The most common and helpful way to diagnose thyroiditis is first for a physician to palpate the thyroid gland during a physical examination. Laboratory tests allow doctors to evaluate the patient for elevated erythrocyte sedimentation rates, elevated thyroglobulin levels, and depressed radioactive iodine uptake (Mather, 2007). Blood tests also help to determine the kind of thyroiditis and to see how much thyroid stimulating hormone the pituitary gland is producing and what antibodies are present in the body. In some cases a biopsy may be needed to find out what is attacking the thyroid.

Various tests can be chosen depending on the presenting symptoms. Doctors may search for Thyroid peroxidase Antibodies (TPOAb) when a person has symptoms of hypothyroidism, or when a person will be started on a drug therapy associated with risks of developing hypothyroidism, such as lithium or Interferon alfa. This antibody is related to Hashimoto's thyroiditis and Graves' disease. If the person presents symptoms of hyperthyroidism, doctors are more likely to test for Thyroid stimulating hormone receptor Antibodies (TRAb), and monitor the effects of anti-thyroid therapy, also associated with Graves' disease.

Doctors may check Thyroglobulin Antibodies (TgAb) also, whenever a thyroglobulin test is performed to see if the antibody is interfering. TgAb may also be ordered in regular intervals after a person has been diagnosed with thyroid cancer, and just like TPOAb, it can be associated with Hashimoto’s thyroiditis.

Diagnosis is usually made by detecting elevated levels of anti-thyroid peroxidase antibodies (TPOAb) in the serum, but seronegative (without circulating autoantibodies) thyroiditis is also possible.

Given the relatively non-specific symptoms of initial hypothyroidism, Hashimoto's thyroiditis is often misdiagnosed as depression, cyclothymia, PMS, chronic fatigue syndrome, fibromyalgia and, less frequently, as erectile dysfunction or an anxiety disorder. On gross examination, there is often presentation of a hard goiter that is not painful to the touch; other symptoms seen with hypothyroidism, such as periorbital myxedema, depend on the current state of progression of the response, especially given the usually gradual development of clinically relevant hypothyroidism. Testing for thyroid-stimulating hormone (TSH), free T3, free T4, and the anti-thyroglobulin antibodies (anti-Tg), anti-thyroid peroxidase antibodies (anti-TPO, or TPOAb) and anti-microsomal antibodies can help obtain an accurate diagnosis. Earlier assessment of the person may present with elevated levels of thyroglobulin owing to transient thyrotoxicosis, as inflammation within the thyroid causes damage to the integrity of thyroid follicle storage of thyroglobulin; TSH secretion from the anterior pituitary increases in response to a decrease in negative feedback inhibition secondary to decreased serum thyroid hormones. Typically T4 is the preferred thyroid hormone test for hypothyroidism. This exposure of the body to substantial amounts of previously isolated thyroid enzymes is thought to contribute to the exacerbation of tolerance breakdown, giving rise to the more pronounced symptoms seen later in the disease. Lymphocytic infiltration of the thyrocyte-associated tissues often leads to the histologically significant finding of germinal center development within the thyroid gland.

Hashimoto's when presenting as mania is known as Prasad's syndrome after Ashok Prasad, the psychiatrist who first described it.

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.

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"]."

Subacute lymphocytic thyroiditis can only be diagnosed correctly by taking a radioactive iodine uptake test (RAIU) test.

During the hyperthyroid phase, iodine uptake is increased, while during the hypothyroid phase, uptake is decreased.

This situation contrasts greatly with the elevated iodine uptake found in patients with Graves' disease.

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.

Autoantibodies to the thyroid gland may be detected in various disease states. There are several anti-thyroid antibodies, including anti-thyroglobulin antibodies (TgAb), anti-microsomal/anti-thyroid peroxidase antibodies (TPOAb), and TSH receptor antibodies (TSHRAb).

- Elevated anti-thryoglobulin (TgAb) and anti-thyroid peroxidase antibodies (TPOAb) can be found in patients with Hashimoto's thyroiditis, the most common autoimmune type of hypothyroidism. TPOAb levels have also been found to be elevated in patients who present with subclinical hypothyroidism (where TSH is elevated, but free T4 is normal), and can help predict progression to overt hypothyroidism. The American Association Thyroid Association thus recommends measuring TPOAb levels when evaluating subclinical hypothyroidism or when trying to identify whether nodular thyroid disease is due to autoimmune thyroid disease.

- When the etiology of hyperthyroidism is not clear after initial clinical and biochemical evaluation, measurement of TSH receptor antibodies (TSHRAb) can help make the diagnosis. In Grave's disease, TSHRAb levels are elevated as they are responsible for activating the TSH receptor and causing increased thyroid hormone production.

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

Thyroid autoantibodies appear mostly with the presence of lymphocytes in the targeted organ. Lymphocytes produce antibodies targeting three different thyroid proteins: Thyroid peroxidase Antibodies (TPOAb), Thyroglobulin Antibodies (TgAb), and Thyroid stimulating hormone receptor Antibodies (TRAb). Some patients who are healthy may be positive for more than one of these antibodies. Doctors who attend to such patients will most likely do routine follow-ups on the patient’s health since, even though it is highly unlikely that they will present any thyroid problems, there is still a chance that they will develop some type of dysfunction with time.

This condition is commonly undiagnosed by physicians due to either unfamiliarity with the disease, the subtlety of symptoms, or the attribution of the symptoms to the stresses of having a newborn. Usual screening begins with assessing the thyroid stimulating hormone (TSH) level. A suppressed TSH could represent the hyperthyroid phase, but warrants further testing to investigate for possible Graves' disease. A normal TSH with persistent symptoms could represent the shift between phases and requires repeat testing 4–6 weeks later; an elevated TSH at this time could indicate the hypothyroid phase.

In the initial phase of damage to the gland, preformed thyroid hormone will 'fall out' of the damaged cells. This leads to symptoms and biochemistry of an overactive thyroid (feels hot, trembly, anxious, loses weight, fast heart rate, sweaty, greasy hair), with raised free T3 and free T4, and a suppressed thyroid stimulating hormone (TSH) value. The damaged cells will no longer be able to take up iodine in order to manufacture further supplies of thyroid hormone, and thus in due course the patient comes to experience the symptoms of an underactive thyroid (feels cold, tired, depressed, gains weight, dry skin and hair) with low free T3 and free T4, and eventually increased TSH.

With the standard overactive thyroid, iodine uptake into the thyroid is avid, whereas if the cells are damaged, then uptake is poor. In this way, if there is doubt about whether the patient has too much thyroid hormone because of de Quervain's thyroiditis, then measuring radio-iodine uptake or technetium uptake gives a clear cut answer as it will be higher than normal in standard thyrotoxicosis and lower than normal in de Quervain's.

Treatment is beta blockers, ASA, and NSAIDs (or corticosteroids if NSAIDs are ineffective).

During pregnancy, the thyroid gland must produce 50% more thyroid hormone to provide enough thyroid hormone for the developing fetus and the expectant mother. In pregnancy, free thyroxine levels may be lower than anticipated due to increased binding to thyroid binding globulin and decreased binding to albumin. They should either be corrected for the stage of pregnancy, or total thyroxine levels should be used instead for diagnosis. TSH values may also be lower than normal (particularly in the first trimester) and the normal range should be adjusted for the stage of pregnancy.

In pregnancy, subclinical hypothyroidism is defined as a TSH between 2.5 and 10 mIU/l with a normal thyroxine level, while those with TSH above 10 mIU/l are considered to be overtly hypothyroid even if the thyroxine level is normal. Antibodies against TPO may be important in making decisions about treatment, and should, therefore, be determined in women with abnormal thyroid function tests.

Determination of TPO antibodies may be considered as part of the assessment of recurrent miscarriage, as subtle thyroid dysfunction can be associated with pregnancy loss, but this recommendation is not universal, and presence of thyroid antibodies may not predict future outcome.

There are several hormones that can be measured in the blood to determine how the thyroid gland is functioning. These include the thyroid hormones triiodothyronine (T3) and its precursor thyroxine (T4), which are produced by the thyroid gland. Thyroid-stimulating hormone (TSH) is another important hormone that is secreted by the anterior pituitary cells in the brain. Its primary function is to increase the production of T3 and T4 by the thyroid gland.

The most useful marker of thyroid gland function is serum thyroid-stimulating hormone (TSH) levels. TSH levels are determined by a classic negative feedback system in which high levels of T3 and T4 suppress the production of TSH, and low levels of T3 and T4 increase the production of TSH. TSH levels are thus often used by doctors as a screening test, where the first approach is to determine whether TSH is elevated, suppressed, or normal.

- Elevated TSH levels can signify inadequate thyroid hormone production (hypothyroidism)

- Suppressed TSH levels can point to excessive thyroid hormone production (hyperthyroidism)

Because a single abnormal TSH level can be misleading, T3 and T4 levels must be measured in the blood to further confirm the diagnosis. When circulating in the body, T3 and T4 are bound to transport proteins. Only a small fraction of the circulating thyroid hormones are unbound or free, and thus biologically active. T3 and T4 levels can thus be measured as free T3 and T4, or total T3 and T4, which takes into consideration the free hormones in addition to the protein-bound hormones. Free T3 and T4 measurements are important because certain drugs and illnesses can affect the concentrations of transport proteins, resulting in differing total and free thyroid hormone levels. There are differing guidelines for T3 and T4 measurements.

- Free T4 levels should be measured in the evaluation of hypothyroidism, and low free T4 establishes the diagnosis. T3 levels are generally not measured in the evaluation of hypothyroidism.

- Free T4 and total T3 can be measured when hyperthyroidism is of high suspicion as it will improve the accuracy of the diagnosis. Free T4, total T3 or both are elevated and serum TSH is below normal in hyperthyroidism. If the hyperthyroidism is mild, only serum T3 may be elevated and serum TSH can be low or may not be detected in the blood.

- Free T4 levels may also be tested in patients who have convincing symptoms of hyper- and hypothyroidism, despite a normal TSH.

Treatment is based on symptoms. Beta-blockers relieve rapid heart rate and excessive sweating during the hyperthyroid phase.

It is often possible to diagnose myxedema on clinical grounds alone. Characteristic symptoms are weakness, cold intolerance, mental and physical slowness, dry skin, typical facies, and hoarse voice. Results of the total serum thyroxine and free thyroxine index tests usually will confirm the diagnosis.

Therapy usually consists of prednisolone, nonetheless some cases may require surgery. Tamoxifen has been proposed as part of a treatment plan.

Treatment is directed to surgical relief of compressive symptoms. Tamoxifen may also be beneficial.

-Harrison's principle of internal medicine, 17th

The type of surgery which is indicated here is isthmectomy.

In overt primary hyperthyroidism, TSH levels are low and T and T levels are high. Subclinical hyperthyroidism is a milder form of hyperthyroidism characterized by low or undetectable serum TSH level, but with a normal serum free thyroxine level. Although the evidence for doing so is not definitive, treatment of elderly persons having subclinical hyperthyroidism could reduce the incidence of atrial fibrillation. There is also an increased risk of bone fractures (by 42%) in people with subclinical hyperthyroidism; there is insufficient evidence to say whether treatment with antithyroid medications would reduce that risk.

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.

Experts have not reached agreement on whether all pregnant women should be routinely screened for thyroid problems. But, if an underactive thyroid with or without symptoms is found during pregnancy it will be treated to lower the risk of pregnancy problems. An underactive thyroid without symptoms occurs in 2 to 3 in every 100 pregnancies. Women can request thyroid screening.

Measuring the level of thyroid-stimulating hormone (TSH), produced by the pituitary gland (which in turn is also regulated by the hypothalamus's TSH Releasing Hormone) in the blood is typically the initial test for suspected hyperthyroidism. A low TSH level typically indicates that the pituitary gland is being inhibited or "instructed" by the brain to cut back on stimulating the thyroid gland, having sensed increased levels of T and/or T in the blood. In rare circumstances, a low TSH indicates primary failure of the pituitary, or temporary inhibition of the pituitary due to another illness (euthyroid sick syndrome) and so checking the T and T is still clinically useful.

Measuring specific antibodies, such as anti-TSH-receptor antibodies in Graves' disease, or anti-thyroid peroxidase in Hashimoto's thyroiditis — a common cause of hypothyroidism — may also contribute to the diagnosis.

The diagnosis of hyperthyroidism is confirmed by blood tests that show a decreased thyroid-stimulating hormone (TSH) level and elevated T and T levels. TSH is a hormone made by the pituitary gland in the brain that tells the thyroid gland how much hormone to make. When there is too much thyroid hormone, the TSH will be low. A radioactive iodine uptake test and thyroid scan together characterizes or enables radiologists and doctors to determine the cause of hyperthyroidism. The uptake test uses radioactive iodine injected or taken orally on an empty stomach to measure the amount of iodine absorbed by the thyroid gland. Persons with hyperthyroidism absorb much more iodine than healthy persons which includes the radioactive iodine which is easy to measure. A thyroid scan producing images is typically conducted in connection with the uptake test to allow visual examination of the over-functioning gland.

Thyroid scintigraphy is a useful test to characterize (distinguish between causes of) hyperthyroidism, and this entity from thyroiditis. This test procedure typically involves two tests performed in connection with each other: an iodine uptake test and a scan (imaging) with a gamma camera. The uptake test involves administering a dose of radioactive iodine (radioiodine), traditionally iodine-131 (I), and more recently iodine-123 (I). Iodine-123 may be the preferred radionuclide in some clinics due to its more favorable radiation dosimetry (i.e. less radiation dose to the patient per unit administered radioactivity) and a gamma photon energy more amenable to imaging with the gamma camera. For the imaging scan, I-123 is considered an almost ideal isotope of iodine for imaging thyroid tissue and thyroid cancer metastasis.

Typical administration involves a pill or liquid containing sodium iodide (NaI) taken orally, which contains a small amount of iodine-131, amounting to perhaps less than a grain of salt. A 2-hour fast of no food prior to and for 1 hour after ingesting the pill is required. This low dose of radioiodine is typically tolerated by individuals otherwise allergic to iodine (such as those unable to tolerate contrast mediums containing larger doses of iodine such as used in CT scan, intravenous pyelogram (IVP), and similar imaging diagnostic procedures). Excess radioiodine that does not get absorbed into the thyroid gland is eliminated by the body in urine. Some patients may experience a slight allergic reaction to the diagnostic radioiodine and may be given an antihistamine.

The patient returns 24 hours later to have the level of radioiodine "uptake" (absorbed by the thyroid gland) measured by a device with a metal bar placed against the neck, which measures the radioactivity emitting from the thyroid. This test takes about 4 minutes while the uptake % is accumulated (calculated) by the machine software. A scan is also performed, wherein images (typically a center, left and right angle) are taken of the contrasted thyroid gland with a gamma camera; a radiologist will read and prepare a report indicating the uptake % and comments after examining the images. Hyperthyroid patients will typically "take up" higher than normal levels of radioiodine. Normal ranges for RAI uptake are from 10-30%.

In addition to testing the TSH levels, many doctors test for T, Free T, T, and/or Free T for more detailed results. Typical adult limits for these hormones are: TSH (units): 0.45 - 4.50 uIU/mL; T Free/Direct (nanograms): 0.82 - 1.77 ng/dl; and T (nanograms): 71 - 180 ng/dl. Persons with hyperthyroidism can easily exhibit levels many times these upper limits for T and/or T. See a complete table of normal range limits for thyroid function at the thyroid gland article.

In hyperthyroidism CK-MB (Creatine kinase) is usually elevated.

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

Cerebrospinal fluid findings:

- Raised protein (25% cases)

- Negative for 14–3–3 protein

- May contain antithyroid antibodies

- Magnetic resonance imaging abnormalities consistent with encephalopathy (26% cases)

- Single photon emission computed tomography shows focal and global hypoperfusion (75% cases)

- Cerebral angiography is normal

Thyroid hormone abnormalities are common (>80% cases):

- subclinical hypothyroidism (35% cases)

- overt hypothyroidism (20% cases)

- hyperthyroidism (5% cases)

- euthyroid on levothyroxine (10% cases)

- euthyroid not on levothyroxine (20% cases)

Thyroid antibodies – both anti-thyroid peroxidase antibodies (anti-TPO, anti-thyroid microsomal antibodies, anti-M) and antithyroglobulin antibodies (anti-Tg) – in the disease are elevated but their levels do not correlate with the severity.

Electroencephalogram studies, while almost always abnormal (98% cases), are usually nondiagnostic. The most common findings are diffuse or generalized slowing or frontal intermittent rhythmic delta activity. Prominent triphasic waves, focal slowing, epileptiform abnormalities, photoparoxysmal and photomyogenic responses may be seen.

Primary treatment is prompted by the administration of adequate doses of either the thyroid hormone l-throxine given intravenously or by giving L-triiodothyronine via a nasogastric tube. It is essential to identify and treat the condition precipitating the coma.

Myxedema coma is rare but often fatal. It occurs most often in elderly women and may be mistaken for one of the chronic debilitating diseases common to this age group.

Though the exact cause of myxedema is still unclear, a wealth of skillful research has demonstrated the importance of iodine. In an important study the researchers showed that in the myxedematous type of cretinism treatment with iodine normalizes thyroid function provided that the treatment is begun early in the postnatal period. If not, the prognosis remains dismal.