Thyroiditis

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Thyroiditis
Illu thyroid parathyroid.jpg
Above shows two parts of the thyroid that could potentially be affected if diagnosed with thyroiditis.
Specialty Endocrinology

Thyroiditis is the inflammation of the thyroid gland. The thyroid gland is located on the front of the neck below the laryngeal prominence, and makes hormones that control metabolism.

Contents

Signs and symptoms

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. [1]

Causes

Thyroiditis is generally caused by an immune system attack on the thyroid, resulting in inflammation and damage to the thyroid cells. This disease is often considered a malfunction of the immune system and can be associated with IgG4-related systemic disease, in which symptoms of autoimmune pancreatitis, retroperitoneal fibrosis and noninfectious aortitis also occur. Such is also the case in Riedel thyroiditis, an inflammation in which the thyroid tissue is replaced by fibrous tissue which can extend to neighbouring structures. Antibodies that attack the thyroid are what causes most types of thyroiditis. It can also be caused by an infection, like a virus or bacteria, which works in the same way as antibodies to cause inflammation in the glands, such as in the case of subacute granulomatous thyroiditis (de Quervain). [2] Certain people make thyroid antibodies, and thyroiditis can be considered an autoimmune disease, because the body acts as if the thyroid gland is foreign tissue. [3] Some drugs, such as interferon, lithium, amiodarone (AIT type-2) and immune check point inhibitors can also cause thyroiditis. [4]

Diagnosis

Diagnosis of thyroiditis depends on the specific cause and clinical context. When the initial presentation is thyrotoxicosis, work-up will include causes of thyroiditis as well as causes of hyperthyroidism. In some types of thyroiditis, a physical exam may reveal an enlarged thyroid and/or tenderness to palpation. If infectious thyroiditis is suspected a neck ultrasound can be utilized to check for an abscess. Color flow doppler is expected to show reduced blood flow in thyroiditis vs. hyperthyroidism. [5] Blood tests will usually include thyroid function tests as well levels of specific thyroid antibodies and thyroglobulin. Inflammatory markers such as white blood cell count, erythrocyte sedimentation rate and c-reactive protein may be elevated in some forms of thyroiditis. The gold-standard for diagnosis of thyroiditis is the lack of tracer uptake in a radionuclide uptake scan such as radioactive iodine, technetium-99m or setamibi. [6] Importantly, recent exposure to an intravenous iodine based radio-contrast agent may lead to falsely low uptake due to saturation with iodine. [7]

Classification

Microscopic image showing inflammation of the thyroid tissue Thyroid colloid - Thyroiditis.jpg
Microscopic image showing inflammation of the thyroid tissue

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, Riedel's thyroiditis. [8]

Treatment

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. [9]

Epidemiology

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. [1]

History

Hashimoto's thyroiditis was first described by Japanese physician Hashimoto Hakaru working in Germany in 1912. Hashimoto's thyroiditis is also known as chronic lymphocytic thyroiditis, and patients with this disease often complain about difficulty swallowing. This condition may be so mild at first that the disease goes unnoticed for years. The first symptom that shows signs of Hashimoto's thyroiditis is a goiter on the front of the neck. Depending on the severity of the disease and how much it has progressed, doctors then decide what steps are taken for treatment.[ citation needed ]

See also

Related Research Articles

<span class="mw-page-title-main">Hyperthyroidism</span> Clinical syndrome caused by excessive thyroid hormone

Hyperthyroidism is the condition that occurs due to excessive production of thyroid hormones by the thyroid gland. Thyrotoxicosis is the condition that occurs due to excessive thyroid hormone of any cause and therefore includes hyperthyroidism. Some, however, use the terms interchangeably. Signs and symptoms vary between people and may include irritability, muscle weakness, sleeping problems, a fast heartbeat, heat intolerance, diarrhea, enlargement of the thyroid, hand tremor, and weight loss. Symptoms are typically less severe in the elderly and during pregnancy. An uncommon but life-threatening complication is thyroid storm in which an event such as an infection results in worsening symptoms such as confusion and a high temperature; this often results in death. The opposite is hypothyroidism, when the thyroid gland does not make enough thyroid hormone.

<span class="mw-page-title-main">Thyroid</span> Endocrine gland in the neck; secretes hormones that influence metabolism

The thyroid, or thyroid gland, is an endocrine gland in vertebrates. In humans, it is in the neck and consists of two connected lobes. The lower two thirds of the lobes are connected by a thin band of tissue called the isthmus (pl.: isthmi). The thyroid gland is a butterfly-shaped gland located in the neck below the Adam's apple. Microscopically, the functional unit of the thyroid gland is the spherical thyroid follicle, lined with follicular cells (thyrocytes), and occasional parafollicular cells that surround a lumen containing colloid. The thyroid gland secretes three hormones: the two thyroid hormones – triiodothyronine (T3) and thyroxine (T4) – and a peptide hormone, calcitonin. The thyroid hormones influence the metabolic rate and protein synthesis and growth and development in children. Calcitonin plays a role in calcium homeostasis. Secretion of the two thyroid hormones is regulated by thyroid-stimulating hormone (TSH), which is secreted from the anterior pituitary gland. TSH is regulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus.

<span class="mw-page-title-main">Graves' disease</span> Autoimmune endocrine disease

Graves disease, also known as toxic diffuse goiter or Basedow’s disease, is an autoimmune disease that affects the thyroid. It frequently results in and is the most common cause of hyperthyroidism. It also often results in an enlarged thyroid. Signs and symptoms of hyperthyroidism may include irritability, muscle weakness, sleeping problems, a fast heartbeat, poor tolerance of heat, diarrhea and unintentional weight loss. Other symptoms may include thickening of the skin on the shins, known as pretibial myxedema, and eye bulging, a condition caused by Graves' ophthalmopathy. About 25 to 30% of people with the condition develop eye problems.

<span class="mw-page-title-main">Hypothyroidism</span> Insufficient production of thyroid hormones by the thyroid gland

Hypothyroidism is a disorder of the endocrine system in which the thyroid gland does not produce enough thyroid hormones. It can cause a number of symptoms, such as poor ability to tolerate cold, extreme fatigue, muscle aches, constipation, slow heart rate, depression, and weight gain. Occasionally there may be swelling of the front part of the neck due to goitre. Untreated cases of hypothyroidism during pregnancy can lead to delays in growth and intellectual development in the baby or congenital iodine deficiency syndrome.

<span class="mw-page-title-main">Myxedema</span> Extreme hypothyroidism

Myxedema is a term used synonymously with severe hypothyroidism. However, the term is also used to describe a dermatological change that can occur in hypothyroidism and (rare) paradoxical cases of hyperthyroidism. In this latter sense, myxedema refers to deposition of mucopolysaccharides in the dermis, which results in swelling of the affected area. One manifestation of myxedema occurring in the lower limb is pretibial myxedema, a hallmark of Graves disease, an autoimmune form of hyperthyroidism. Myxedema can also occur in Hashimoto thyroiditis and other long-standing forms of hypothyroidism.

<span class="mw-page-title-main">Hashimoto's thyroiditis</span> Autoimmune disease

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. A slightly broader term is autoimmune thyroiditis, identical other than that it is also used to describe a similar condition without a goiter.

The Jod-Basedow effect is hyperthyroidism following administration of iodine or iodide, either as a dietary supplement, for iodinated contrast medical imaging, or as a medication.

<span class="mw-page-title-main">Thyroid disease</span> Medical condition

Thyroid disease is a medical condition that affects the function of the thyroid gland. The thyroid gland is located at the front of the neck and produces thyroid hormones that travel through the blood to help regulate many other organs, meaning that it is an endocrine organ. These hormones normally act in the body to regulate energy use, infant development, and childhood development.

Thyroid storm is a rare but severe and life-threatening complication of hyperthyroidism. It occurs when an overactive thyroid leads to hypermetabolism, which can cause death from cardiac arrest or multiple organ failure.

<span class="mw-page-title-main">De Quervain's thyroiditis</span> Medical condition

De Quervain's thyroiditis, also known as subacute granulomatous thyroiditis or giant cell thyroiditis, is a self-limiting inflammatory illness of the thyroid gland. De Quervain thyroiditis is characterized by fever, flu-like symptoms, a painful goiter, and neck pain. The disease has a natural history of four phases: thyroid pain, thyrotoxicosis, euthyroid phase, hypothyroid phase, and recovery euthyroid phase.

Subacute lymphocytic thyroiditis is a form of 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.

<span class="mw-page-title-main">Subacute thyroiditis</span> Medical condition

Subacute thyroiditis refers to a temporal classification of the different forms of thyroiditis based on onset of symptoms. The temporal classification of thyroiditis includes presentation of symptoms in an acute, subacute, or chronic manner. There are also other classification systems for thyroiditis based on factors such as clinical symptoms and underlying etiology.

Postpartum thyroiditis refers to thyroid dysfunction occurring in the first 12 months after pregnancy and may involve hyperthyroidism, hypothyroidism or the two sequentially. According to the National Institute of Health, postpartum thyroiditis affects about 8% of pregnancies. There are, however, different rates reported globally. This is likely due to the differing amounts of average postpartum follow times around the world, and due to humans' own innate differences. For example, in Bangkok, Thailand the rate is 1.1%, but in Brazil it is 13.3%. 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.

Thyrotoxicosis factitia is a condition of thyrotoxicosis caused by the ingestion of exogenous thyroid hormone. It can be the result of mistaken ingestion of excess drugs, such as levothyroxine and triiodothyronine, or as a symptom of Munchausen syndrome. It is an uncommon form of hyperthyroidism.

Thyroid disease in pregnancy can affect the health of the mother as well as the child before and after delivery. Thyroid disorders are prevalent in women of child-bearing age and for this reason commonly present as a pre-existing disease in pregnancy, or after childbirth. Uncorrected thyroid dysfunction in pregnancy has adverse effects on fetal and maternal well-being. The deleterious effects of thyroid dysfunction can also extend beyond pregnancy and delivery to affect neurointellectual development in the early life of the child. Due to an increase in thyroxine binding globulin, an increase in placental type 3 deioidinase and the placental transfer of maternal thyroxine to the fetus, the demand for thyroid hormones is increased during pregnancy. The necessary increase in thyroid hormone production is facilitated by high human chorionic gonadotropin (hCG) concentrations, which bind the TSH receptor and stimulate the maternal thyroid to increase maternal thyroid hormone concentrations by roughly 50%. If the necessary increase in thyroid function cannot be met, this may cause a previously unnoticed (mild) thyroid disorder to worsen and become evident as gestational thyroid disease. Currently, there is not enough evidence to suggest that screening for thyroid dysfunction is beneficial, especially since treatment thyroid hormone supplementation may come with a risk of overtreatment. After women give birth, about 5% develop postpartum thyroiditis which can occur up to nine months afterwards. This is characterized by a short period of hyperthyroidism followed by a period of hypothyroidism; 20–40% remain permanently hypothyroid.

Antithyroid autoantibodies (or simply antithyroid antibodies) are autoantibodies targeted against one or more components on the thyroid. The most clinically relevant anti-thyroid autoantibodies are anti-thyroid peroxidase antibodies (anti-TPO antibodies, TPOAb), thyrotropin receptor antibodies (TRAb) and thyroglobulin antibodies (TgAb). TRAb's are subdivided into activating, blocking and neutral antibodies, depending on their effect on the TSH receptor. Anti-sodium/iodide (Anti–Na+/I) symporter antibodies are a more recent discovery and their clinical relevance is still unknown. Graves' disease and Hashimoto's thyroiditis are commonly associated with the presence of anti-thyroid autoantibodies. Although there is overlap, anti-TPO antibodies are most commonly associated with Hashimoto's thyroiditis and activating TRAb's are most commonly associated with Graves' disease. Thyroid microsomal antibodies were a group of anti-thyroid antibodies; they were renamed after the identification of their target antigen (TPO).

Thyroid disease in women is an autoimmune disease that affects the thyroid in women. This condition can have a profound effect during pregnancy and on the child. It also is called Hashimoto's thyroiditis (theye-royd-EYET-uhss). During pregnancy, the infant may be seriously affected and have a variety of birth defects. Many women with Hashimoto's disease develop an underactive thyroid. They may have mild or no symptoms at first, but symptoms tend to worsen over time. If a woman is pregnant and has symptoms of Hashimoto's disease, the clinician will do an exam and order one or more tests.

<span class="mw-page-title-main">Amiodarone induced thyrotoxicosis</span> Form of hyperthyroidism

Amiodarone induced thyrotoxicosis (AIT) is a form of hyperthyroidism due to treatment with antiarrhythmic drug, amiodarone.

<span class="mw-page-title-main">Hypothyroidism in dogs</span> Medical condition

Hypothyroidism is an endocrine disorder in which the thyroid gland fails to produce sufficient thyroid hormones. Hypothyroidism is one of the most common endocrinopathies in dogs. It is either acquired or congenital.

Feline hyperthyroidism is an endocrine disorder in which the thyroid gland produces too much thyroid hormone. Hyperthyroidism is the most common endocrinopathy of cats. The complete pathogenesis is not fully understood.

References

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