hashimoto's disease

- Ord's thyroiditis

- Postpartum thyroiditis

- Silent thyroiditis

- Acute thyroiditis

- Riedel's thyroiditis (the majority of cases do not affect thyroid function, but approximately 30% of cases lead to hypothyroidism)

- Iatrogenic hypothyroidism

- Postoperative hypothyroidism

- Medication- or radiation-induced hypothyroidism

- Thyroid hormone resistance

- Euthyroid sick syndrome

- Congenital hypothyroidism: a deficiency of thyroid hormone from birth, which untreated can lead to cretinism

Riedel's thyroiditis is classified as rare. Most patients remain euthyroid, but approximately 30% of patients become hypothyroid and very few patients are hyperthyroid. It is most seen in women.

Some cases may be viral in origin, perhaps preceded by an upper respiratory tract infection. Viral causes include Coxsackie virus, mumps and adenoviruses. Some cases develop postpartum .

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

It is named for Fritz de Quervain. It should not be confused with De Quervain syndrome.

Treatment is as with hypothyroidism, daily thyroxine(T4) and/or triiodothyronine(T3).

Outside Europe a goitrous form of autoimmune thyroiditis (Hashimoto's Thyroiditis) is more common than Ord's disease.

Subacute thyroiditis is a form of thyroiditis that can be a cause of both thyrotoxicosis and hypothyroidism. It is uncommon and can affect individuals of both sexes and people of all ages. The most common form, subacute granulomatous, or de Quervain's, thyroiditis manifests as a sudden and painful enlargement of the thyroid gland accompanied with fever, malaise and muscle aches. Indirect evidence has implicated viral infection in the aetiology of subacute thyroiditis. This evidence is limited to preceding upper respiratory tract infection, elevated viral antibody levels, and both seasonal and geographical clustering of cases. There may be a genetic predisposition.

Nishihara and coworkers studied the clinical features of subacute thyroiditis in 852 mostly 40- to 50-year-old women in Japan. They noted seasonal clusters (summer to early autumn) and most subjects presented with neck pain. Fever and symptoms of thyrotoxicosis was present in two thirds of subjects. Upper respiratory tract infections in the month preceding presentation were reported in only 1 in 5 subjects. Recurrent episodes following resolution of the initial episode were rare, occurring in just 1.6% of cases. Laboratory markers for thyroid inflammation and dysfunction typically peaked within one week of onset of illness.

Types include:

- Subacute granulomatous thyroiditis (De Quervain thyroiditis)

- Subacute lymphocytic thyroiditis

- Postpartum thyroiditis

- Palpation thyroiditis

Subacute lymphocytic thyroiditis is a form of thyroiditis that is also known as silent thyroiditis or painless thyroiditis. Subacute lymphocytic thyroiditis may occur at any age and is more common in females.

A variant of subacute lymphocytic thyroiditis occurs postpartum, postpartum thyroiditis. Both of these entities can be considered subtypes of Hashimoto's thyroiditis and have an autoimmune basis. Anti-thyroid antibodies are common in all three and the underlying histology is similar. This disorder should not be confused with de Quervain's thyroiditis which is another form of subacute thyroiditis.

Women being treated for Hashimoto's disease can become pregnant. It is recommended that thyroid function be well-controlled before getting pregnant.

Untreated or poorly treated underactive thyroid can lead to problems for the mother, such as:

- Preeclampsia

- Anemia

- Miscarriage

- Placental abruption

- High cholesterol

- Postpartum bleeding

It also can cause serious problems for the baby, such as:

- Preterm birth

- Low birth weight

- Stillbirth

- Birth defects

- Thyroid problems

Risk factors of progressive and severe thyroid-associated orbitopathy are:

- Age greater than 50 years

- Rapid onset of symptoms under 3 months

- Cigarette smoking

- Diabetes

- Severe or uncontrolled hyperthyroidism

- Presence of pretibial myxedema

- High cholesterol levels (hyperlipidemia)

- Peripheral vascular disease

During pregnancy, immunologic suppression occurs which induces tolerance to the presence of the fetus. Without this suppression, the fetus would be rejected causing miscarriage. As a result, following delivery, the immune system rebounds causing levels of thyroids antibodies to rise in susceptible women.

Specifically, the immunohistological features of susceptible women are indicated by:

- antibodies to thyroglobulin (TgAb)

- antibodies to thyroid peroxidase (TPOAb)

- increase in TPOAb subclasses IgG-IgG

- lymphocyte infiltration and follicle formation within thyroid gland (Hashimoto's thyroiditis)

- T-cell changes (increased CD4:CD8 ratio)

- TSH-receptor antibodies (TSH-R Abs)

Riedel's thyroiditis is characterized by a replacement of the normal thyroid parenchyma by a dense fibrosis that invades adjacent structures of the neck and extends beyond the thyroid capsule. This makes the thyroid gland stone-hard (woody) and fixed to adjacent structures. The inflammatory process infiltrates muscles and causes symptoms of tracheal compression. Surgical treatment is required to relieve tracheal or esophageal obstruction.

Normal hormone changes during pregnancy cause thyroid hormone levels to increase. The thyroid may enlarge slightly in healthy women during pregnancy, but not enough to be felt. These changes do not affect the pregnancy or unborn baby. Yet, untreated thyroid problems can threaten pregnancy and the growing baby. Symptoms of normal pregnancy, like fatigue, can make it easy to overlook thyroid problems in pregnancy.

Thyroid hormone is vital during pregnancy. The unborn baby's brain and nervous system need thyroid hormone to develop. During the first trimester, the baby depends on the mother's supply of thyroid hormone. At 10 to 12 weeks of pregnancy, the baby's thyroid begins to work on its own. But the baby still depends on the mother for iodine, which the thyroid uses to make thyroid hormone. Pregnant women need about 250 micrograms (mcg) of iodine a day. Some women might not get all the iodine they need through the foods they eat or prenatal vitamins. Using iodized salt — salt that has had iodine added to it over plain table salt is recommended. Prenatal vitamins that contain iodine are also recommended.

Some women develop thyroid problems in the first year after giving birth. This is called postpartum thyroiditis. It often begins with symptoms of an overactive thyroid, which last 2 to 4 months. Mild symptoms might be overlooked. Affected women then develop symptoms of an underactive thyroid, which can last up to a year. An underactive thyroid needs to be treated. In most cases, thyroid function returns to normal as the thyroid heals.

Subacute lymphocytic thyroiditis features a small goiter without tenderness. This condition tends to have a phase of hyperthyroidism followed by a return to a euthyroid state, and then a phase of hypothyroidism, followed again by a return to the euthyroid state. The time span of each phase can vary; however, each phase usually lasts 2–3 months.

Worldwide reporting of postpartum thyroiditis cases is highly varied. This variation may be due to methodological discrepancies in assessing women for this condition. Factors such as length of follow-up after delivery, diagnostic criteria, frequency of postpartum blood sampling, and thyroid hormone assay methodology likely contribute to this variation. On average, 5-7% of pregnant women from most iodine-replete populations develop this condition.

Women with type I diabetes mellitus have a threefold increase in the prevalence of postpartum thyroiditis than non-diabetic women in the same region.

Hypothyroidism is diagnosed by noting a high TSH associated with a subnormal T4 concentration. Subclinical hypothyroidism (SCH) is present when the TSH is high but the T4 level is in the normal range but usually low normal. SCH is the commonest form of hypothyroidism in pregnancy and is usually due to progressive thyroid destruction due to autoimmune thyroid disease.

Several studies, mostly retrospective, have shown an association between overt hypothyroidism and adverse fetal and obstetric outcomes (e.g. Glinoer 1991). Maternal complications such as miscarriages, anaemia in pregnancy, pre-eclampsia, abruptio placenta and postpartum haemorrhage can occur in pregnant women with overt hypothyroidism. Also, the offspring of these mothers can have complications such as premature birth, low birth weight and increased neonatal respiratory distress. Similar complications have been reported in mothers with subclinical hypothyroidism. A three-fold risk of placental abruption and a two-fold risk of pre-term delivery were reported in mothers with subclinical hypothyroidism. Another study showed a higher prevalence of subclinical hypothyroidism in women with pre-term delivery (before 32 weeks) compared to matched controls delivering at term. An association with adverse obstetrics outcome has also been demonstrated in pregnant women with thyroid autoimmunity independent of thyroid function. Treatment of hypothyroidism reduces the risks of these adverse obstetric and fetal outcomes; a retrospective study of 150 pregnancies showed that treatment of hypothyroidism led to reduced rates of abortion and premature delivery. Also, a prospective intervention trial study showed that treatment of euthyroid antibody positive pregnant women led to fewer rates of miscarriage than non treated controls.

It has long been known that cretinism (i.e. gross reduction in IQ) occurs in areas of severe iodine deficiency due to the fact that the mother is unable to make T4 for transport to the fetus particularly in the first trimester. This neurointellectual impairment (on a more modest scale) has now been shown in an iodine sufficient area (USA) where a study showed that the IQ scores of 7-9 year old children, born to mothers with undiagnosed and untreated hypothyroidism in pregnancy, were seven points lower than those of children of matched control women with normal thyroid function in pregnancy. Another study showed that persistent hypothyroxinaemia at 12 weeks gestation was associated with an 8-10 point deficit in mental and motor function scores in infant offspring compared to children of mothers with normal thyroid function. Even maternal thyroid peroxidase antibodies were shown to be associated with impaired intellectual development in the offspring of mothers with normal thyroid function. Interestingly, it has been shown that it is only the maternal FT4 levels that are associated with child IQ and brain morphological outcomes, as opposed to maternal TSH levels.

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.

A person's sex also seems to have some role in the development of autoimmunity; that is, most autoimmune diseases are "sex-related". Nearly 75% of the more than 23.5 million Americans who suffer from autoimmune disease are women, although it is less-frequently acknowledged that millions of men also suffer from these diseases. According to the American Autoimmune Related Diseases Association (AARDA), autoimmune diseases that develop in men tend to be more severe. A few autoimmune diseases that men are just as or more likely to develop as women include: ankylosing spondylitis, type 1 diabetes mellitus, granulomatosis with polyangiitis, Crohn's disease, Primary sclerosing cholangitis and psoriasis.

The reasons for the sex role in autoimmunity vary. Women appear to generally mount larger inflammatory responses than men when their immune systems are triggered, increasing the risk of autoimmunity. Involvement of sex steroids is indicated by that many autoimmune diseases tend to fluctuate in accordance with hormonal changes, for example: during pregnancy, in the menstrual cycle, or when using oral contraception. A history of pregnancy also appears to leave a persistent increased risk for autoimmune disease. It has been suggested that the slight, direct exchange of cells between mothers and their children during pregnancy may induce autoimmunity. This would tip the gender balance in the direction of the female.

Another theory suggests the female high tendency to get autoimmunity is due to an imbalanced X chromosome inactivation. The X-inactivation skew theory, proposed by Princeton University's Jeff Stewart, has recently been confirmed experimentally in scleroderma and autoimmune thyroiditis. Other complex X-linked genetic susceptibility mechanisms are proposed and under investigation.