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.

Patients will experience a hyperthyroid period as the cellular lining of colloid spaces fails, allowing abundant colloid into the circulation, with neck pain and fever. Patients typically then become hypothyroid as the pituitary reduces TSH production and the inappropriately released colloid is depleted before resolving to euthyroid. The symptoms are those of hyperthyroidism and hypothyroidism. In addition, patients may suffer from painful dysphagia. There are multi-nucleated giant cells on histology. Thyroid antibodies can be present in some cases. The clinical presentation during the hyperthyroid phase can mimic those of Diffuse Toxic Goiter or Graves' disease. In such cases, a radionuclide thyroid uptake and scan can be helpful, since subacute thyroiditis will result in decreased isotope uptake, while Graves' disease will generally result in increased uptake. Distinguishing between these two types of disease is important, since Graves' disease and Diffuse Toxic Goiter can be treated with radioiodine therapy, but subacute thyroiditis is usually self-limited and is not treated with radioiodine.

There are many different signs and symptoms for thyroiditis, none of which are exclusively limited to this disease. Many of the signs imitate symptoms of other diseases, so thyroiditis can sometimes be difficult to diagnose. Common hypothyroid symptoms manifest when thyroid cell damage is slow and chronic, and may include fatigue, weight gain, feeling "fuzzy headed", depression, dry skin, and constipation. Other, rarer symptoms include swelling of the legs, vague aches and pains, decreased concentration and so on. When conditions become more severe, depending on the type of thyroiditis, one may start to see puffiness around the eyes, slowing of the heart rate, a drop in body temperature, or even incipient heart failure. On the other hand, if the thyroid cell damage is acute, the thyroid hormone within the gland leaks out into the bloodstream causing symptoms of thyrotoxicosis, which is similar to those of hyperthyroidism. These symptoms include weight loss, irritability, anxiety, insomnia, fast heart rate, and fatigue. Elevated levels of thyroid hormone in the bloodstream cause both conditions, but thyrotoxicosis is the term used with thyroiditis since the thyroid gland is not overactive, as in the case of hyperthyroidism.

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 .

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.

Thyroiditis is a group of disorders that all cause thyroidal inflammation. Forms of the disease are Hashimoto's thyroiditis, the most common cause of hypothyroidism in the US, postpartum thyroiditis, subacute thyroiditis, silent thyroiditis, drug-induced thyroiditis, radiation-induced thyroiditis, acute thyroiditis, and Riedel's thyroiditis.

Each different type of this disease has its own causes, clinical features, diagnoses, durations, resolutions, conditions and risks.

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

Symptoms of Ord's thyroiditis include symptoms of hypothyroidism and atrophy of the thyroid gland.

The symptoms may vary depending on the thyroid function, i.e. hyperthyroidism or hypothyroidism. Hyperthyroidism can cause sweating, rapid heart rate, anxiety, tremors, fatigue, difficulty sleeping, sudden weight loss, and protruding eyes. Hypothyroidism can cause weight gain, fatigue, dry skin, hair loss, intolerance to cold, and constipation. The effects of this disease may be permanent but can sometimes be transient. Symptoms may come and go depending on whether the person receives treatment, and whether the treatment takes effect.

Physiologically, antibodies to thyroid peroxidase and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland. Accordingly, the disease can be detected clinically by looking for these antibodies in the blood. It is also characterised by invasion of the thyroid tissue by leukocytes, chiefly T-lymphocytes.

Ord's thyroiditis usually results in hypothyroidism.

Transient hyperthyroid states in the acute phase, (a common observation in Hashimoto's thyroiditis), are rare in Ord's disease.

Autoimmune thyroiditis, (or Chronic Autoimmune thyroiditis), is a chronic disease in which the body interprets the thyroid glands and its hormone products T3, T4 and TSH as threats, therefore producing special antibodies that target the thyroid’s cells, thereby destroying it.

It may present with hypothyroidism or hyperthyroidism and with or without a goiter.

Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis and Hashimoto's disease, is an autoimmune disease in which the thyroid gland is gradually destroyed. Early on there may be no symptoms. Over time the thyroid may enlarge forming a painless goiter. Some people eventually develop hypothyroidism with its accompanying weight gain, feeling tired, constipation, depression, and general pains. After many years the thyroid typically shrinks in size. Potential complications include thyroid lymphoma.

Hashimoto's thyroiditis is thought to be due to a combination of genetic and environmental factors. Risk factors include a family history of the condition and having another autoimmune disease. Diagnosis is confirmed with blood tests for TSH, T4, and antithyroid antibodies. Other conditions that can produce similar symptoms include Graves’ disease and nontoxic nodular goiter.

Hashimoto's thyroiditis is typically treated with levothyroxine. If hypothyroidism is not present some may recommend no treatment while others may treat to try to reduce the size of the goiter. Those affected should avoid eating large amounts of iodine; however, sufficient iodine is required especially during pregnancy. Surgery is rarely required to treat the goiter.

Hashimoto's thyroiditis affects about 5% of the population at some point in their life. It typically begins between the ages of 30 and 50 and is much more common in women than men. Rates of disease appear to be increasing. It was first described by the Japanese physician Hakaru Hashimoto in 1912. In 1957 it was recognized as an autoimmune disorder.

There are many symptoms that are attributed to Hashimoto's thyroiditis or Hashimoto's disease. The most common symptoms include the following: fatigue, weight gain, pale or puffy face, feeling cold, joint and muscle pain, constipation, dry and thinning hair, heavy menstrual flow or irregular periods, depression, panic disorder, a slowed heart rate, and problems getting pregnant and maintaining pregnancy.

Hashimoto’s disease is about seven times more common in women than in men. It can occur in teens and young women, but more commonly shows up in middle age, particularly for men. People who develop Hashimoto’s disease often have family members who have thyroid or other autoimmune diseases, and sometimes have other autoimmune diseases themselves.

The thyroid gland may become firm, large, and lobulated in Hashimoto's thyroiditis, but changes in the thyroid can also be nonpalpable. Enlargement of the thyroid is due to lymphocytic infiltration and fibrosis rather than tissue hypertrophy. Physiologically, antibodies against thyroid peroxidase (TPO) (also called TPOAb) and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland. Accordingly, the disease can be detected clinically by looking for these antibodies in the blood. It is also characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. A rare but serious complication is thyroid lymphoma, generally the B-cell type, non-Hodgkin lymphoma.

The initial phase of hyperthyroid symptoms occurs transiently about two to six months postpartum. Typical symptoms include irritability, nervousness, palpitations, and heat intolerance. Hormonal disturbances during this phase tend to occur with lower intensity compared with the hypothyroid phase. As a result, the hyperthyroid phase may pass undetected. The second phase of hypothyroid symptoms is also transient and can occur anytime within the three- to twelve-month period postpartum. Women in this phase experience low energy, poor memory, impaired concentration, carelessness, dry skin, cold intolerance, and general aches and pains. After one year postpartum, euthyroid function resumes. Any case with hypothyroid symptoms extending beyond one year postpartum is not considered postpartum thyroiditis.

Women who test positive for thyroid antibodies may be at increased risk of developing symptoms associated with postpartum depression than women without thyroid antibodies.

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.

Riedel's thyroiditis, also called Riedel's struma is a chronic form of thyroiditis.

It is now believed that Riedel's thyroiditis is one manifestation of a systemic disease that can affect many organ systems called IgG4-related disease. It is often a multi-organ disease affecting pancreas, liver, kidney, salivary and orbital tissues and retroperitoneum. The hallmarks of the disease are fibrosis and infiltration by IgG4 secreting plasma cells.

Postpartum thyroiditis is a phenomenon observed following pregnancy and may involve hyperthyroidism, hypothyroidism or the two sequentially. It affects about 5% of all women within a year after giving birth. The first phase is typically hyperthyroidism. Then, the thyroid either returns to normal or a woman develops hypothyroidism. Of those women who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop permanent hypothyroidism requiring lifelong treatment.

Postpartum thyroiditis is believed to result from the modifications to the immune system necessary in pregnancy, and histologically is a subacute lymphocytic thyroiditis. The process is normally self-limiting, but when conventional antibodies are found there is a high chance of this proceeding to permanent hypothyroidism. Postpartum thyroiditis is a member of the group of thyroiditis conditions known as resolving thyroiditis.

A relapsing encephalopathy occurring in association with Hashimoto's thyroiditis, with high titers of anti-thyroid antibodies. Clinically, the condition may present one or more symptoms.

Onset is often gradual and may go unnoticed by the patient and close associates to the patients.

Symptoms sometimes resolve themselves within days to weeks, leaving a patient undiagnosed. For many other patients, the condition may result in ongoing problems with a variety of manifestations, often confusing clinicians due to the diffuse nature of symptoms.

Symptoms of the condition vary with type: hypo- vs. hyperthyroidism, which are further described below.

Possible symptoms of hypothyroidism are:

Possible symptoms of hyperthyroidism are:Note: certain symptoms and physical changes can be seen in both hypothyroidism and hyperthyroidism —fatigue, fine / thinning hair, menstrual cycle irregularities, muscle weakness / aches (myalgia), and different forms of myxedema.

The onset of symptoms tends to be fairly gradual and to occur over 1–7 days.

Symptoms of Hashimoto's encephalopathy may include:

- personality changes

- aggression

- delusional behavior

- concentration and memory problems

- coma

- disorientation

- headaches

- jerks in the muscles (myoclonus – 65% cases)

- lack of coordination (ataxia – 65% cases)

- partial paralysis on the right side

- psychosis

- seizures (60% cases)

- sleep abnormalities (55% cases)

- speech problems (transient aphasia – 80% cases)

- status epilepticus (20% cases)

- tremors (80% cases)

Palpation thyroiditis refers to the development of thyroid inflammation due to mechanical damage to thyroid follicles.This can occur by vigorous repeated palpation (as with thyroid examination) or surgical manipulation (as can occur with radical neck dissection). It is a type of subacute thyroiditis. Pathology shows multifocal granulomatous folliculitis. T cells predominate compared to B cells. There may be initial transient hyperthyroidism due to leakage of preformed thyroid hormone in blood.

In most cases AIT is characterized by onset of pain, firmness, tenderness, redness or swelling in the anterior aspect of the neck. Patients will also present with a sudden fever, dysphagia and dysphonia. Symptoms may be present from 1 to 180 days, with most symptoms lasting an average of about 18 days. The main issue associated with the diagnosis of AIT is differentiating it from other more commonly seen forms of thyroid conditions. Pain, fever and swelling are often much more severe and continue to get worse in patients who have AIT compared to those with other thyroid conditions. Patients who are suspected of having AIT often undergo tests to detect for elevated levels of white blood cells as well as an ultrasound to reveal unilobular swelling. Depending on the age and immune status of the patient more invasive procedures may be performed such as fine needle aspiration of the neck mass to facilitate a diagnosis.

In cases where the infection is thought to be associated with a sinus fistula it is often necessary to confirm the presence of the fistula through surgery or laryngoscopic examination. While invasive procedures can often tell definitively whether or not a fistula is present, new studies are working on the use of computed tomography as a useful method to visualize and detect the presence of a sinus fistula.

Thyroid disease is a medical condition that affects the function of the thyroid gland (the endocrine organ found at the front of the neck that produces thyroid hormones). The symptoms of thyroid disease vary depending on the type. There are four general types: 1) hypothyroidism (low function) caused by not having enough thyroid hormones; 2) hyperthyroidism (high function) caused by having too much thyroid hormones; 3) structural abnormalities, most commonly an enlargement of the thyroid gland; and 4) tumors which can be benign or cancerous. It is also possible to have abnormal thyroid function tests without any clinical symptoms. Common hypothyroid symptoms include fatigue, low energy, weight gain, inability to tolerate the cold, slow heart rate, dry skin and constipation. Common hyperthyroid symptoms include irritability, weight loss, fast heartbeat, heat intolerance, diarrhea, and enlargement of the thyroid. In both hypothyroidism and hyperthyroidism, there may be swelling of a part of the neck, which is also known as goiter.

Diagnosis can often be made through laboratory tests. The first is thyroid-stimulating hormone (TSH), which is generally below normal in hyperthyroidism and above normal in hypothyroidism. The other useful laboratory test is non-protein-bound thyroxine or free T4. Total and free triiodothyronine (T3) levels are less commonly used. Anti-thyroid autoantibodies can also be used, where elevated anti-thyroglobulin and anti-thyroid peroxidase antibodies are commonly found in hypothyroidism from Hashimoto's thyroiditis and TSH-receptor antibodies are found in hyperthyroidism caused by Graves' disease. Procedures such as ultrasound, biopsy and a radioiodine scanning and uptake study may also be used to help with the diagnosis.

Treatment of thyroid disease varies based on the disorder. Levothyroxine is the mainstay of treatment for people with hypothyroidism, while people with hyperthyroidism caused by Graves' disease can be managed with iodine therapy, antithyroid medication, or surgical removal of the thyroid gland. Thyroid surgery may also be performed to remove a thyroid nodule or lobe for biopsy, or if there is a goiter that is unsightly or obstructs nearby structures.

Hypothyroidism affects 3-10% percent of adults, with a higher incidence in women and the elderly. An estimated one-third of the world's population currently lives in areas of low dietary iodine levels, making iodine-deficiency the most common cause of hypothyroidism and endemic goiter. In regions of severe iodine deficiency, the prevalence of goiter is as high as 80%. In areas where iodine-deficiency is not found, the most common type of hypothyroidism is an autoimmune subtype called Hashimoto's thyroiditis, with a prevalence of 1-2%. As for hyperthyroidism, Graves' disease, another autoimmune condition, is the most common type with a prevalence of 0.5% in males and 3% in females. Although thyroid nodules are common, thyroid cancer is rare. Thyroid cancer accounts for less than 1% of all cancer in the UK, though it is the most common endocrine tumor and makes up greater than 90% of all cancers of the endocrine glands.

People with hypothyroidism often have no or only mild symptoms. Numerous symptoms and signs are associated with hypothyroidism, and can be related to the underlying cause, or a direct effect of having not enough thyroid hormones. Hashimoto's thyroiditis may present with the mass effect of a goiter (enlarged thyroid gland).

Delayed relaxation after testing the ankle jerk reflex is a characteristic sign of hypothyroidism and is associated with the severity of the hormone deficit.

Myxedema can occur in the lower leg (pretibial myxedema) and behind the eyes (exophthalmos).