Hashimoto's thyroiditis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Hashimoto’s thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease where the body’s own antibodies attack the cells of the thyroid. Hashimoto’s thyroiditis was first described by Hashimoto Hakaru in 1912. He named it struma lymphomatosa which was renamed as Hashimoto’s thyroiditis in 1931. Hashimoto’s thyroiditis can be classified as primary or secondary types. Rarely, Hashimoto’s thyroiditis can be categorized under the polyglandular syndromes. Hashimoto’s thyroiditis (HT) is characterized by lymphocytic infiltration of the thyroid gland and production of antibodies that recognize thyroid-specific antigens. The pathogenesis is not yet completely understood. Thyroid cells undergo atrophy or transform into a type of follicular cell rich in mitochondria called Hurthle cell. It is currently thought that the disease is caused by abnormalities in cellular and humoral immunity which results in a localized cell-mediated immune response directed toward the thyroid parenchymal cells. This results in the decreased production of thyroid hormones. Hashimoto’s thyroiditis is particularly common in middle aged women, Asians, and Whites. Hashimoto’s thyroiditis usually begins slowly and may progress to hypothyroidism. Complications include heart failure, lymphoma, myxedema, and cervical compression. A positive history of autoimmune diseases and certain drug use are suggestive of Hashimoto’s thyroiditis. The most common symptoms of Hashimoto’s thyroiditis include fatigue, constipation, and cold intolerance. Laboratory findings consistent with the diagnosis of Hashimoto’s thyroiditis usually include increased thyroid stimulating hormone, decreased free T3 and free T4, and anti-thyroid peroxidase antibodies. Ultrasound findings associated with Hashimoto’s thyroiditis are reduced echogenicity, glandular irregularities, and nodules. 24-hour iodine-123 uptake is decreased in Hashimoto’s thyroiditis. The mainstay of therapy for Hashimoto’s thyroiditis is synthetic levothyroxine. Corticosteroids and selenium can also be used in certain cases. Thyroidectomy is usually performed when the enlarged thyroid produces cervical compression symptoms and there is a high suspicion for malignancy.

Hashimoto’s thyroiditis was first described by Hashimoto Hakaru in 1912. He named it struma lymphomatosa which was renamed as Hashimoto’s thyroiditis in 1931.

On the basis of the etiology, Hashimoto’s thyroiditis can be classified as primary or secondary types. Rarely, Hashimoto’s thyroiditis can be categorized under the polyglandular syndromes.

Hashimoto’s thyroiditis (HT) is characterized by lymphocytic infiltration of the thyroid gland and production of antibodies that recognize thyroid-specific antigens.The pathogenesis is not yet completely understood. Thyroid cells undergo atrophy or transform into a type of follicular cell rich in mitochondria called Hurthle cell. It is currently thought that the disease is caused by abnormalities in cellular and humoral immunity which results in a localized cell-mediated immune response directed toward the thyroid parenchymal cells. This results in the decreased production of thyroid hormones.

Hashimoto’s thyroiditis may be caused by T cells and B cells auto activation, genetic factors, and autoimmune antibodies against thyrotropin receptors.

Hashimoto’s thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. Hashimoto’s thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. Hashimoto’s thyroiditis must also be differentiated from other diseases which cause hypothyroidism. As Hashimoto’s thyroiditis may cause transient thyrotoxic symptoms, the diseases causing thyrotoxicosis must also be considered in the differential diagnosis.

Hashimoto’s thyroiditis is particularly common in middle aged women, Asians, and Whites. Annually, there are around 22 per 100,000 individuals worldwide.

Common risk factors in the development of Hashimoto’s thyroiditis are family history, female gender, and other autoimmune diseases.

There is insufficient evidence to recommend routine screening for Hashimoto’s thyroiditis.

Hashimoto’s thyroiditis usually begins slowly and may progress to hypothyroidism. Complications include heart failure, lymphoma, myxedema, and cervical compression.

There are no established criteria for the diagnosis of Hashimoto’s thyroiditis. The diagnosis of Hashimoto’s thyroiditis is made on laboratory and pathological findings after the clinical suspicion. It includes the TPO antibodies, hypothyroidism, reduced echogenicity on the ultrasound, the presence of germinal centers and lymphocytic infiltration of the thyroid gland.

The hallmark of Hashimoto’s thyroiditis is hypothyroidism. A positive history of autoimmune diseases and certain drug use are suggestive of Hashimoto’s thyroiditis. The most common symptoms of Hashimoto’s thyroiditis include fatigue, constipation, and cold intolerance.

Patients with Hashimoto’s thyroiditis usually appear fatigued and have myxedema. Physical examination of patients with Hashimoto’s thyroiditis is usually remarkable for bradycardia, bradypnea and delayed reflexes.

Laboratory findings consistent with the diagnosis of Hashimoto’s thyroiditis usually include increased thyroid stimulating hormone, decreased free T3 and free T4, and anti-thyroid peroxidase antibodies.

The findings associated with ECG in Hashimoto’s thyroiditis are bradycardia and low voltage QRS complex.

The findings associated with Chest X ray in Hashimoto’s thyroiditis are pleural effusion and cardiomegaly.

Non-contrast CT may be used in Hashimoto’s thyroiditis to assess the tracheal or esophageal compression.

There are no MRI findings associated with Hashimoto’s thyroiditis.

Ultrasound findings associated with Hashimoto’s thyroiditis are reduced echogenicity, glandular irregularities, and nodules.

24-hour iodine-123 uptake is decreased in Hashimoto’s thyroiditis.

The histological analysis in Hashimoto’s thyroiditis may show inflammatory cell infiltration and hurthle cells. Fine needle aspiration cytology helps to differentiate between the benign and malignant nodules. ^[1][2]

The mainstay of therapy for Hashimoto’s thyroiditis is synthetic levothyroxine. Corticosteroids and selenium can also be used in certain cases.

Thyroidectomy is usually performed when the enlarged thyroid produces cervical compression symptoms and there is a high suspicion for malignancy.

There are no primary preventive measures available for Hashimoto’s thyroiditis.

There are no secondary preventive measures available for Hashimoto’s thyroiditis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Hashimoto’s thyroiditis was first described by Hashimoto Hakaru in 1912. He named it struma lymphomatosa which was renamed as Hashimoto’s thyroiditis in 1931.

Hashimoto’s thyroiditis was first described by a Japanese physician Hashimoto Hakaru (1881−1934) of the medical school at Kyushu University. Hashimoto’s thyroiditis is also known as Hashimoto’s disease. ^[1]

• Hashimoto thyroiditis was initially considered to be an earlier manifestation of Riedel’s thyroiditis.
• Hashimoto Hakaru was the first who described four patients with a chronic disorder of the thyroid. Hakaru Hashimoto explained in his report that the new pathological characteristics he had identified, namely infiltration of lymphoid and plasma cells, the formation of lymphoid follicles with germinal centers, fibrosis, degenerated thyroid epithelial cells and leukocytes in the lumen, were histologically similar to those of Mikulicz’s disease.^[2][3]
• Hashimoto Hakaru termed the new disease struma lymphomatosa due to the lymphoid cell infiltration and formation of lymphoid follicles with germinal centers.^[3]
• Hashimoto’s struma lymphomatosa was then ignored and forgotten until 1931, when Allen Graham and his team at Cleveland reported struma lymphomatosa as detailed by Hashimoto Hakaru and recommended it to be considered a separate disease as Hashimoto suggested. Since then, this disease has been referred to as Hashimoto thyroiditis.^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

On the basis of the etiology, Hashimoto’s thyroiditis can be classified as primary or secondary types. Rarely, Hashimoto’s thyroiditis can be categorized under the polyglandular syndromes.

Hashimoto’s thyroiditis (HT) can be classified on the basis of the etiology to the primary and secondary types as follows:^[1]

Primary HT is the most common form of thyroiditis and comprises the cases that do not currently have identifiable causes. Primary HT encompasses a spectrum of the following main types:

• Classic form
• Fibrous variant
• IgG4-related variant
• Juvenile form
• Hashitoxicosis

Two forms of painless thyroiditis, sporadic and postpartum thyroiditis were considered the form of Hashimoto’s thyroiditis. These are now regarded as different from Hashimoto’s thyroiditis.

Secondary HT is of more recent description. It includes the forms where an etiologic agent can be clearly identified. It is more commonly iatrogenic and induced by the administration of:

• Immunomodulatory drugs (e.g, interferon-alpha)
• Monoclonal antibodies that block CTLA-4
• Cancer vaccines

In rare cases, Hashimoto’s thyroiditis may be associated with other endocrine disorders caused by the immune system. On the basis of the involvement of other endocrine disease involvements, Hashimoto’s thyroiditis may be classified under the polyglandular autoimmune syndromes. ^[2]

• Type 2 polyglandular autoimmune syndrome (PGA II):
  • Hashimoto’s thyroiditis/hypothyroidism
  • Adrenal insufficiency
  • Type 1 diabetes
• Type 1 polyglandular autoimmune syndrome (PGA I):
  • Hashimoto’s disease/hypothyroidism
  • Adrenal insufficiency
  • Fungal infections of the mouth and nails
  • Hypoparathyroidism

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Hashimoto’s thyroiditis (HT) is characterized by lymphocytic infiltration of the thyroid gland and production of antibodies that recognize thyroid-specific antigens. The pathogenesis is not yet completely understood. Thyroid cells undergo atrophy or transform into a type of follicular cell rich in mitochondria called Hurthle cell. It is currently thought that the disease is caused by abnormalities in cellular and humoral immunity which results in a localized cell-mediated immune response directed toward the thyroid parenchymal cells. This results in the decreased production of thyroid hormones.

The control, synthesis, and release of the thyroid hormones is usually controlled by hypothalamus and pituitary gland.[1][2] Thyroid hormones (T3 and T4) that regulate basal metabolic rate, influence oxygen consumption by tissues. They are crucial for normal development of the brain and growth of the body. Secretion of thyroid hormones follows upper control from the hypothalamus and the pituitary. Thyroid releasing hormone (TRH) acts on thyrotropes releasing cells in the pituitary causing them to release thyroid stimulating hormone (TSH). TSH acts on thyroid gland by binding to specific membrane receptors and activating an intracellular pathway involving cAMP that ends in the formation and secretion of thyroid hormones. Iodine is essential for the synthesis of thyroid hormones. Iodide is uptaken through a special Na/I transporter found in the membrane of thyroid follicular cell. After the iodide uptake, it goes through a series of organic reactions ending in the formation of the two forms of thyroid hormones: T3 (Triiodothyronine) and T4 (Thyroxine). T3 and T4 remain stored in the thyroglobulin of the follicles and are released in response to further stimulation by TSH to the thyroid follicles. While T3 is 3 to 5 times more potent than T4, it represents only one-fourth of the total hormone secretion. T3 is thought to be the biologically active form of the hormone. Most of the circulating T3 is due to peripheral conversion of T4 in the liver and peripheral tissues while only a small percentage is secreted directly from the thyroid gland itself. T3 and T4 act on nuclear receptors (DNA binding proteins) and cause the regulate the transcription of many proteins to regulate the metabolic rate of the body. The higher regulation of thyroxine secretion follows the negative feedback role, meaning that high levels of T3 and T4 will suppress TRH and TSH secretion and vice versa (Low levels of thyroxine will stimulate TRH and TSH secretion). This is useful in diagnosing the cause of hyperthyroidism. TSH will be low in primary hyperthyroidism where the gland is the source of the excess hormones. In secondary hyperthyroidism, TSH will be high as the pituitary or the hypothalamus are the sources of the disease.

Thyroid cells undergo atrophy or transform into a type of follicular cell rich in mitochondria called Hurthle cell. Cellular and humoral immunity is thought to be involved in the pathophysiology of Hashimoto’s thyroiditis:^[3][4]

• Defects in regulatory T cell response to thyroid-specific antigens in autoimmune hypothyroidism resulting in failure of regulatory T cell function.
• Regulatory T cells can also dampen the immune response. Regulatory T cells are high in CD25 expression and have altered activity in Hashimoto thyroiditis.
• CD4+ cells are less sensitive to the inhibitory effect of TGFβ in Hashimoto thyroiditis.
• There is an increased number of follicular helper T cells in patients Hashimoto’s thyroiditis, which correlates with thyroid-specifc antibody levels.

• Patients with Hashimoto thyroiditis have positive antibodies against thyroglobulin (TG) and thyroid peroxidase (TPO).
• Recently, a distinct variant of HT has been documented where the thyroid gland is infiltrated with IgG4-positive cells.
• Thyroid hormone receptor antibodies might be involved in the disease presentation as sometimes thyroiditis presents as hyperthyroidism. The balance between the thyroid stimulating antibodies (TSAb) and thyroid blocking antibodies (TBAb) explains the fluctuating hormone levels in patients with Hashimoto’s thyroiditis. It should also be noted that thyroid stimulating antibodies (TSAb) might have a minor blocking action.
• The sodium-iodide symporter (NIS) mediates iodine uptake by the thyroid gland, while pendrin is responsible for the efflux of iodine through thyroid follicles. Antibodies against NIS and pendrin are also found in Hashimoto thyroiditis (HT).

• Increased plasma level and expressions of IL-17 and IL-22 are seen in HT.

• MicroRNAs (miRNA), which are small noncoding RNA regions, have also been implicated in the pathogenesis of thyroid immunity. In HT tissue, a decreased level of miR-155_2 and an increase in miR-200a1 was found.

• A family history of thyroid disorders is common, with HLA-B* 46:01 confers an increased risk of HT developing in Han Chinese children. HLA-A* 02:07 and HLA-DRB4 conferred susceptibility. The genes implicated vary in different groups and the incidence is increased in patients with chromosomal disorders, including Down’s syndrome and Turner syndrome.^[3][5]

The following conditions are associated with Hashimoto’s thyroiditis:^[6]

• Type 1 diabetes
• Addison’s disease
• Pernicious anemia
• Vitiligo
• Rheumatoid arthritis
• Premature ovarian failure

On gross pathology the characteristic findings of Hashimoto’s thyroiditis are.^[4][7]

• The gland is usually diffusely enlarged, firm, and slightly lobular.
• The capsule is intact, and the cut surface is light-tan and has a slight lobular pattern.

On microscopic histopathological analysis, characteristic findings of Hashimoto’s thyroiditis include:^[4][7]

• Massive infiltration of the thyroid gland by lymphocytes and plasma cells
• Germinal centers
• Thyroid follicles are usually absent and the few remaining follicles are devoid of colloid
• Hurthle cells
  • Large polygonal cells with eosinophilic cytoplasm
  • Have an abundance of mitochondria

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Hashimoto’s thyroiditis may be caused by T cells and B cells auto-activation, genetic factors, and autoimmune antibodies against thyrotropin receptors.

Hashimoto’s thyroiditis usually caused by:^[1][2]

• Autoantibodies against thyroid peroxidase and thyroglobulin
• Abnormalities in the suppressor T cells and regulatory T cells
• HLA-B* 46:01, HLA-A* 02:07 and HLA-DRB4 involvement

• Immunomodulatory drugs (e.g, interferon-alpha)
• Monoclonal antibodies that block CTLA-4
• Cancer vaccines
• Micro RNA involvement
• Polyglandular Syndrome

For the factors involved in the development of Hashimoto’s thyroiditis, please click here.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Hashimoto’s thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. Hashimoto’s thyroiditis must also be differentiated from other diseases which cause hypothyroidism. As Hashimoto’s thyroiditis may cause transient thyrotoxic symptoms, the diseases causing thyrotoxicosis must also be considered in the differential diagnosis.

• Hashimoto’s thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis.^[1]

Conditions	Causes	Age at onset	Pathological findings	Diagnostic approach
Hashimoto’s thyroiditis	Autoimmune	All ages, peak at 30-50	Lymphocytic infiltration Germinal centers Fibrosis (in some variants)	Increased TSH (hypothyroidism) TPO antibodies present in high titer I-123 uptake usually decreased
Painful subacute (De Quervain’s) thyroiditis	Unknown	20-60	Giant cells Granulomas	Increased TSH (hypothyroidism) and/or Decreased TSH (Thyrotoxicosis) TPO antibodies absent or very low titer I-123 uptake decreased
Silent thyroiditis	Autoimmune	All ages, peak at 30-40	Lymphocytic infiltration Lymphoid follicles	Increased TSH (hypothyroidism) and/or Decreased TSH (transient hypothyroidism) TPO antibodies present in high titer I-123 uptake usually decreased
Postpartum thyroiditis	Autoimmune	Childbearing age	Lymphocytic infiltration	Increased TSH (hypothyroidism) and/or Decreased TSH (transient hypothyroidism) TPO antibodies present in high titer I-123 uptake usually decreased
Riedel’s thyroiditis	Unknown	30-60	Dense fibrosis	Normal TSH (euthyroidism) TPO antibodies usually present I-123 uptake decreased or normal
Suppurative thyroiditis	Infection	Children, 20-40	Abscess formation	Normal TSH (euthyroidism) TPO antibodies absent I-123 uptake normal

• Hashimoto’s thyroiditis must be differentiated from other causes of hypothyroidism on the basis of history and symptoms and laboratory findings:^{[2][3][1][4][5][6]}

Disease		History and symptoms		Laboratory findings							Additional findings
		Fever	Pain	TSH	Free T4	T3	T3RU†	Thyroglobin	TRH	TPOAb^
Primary hypothyroidism	Autoimmune (Hashimoto’s thyroiditis)	–	–	↑*	↓	Normal/↓	Normal/↓	Normal/↑	Normal	Present (high titer)	May be accompanied by other autoimmune diseases
	Riedel’s thyroiditis	–	–	Normal/↑	Normal/↓	Normal/↓	Normal/↓	Normal	Normal	Usually present	Riedel’s thyroiditis usually presents with hard and fixed thyroid mass.
	Infectious thyroiditis	+	+	Normal	Normal	Normal	Normal	Normal	Normal	Absent	Infectious thyroiditis associated with neck pain
Transient hypothyroidism	Subacute (de Quervain’s) thyroiditis	+/-	+/-	↑/↓	↓/↑	Normal	↓	↑	Normal	Low/absent	May present primarily with hyperthyroidism
	Postpartum thyroiditis	+/-	+/-	↑/↓	↓/↑	Normal	↓	↑	Normal/↑	Present (high titer)	May present primarily with hyperthyroidism
	Silent thyroiditis	–	–	↑/↓	↓/↑	Normal	↓	↑	Normal	Present (high titer)	May present primarily with hyperthyroidism
Others	Drug-induced	–	–	↑/↓	↓/↑	Normal	↓	Normal/↑	Normal	Absent**	History of hyperthyroidism History of trauma History of drug use, surgery, or radiation
	Radiation-induced
	Trauma induced
	Radioiodine induced
	Thyroidectomy
	Subclinical hypothyroidism	–	–	↑	Normal	Normal	Normal	Normal	Normal	Normal/↑	Asymptomatic

(†)T3RU; Triiodothyronine Resin uptake. (^)TPOAb; Thyroid peroxidase antibodies. (*)TSH may be decreased transiently in the thyrotoxicosis. (**)TPOAb may be present in drug-induced hypo/hyperthyroidism such as Interferon-alpha, interleukin-2, and lithium.

• Hashimoto’s thyroiditis can initially present with thyrotoxicosis (hashitoxicosis) which must be differentiated from other causes of thyrotoxicosis.^{[2][3][1][4][5][6][7][8][9]}

Disease		History and symptoms		Laboratory findings								Additional findings
		Fever	Pain	TSH	Free T4	T3	T3RU†	Thyroglobin	TRH	TSH Receptor Antibody	TPOAb^
Thyroiditis	Hashimoto’s thyroiditis (Hashitoxicosis)	–	–	↑*	↓	Normal/↓	Normal/↓	Normal/↑	Normal	Absent	Present (high titer)	May be accompanied by other autoimmune diseases
	Subacute (de Quervain’s) thyroiditis	+/-	+/-	↑/↓	↓/↑	Normal	↓	↑	Normal	Absent	Low/absent	May present with hypothyroidism
	Postpartum thyroiditis	+/-	+/-	↑/↓	↓/↑	Normal	↓	↑	Normal/↑	Absent	Present (high titer)	May present with hypothyroidism
	Silent thyroiditis	–	–	↑/↓	↓/↑	Normal	↓	↑	Normal	Absent	Present (high titer)	May present with hypothyroidism
Primary hyperthyroidism	Grave’s disease	–	–	↓	↑	Normal/↑	↑	↑	Normal	Present	Absent	Patient may have opthalmopathy and dermopathy
	Toxic thyroid nodule	–	–	↓	↑	Normal/↑	↑(hot nodule)	Normal/↑	Normal	Absent	Absent	–
Secondary hyperthyroidism	Pituitary adenoma	–	–	↑	↑	Normal/↑	↑	Normal/↑	Normal	Absent	Absent	Inappropriately normal or increased TSH
Tertiary hyperthyroidism	Tertiary hyperthyroidism	–	–	↑	↑	↑	↑	Normal/↑	↑	Absent	Absent	Inappropriately normal or increased TSH
Drug induced	Amiodarone type 1	–	–	↓	↑	Normal/↑	↓	Normal/↑	Normal	Absent	Absent	High urinary iodine
	Amiodarone type 2	–	–	↓	↑	Normal/↑	Absent/↓	Normal/↑	Normal	Absent	Absent	High urinary iodine
Others	Factitious thyrotoxicosis	–	–	↓	↑	Normal/↑	↓	↓	Normal	Absent	Absent	Decreased thyroglobulin
	Trophoblastic disease	–	–	↓	↑	Normal/↑	↑	–	Normal	Absent	Absent	–
	Struma ovarii	–	–	↓	↑	Normal/↑	↓	–	Normal	Absent	Absent	–

(†)T3RU; Triiodothyronine Resin uptake. (^)TPOAb; Thyroid peroxidase antibodies.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Hashimoto’s thyroiditis is particularly common in middle aged women, Asians, and Whites. Annually, there are around 22 cases per 100,000 individuals worldwide.

Hashimoto’s thyroiditis is more common in middle aged women, Asians, and Whites.^[1]

The prevalence of Hashimoto’s thyroiditis is 800 cases per 100,000 when estimated from a review of published articles and 4600 cases per 100,000 when estimated from the biochemical evidence of hypothyroidism and thyroid autoantibodies.^[1][2]

The overall incidence of endogenous Hashimoto’s thyroiditis is approximately 22 per 100,000 individuals per year. The incidence varies according to the disease definition and case detection methods. ^[1][2]

Hashimoto’s thyroiditis is most prevalent between 45 and 65 years of age.^[1]

Hashimoto’s thyroiditis is more common in females.^[1]

Hashimoto’s thyroiditis is more common in Whites and Asians than in African-Americans.^[1]

Hashimoto’s thyroiditis is believed to be the most common cause of primary hypothyroidism in North America. In European countries, an atrophic form of autoimmune thyroiditis (Ord’s thyroiditis) is more common than Hashimoto’s thyroiditis. It affects between 0.1% and 5% of all adults in Western countries.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Common risk factors in the development of Hashimoto’s thyroiditis are family history, female gender, and other autoimmune diseases.

The risk factors for Hashimoto’s thyroiditis are:^[1]

• Female gender
• Family history
• Other autoimmune diseases like vitiligo, rheumatoid arthritis, Addison’s disease, type 1 diabetes and pernicious anemia.

• Hygienic environment
• Selenium deficiency
• Irradiation
• Drugs (cytokines, especially interferon-α, tyrosine kinase inhibitors, alemtuzumab)
• HHV-6 and Yersinia infection (low level of evidence)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

There is insufficient evidence to recommend routine screening for Hashimoto’s thyroiditis.

There is insufficient evidence to recommend routine screening for Hashimoto’s thyroiditis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Hashimoto’s thyroiditis usually begins slowly and may progress to hypothyroidism. Complications include heart failure, lymphoma, myxedema, and cervical compression.

The disease begins slowly. The patient usually has the neck swelling and presents with symptoms of hypothyroidism such as fatigue, weight gain, constipation, and dry skin. Some patients may also present with hyperthyroidism. It may take months or even years for the condition to be detected. If left untreated, Hashimoto’s thyroiditis may lead to muscle failure including heart failure, other features associated with hypothyroidism and complications such as myxedema Coma and Hashimoto’s encephalopathy.^[1]

Complications that can develop as a result of Hashimoto’s thyroiditis are:^{[1][2][3][4][5]}

• Hypothyroidism
• Hyperthyroidism
• Heart failure
• Myxedema Coma
• Tracheal and/or esophageal compression
• Hashimoto’s encephalopathy
• Papillary thyroid carcinoma (PTC)
• Thyroid lymphoma

The outcome is usually very good. The disease stays stable for years. If it does slowly progress to thyroid hormone deficiency (hypothyroidism), it can be treated with thyroid replacement therapy.

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