Riedel'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]

Riedel’s thyroiditis was first described by Semple, in 1864 and Bolby in 1888. Riedel’s thyroiditis was reported to the International Congress of Surgery by Bernhard Riedel in 1894 and 1896. It was initially considered to be the fibrous variant of Hashimoto’s thyroiditis but was later recognized as a separate disease. The exact pathogenesis of Riedel’s thyroiditis is not fully understood. The presence of thyroid autoantibodies and lymphoid infiltration of the thyroid gland resembling that of Hashimoto’s thyroiditis might indicate an autoimmune etiology. It is considered that the infiltrating lymphocytes release cytokines which are responsible for the activation of fibroblasts responsible for the fibrosis. 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 and fixed to adjacent structures. A shared mechanism with retroperitoneal fibrosis and sclerosing cholangitis has been suggested. Riedel’s thyroiditis is considered to have autoimmune etiology and may be caused by the eosinophilia and the proliferation fibroblast as a result of cytokines released by inflammatory cells. Riedel’s thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Hashimoto’s thyroiditis, and suppurative thyroiditis. Riedel’s thyroiditis is a rare disease with an approximate incidence of 1.06 cases per 100,000 individuals worldwide. Riedel’s thyroiditis commonly affects individuals between 30-50 years of age. Females are more commonly affected by Riedel’s thyroiditis. Common risk factors in the development of Riedel’s thyroiditis include genetic factors, medications such as lysergic acid, ergotamine, serotonin, and other autoimmune diseases such as Graves’ disease and Hashimoto’s thyroiditis. If left untreated, patients with Riedel’s thyroiditis may progress to develop complications such as painless neck pressure, hoarseness, stridor, dysphagia, hypothyroidism, hypoparathyroidism, Horner’s syndrome, and occlusive phlebitis. Prognosis is generally good and the disease-specific death rate ranges from 6 to 10%. Diagnostic criteria of Riedel’s thyroiditis is based on the histopathological findings and includes infiltration of inflammatory cells in the thyroid gland, extension beyond the capsule, evidence of occlusive phlebitis and absence of giant cells, lymphoid follicles, or granulomas. The hallmark of Riedel’s thyroiditis is hard and fixed thyroid mass. A positive history of other autoimmune diseases and the use of certain medications is suggestive of Riedel’s thyroiditis. The most common symptoms of Riedel’s thyroiditis include hard and fixed neck mass, painless goiter, dysphagia, dyspnea, and hoarseness. Less common symptoms of Riedel’s thyroiditis include muscular cramps, paresthesias, fatigue, and dry skin. Patients may have the clinical signs of hypocalcemia such as positive Chvostek sign and positive Trousseau sign. Laboratory findings consistent with the diagnosis of Riedel’s thyroiditis include elevated ESR, mild elevation of thyroid peroxidase antibodies and occasionally elevated TSH levels. X-ray is helpful to identify esophageal or tracheal compression. CT scan findings suggestive of Riedel’s thyroiditis include hypodense infiltrative mass, invasion of nearby soft tissues, compression of the trachea, and esophageal compression. MRI findings suggestive of Riedel’s thyroiditis include focal, homogeneous hypointensity in T1 and T2. Ultrasound findings suggestive of Riedel’s thyroiditis include hypoechogenicity, thyroid nodule infiltrating adjacent structures, and absence of blood flow on Doppler ultrasound. 24-hour iodine-123 uptake is absent or decreased in Riedel’s thyroiditis. Other diagnostic studies for Riedel’s thyroiditis include pathological analysis, which demonstrates inflammatory cells infiltration, fibrosis with hyalinization, and extension of fibrosis outside the capsule, and immunohistochemical analysis, which demonstrates the predominance of T lymphocytes, strong positive stain to thyroglobulin, the presence of CD8+, CD4+ and plasma cells. Pharmacologic medical therapies for Riedel’s thyroiditis include corticosteroids, tamoxifen, and mycophenolate mofetil. Surgery is usually reserved for patients with esophageal or tracheal compressive symptoms.

Riedel’s thyroiditis was first described by Semple, in 1864 and Bolby in 1888. Riedel’s thyroiditis was reported to the International Congress of Surgery by Bernhard Riedel in 1894 and 1896. It was initially considered to be the fibrous variant of Hashimoto’s thyroiditis but was later recognized as a separate disease.

There is no established system for the classification of Riedel’s thyroiditis.

The exact pathogenesis of Riedel’s thyroiditis is not fully understood. The presence of thyroid autoantibodies and lymphoid infiltration of the thyroid gland resembling that of Hashimoto’s thyroiditis might indicate an autoimmune etiology. It is considered that the infiltrating lymphocytes release cytokines which are responsible for the activation of fibroblasts responsible for the fibrosis. 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 and fixed to adjacent structures. A shared mechanism with retroperitoneal fibrosis and sclerosing cholangitis has been suggested.

Riedel’s thyroiditis is considered to have autoimmune etiology and may be caused by the eosinophilia and the proliferation fibroblast as a result of cytokines released by inflammatory cells. Although some drugs such as methysergide, serotonin, lysergic acid, and ergotamine have also been identified as the cause of retroperitoneal fibrosis, there are no reports of the direct association with Riedel’s thyroiditis.

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

Riedel’s thyroiditis is a rare disease with an approximate incidence of 1.06 cases per 100,000 individuals worldwide. Riedel’s thyroiditis commonly affects individuals between 30-50 years of age. Females are more commonly affected by Riedel’s thyroiditis.

Common risk factors in the development of Riedel’s thyroiditis include genetic factors, medications such as lysergic acid, ergotamine, serotonin, and other autoimmune diseases such as Graves’ disease and Hashimoto’s thyroiditis.

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

If left untreated, patients with Riedel’s thyroiditis may progress to develop complications such as painless neck pressure out of proportion to the size of the goiter, hoarseness, stridor, dysphagia, hypothyroidism, hypoparathyroidism, Horner’s syndrome, and occlusive phlebitis. Prognosis is generally good and the disease-specific death rate ranges in frequency from 6-10% in the patients with Riedel’s thyroiditis.

Diagnostic criteria of Riedel’s thyroiditis is based on the histopathological findings and includes infiltration of inflammatory cells in the thyroid gland, extension beyond the capsule, evidence of occlusive phlebitis and absence of giant cells, lymphoid follicles, or granulomas.

The hallmark of Riedel’s thyroiditis is hard and fixed thyroid mass. A positive history of other autoimmune diseases and the use of certain medications is suggestive of Riedel’s thyroiditis. The most common symptoms of Riedel’s thyroiditis include hard and fixed neck mass, painless goiter, dysphagia, dyspnea, and hoarseness. Less common symptoms of Riedel’s thyroiditis include muscular cramps, paresthesias, fatigue, and dry skin.

Physical examination of patients with Riedel’s thyroiditis is usually remarkable for hard thyroid mass and clinical signs of hypothyroidism such as fatigue, bradycardia, bradypnea. Patients may have the clinical signs of hypocalcemia such as positive Chvostek sign and positive Trousseau sign.

Laboratory findings consistent with the diagnosis of Riedel’s thyroiditis include elevated ESR, mild elevation of thyroid peroxidase antibodies and occasionally elevated TSH levels.

There are no ECG findings associated with Riedel’s thyroiditis.

X-ray findings in Riedel’s thyroiditis are helpful to identify esophageal or tracheal compression.

CT scan may be helpful in the diagnosis of Riedel’s thyroiditis. Findings on CT scan suggestive of Riedel’s thyroiditis include hypodense infiltrative mass, invasion of nearby soft tissues, compression of the trachea, and esophageal compression.

MRI may be helpful in the diagnosis of Riedel’s thyroiditis. Findings on MRI suggestive of Riedel’s thyroiditis include focal, homogeneous hypointensity in T1 and T2.

Ultrasound may be helpful in the diagnosis of Riedel’s thyroiditis. Findings on an ultrasound suggestive of Riedel’s thyroiditis include hypoechogenicity, thyroid nodule infiltrating adjacent structures, and absence of blood flow on Doppler ultrasound.

24-hour iodine-123 uptake is absent or decreased in Riedel’s thyroiditis.

Other diagnostic studies for Riedel’s thyroiditis include pathological analysis, which demonstrates inflammatory cells infiltration, fibrosis with hyalinization, and extension of fibrosis outside the capsule, and immunohistochemical analysis, which demonstrates the predominance of T lymphocytes, strong positive stain to thyroglobulin, the presence of CD8+, CD4+ and plasma cells.

Pharmacologic medical therapies for Riedel’s thyroiditis include corticosteroids, tamoxifen, and mycophenolate mofetil.

Surgery is usually reserved for patients with esophageal or tracheal compressive symptoms.

There are no established measures for the primary prevention of Riedel’s thyroiditis.

There are no established measures for the secondary prevention of Riedel’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]

Riedel’s thyroiditis was first described by Semple, in 1864 and Bolby in 1888. Riedel’s thyroiditis was reported to the International Congress of Surgery by Bernhard Riedel in 1894 and 1896. It was initially considered to be the fibrous variant of Hashimoto’s thyroiditis but was later recognized as a separate disease.

Riedel’s thyroiditis was initially thought to be the fibrous variant of Hashimoto’s thyroiditis and was later differentiated from Hashimoto’s thyroiditis.^[1][2][3]

• Riedel’s thyroiditis was first described by Semple, in 1864 and Bolby in 1888 even before the description of Bernhard Riedel.
• Riedel’s thyroiditis was reported to the International Congress of Surgery by Bernhard Riedel in 1894 and 1896. He gave a complete description of the disease.
• Riedel described 2 patients with a hard goiter and tracheal compressive symptoms. Initially, it was considered to be a fibrous variant of 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]

There is no established system for the classification of Riedel’s thyroiditis.

There is no established system for the classification of Riedel’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]

The exact pathogenesis of Riedel’s thyroiditis is not fully understood. The presence of thyroid autoantibodies and lymphoid infiltration of the thyroid gland resembling that of Hashimoto’s thyroiditis might indicate an autoimmune etiology. It is considered that the infiltrating lymphocytes release cytokines which are responsible for the activation of fibroblasts responsible for the fibrosis. 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 and fixed to adjacent structures. A shared mechanism with retroperitoneal fibrosis and sclerosing cholangitis has been suggested.

The control, synthesis, and release of the thyroid hormone is usually controlled by hypothalamus and pituitary gland.[1][2] Thyroid hormones (T3 and T4) are regulating 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 up taken through a special Sodium-iodide symporter(Na/I) 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 and T4. 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.

The exact pathogenesis of Riedel’s thyroiditis is not fully understood. The presence of thyroid autoantibodies and lymphoid infiltration of the thyroid gland resembling that of Hashimoto’s thyroiditis might indicate an autoimmune etiology.^[3]

• It is considered that the infiltrating lymphocytes (CD4+ and CD8+) release cytokines which are responsible for the activation of fibroblasts responsible for the fibrosis.^[4]
• 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 and fixed to adjacent structures.^[5]
• Tissue eosinophilia and Major basic protein (MBP) identified in the thyroid gland on the histopathological analysis are also thought to play a role in the proliferation of fibroblasts.^[6]
• A shared mechanism with retroperitoneal fibrosis and sclerosing cholangitis is also suggested.^[7]

The following hypotheses regarding the pathogenesis of Riedel’s thyroiditis have been proposed:^[8]

According to this theory, Riedel’s thyroiditis (RT) might be a primary disease of fibroblasts triggered by autoimmune stimuli.^{[8][9][10][11][12][13]}

• It is proposed that the endothelial cells release oxidized low-density lipoprotein from atheromatous plaques following the injury resulting in an allergic hypersensitivity reaction.
• The natural consequence of this hypothesis is that the antigen initiating fibrosis is not localized within the thyroid but is affected secondarily by a systemic fibroinflammatory process.
• Thyroid follicular cells, peri-thyroid muscular cells, or intrathyroidal endothelial cells express antigens, cytokines, or adhesion molecules that might contribute to local activation of the disease. The evidence of a perivascular concentration of inflammatory cells in RT (occlusive phlebitis) might support the theory that the allergic process first involves blood vessels.
• Once the allergic reaction has started, a heavy inflammatory cell population such as B and T lymphocytes, plasma cells, monocytes, and eosinophils infiltrate tissues and produce several cytokines.
• The role of eosinophils in this context probably is central. When eosinophils migrate into the tissues involved by the disease, they degranulate and release cationic toxins into connective tissue including Major basic protein (MBP), eosinophil cationic protein, eosinophil peroxidase, and eosinophil-derived neurotoxin.
• Eosinophils also release cytokines, the most important of which are transforming growth factor β, transforming growth factor α, and granulocyte-macrophage colony-stimulating factor. This stimulates fibroblast proliferation that finally causes fibrosis.

This hypothesis was proposed for the multifocal fibrosclerosis which is associated with Riedel’s thyroiditis.^[14]

• The basis of this hypothesis was a report of multifocal fibrosclerotic disease in two brothers, whose parents were first cousins. They developed different combinations of the multifocal fibrosclerotic disease and a familial multifocal fibrosclerosis was hypothesized.
• It was thought that genetic factors might have played a partial role in an enzymatic defect in the tryptophan → serotonin → 5-hydroxyindolacetic acid pathway. However, such a relationship has never been proven, and the siblings described remain the only case of familial multifocal fibrosclerosis reported in the literature.

Riedel’s thyroiditis is associated with Hashimoto’s thyroiditis and de Quervain’s thyroiditis.^[15]

• It is proposed that Riedel’s thyroiditis might represent a late fibrotic stage of subacute or chronic thyroiditis. The fundamental concept of this theory is that the fibrosing process of RT is specific to the thyroid gland.

This hypothesis is also proposed primarily for multifocal fibrosclerosis. As Riedel’s thyroiditis is associated with multifocal fibrosclerosis this theory might explain the indirect association of Riedel’s thyroiditis with drugs.^[8][16]

• The production of fibrosis by the drugs might be determined by an increased serum serotonin concentration through competitive inhibition at the serotonin receptor level and a reaction of hypersensitivity causing vasculitis and plasma exudation resulting in fibrosis.
• Although drugs have been found to cause multi organ fibrosis, there are no reports regarding medication induced Riedel’s thyroiditis. This theory might explain the indirect association of Riedel’s thyroiditis with drugs as Riedel’s thyroiditis is associated with multifocal fibrosclerosis.

Riedel’s thyroiditis is associated various other autoimmune conditions including:^{[4][17][18][19][20][16]}

• Graves’ disease
• Hashimoto’s thyroiditis
• Multifocal idiopathic fibrosclerosis
• Addison’s disease
• Pernicious anemia
• Type 1 diabetes

On gross pathology the following findings are characteristic of Riedel’s thyroiditis:^[21]

• Dense, avascular white fibrous tissue
• Absence of a capsule
• Absence thyroid tissue

On microscopic histopathological analysis the following findings are usually seen:^[22][8]

• Destruction of thyroid follicle by inflammatory cells
• Inflammatory cells including lymphocytes, plasma cells, and eosinophils in a dense matrix of hyalinized connective tissue
• Fibrous tissues and invasion of surrounding structures

• 
  Histology of Riedel’s thyroiditis (Image courtesy of AFIP and PathologyOutlines.com; http://www.pathologyoutlines.com/topic/thyroidriedel.html )
• 
  Histology of Riedel’s thyroiditis (Image courtesy of AFIP and PathologyOutlines.com; http://www.pathologyoutlines.com/topic/thyroidriedel.html )
• 
  Histology of Riedel’s thyroiditis (Image courtesy of AFIP and PathologyOutlines.com; http://www.pathologyoutlines.com/topic/thyroidriedel.html )

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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]

Riedel’s thyroiditis is considered to have autoimmune etiology and may be caused by the eosinophilia and the proliferation fibroblast as a result of cytokines released by inflammatory cells. Although some drugs such as methysergide, serotonin, lysergic acid, and ergotamine have also been identified as the cause of retroperitoneal fibrosis, there are no reports of the direct association with Riedel’s thyroiditis.

Causes of Riedel’s thyroiditis may include:^[1][2][3][4]

• Autoimmunity
  • T and B Lymphocyte and macrophage infiltration
  • Eosinophilic infiltration

• Drugs
  • There are no reports of the direct association with Riedel’s thyroiditis with drugs. Some drugs have been identified as the cause of retroperitoneal fibrosis. As Riedels’ thyroiditis can develop as a manifestation of multi organ fibrosis these drugs are still relevant even though the direct link is not established. Some of the drugs which can cause retroperitoneal fibrosis are:
    • Methysergide
    • Serotonin
    • Lysergic acid
    • Ergotamine
    • Dihydroergotamine
    • Hydralazine
    • Methyldopa
    • Acetazolamide
    • Phenacetin
    • Beta-blockers

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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]

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

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

Conditions	Causes	Age at onset	Pathological findings	Diagnostic findings
Riedel’s thyroiditis	Unknown	30-60	Dense fibrosis	Normal TSH (euthyroidism) TPO antibodies usually present I-123 uptake decreased or normal
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
Suppurative thyroiditis	Infection	Children, 20-40	Abscess formation	Normal TSH (euthyroidism) TPO antibodies absent I-123 uptake normal

• Riedel’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	Riedel’s thyroiditis	–	–	Normal/↑	Normal/↓	Normal/↓	Normal/↓	Normal	Normal	Usually present	Riedel’s thyroiditis usually presents with hard and fixed thyroid mass.
	Autoimmune (Hashimoto’s thyroiditis)	–	–	↑*	↓	Normal/↓	Normal/↓	Normal/↑	Normal	Present (high titer)	May be accompanied by other autoimmune diseases
	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.

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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]

Riedel’s thyroiditis is a rare disease with an approximate incidence of 1.06 cases per 100,000 individuals worldwide. Riedel’s thyroiditis commonly affects individuals between 30-50 years of age. Females are more commonly affected by Riedel’s thyroiditis.

• The incidence of Riedel’s thyroiditis is estimated to be approximately 1.06 cases per 100,000 individuals worldwide.^[1]

• Riedel’s thyroiditis is rare. In 1985, 37 patients reported were identified with Riedel’s thyroiditis over a 64 years period during which more than 56,000 thyroidectomies were performed in a study.^[1]

• There are no reports of reduced life expectancy in subjects with Riedel’s thyroiditis (RT). One lethal case of RT has been described up until now.^[2]

• Riedel’s thyroiditis commonly affects individuals between 30-50 years of age.^[3][4]

• There is no racial predilection to Riedel’s thyroiditis.

• Females are more commonly affected by Riedel’s thyroiditis than men. Women have been noted to be affected 3-fold more frequently than men.^[3][4]

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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 Riedel’s thyroiditis include genetic factors, medications such as lysergic acid, ergotamine, serotonin, and other autoimmune diseases such as Graves’ disease and Hashimoto’s thyroiditis.

Common risk factors in the development of Riedel’s thyroiditis include:^{[1][2][3][4][5][6][7]}

• Genetic factors
• Medications
  • Lysergic acid
  • Ergotamine
  • Serotonin
  • Dihydroergotamine
  • Hydralazine
  • Methyldopa
  • Methysergide
  • Acetazolamide
  • Phenacetin
  • β-blockers
• Other autoimmune diseases
  • Graves’ disease
  • Hashimoto’s thyroiditis
  • Multifocal idiopathic fibrosclerosis
  • Addison’s disease
  • Pernicious anemia
• Smoking

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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 Riedel’s thyroiditis.

There is insufficient evidence to recommend routine screening for Riedel’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]

If left untreated, patients with Riedel’s thyroiditis may progress to develop complications such as painless neck pressure out of proportion to the size of the goiter, hoarseness, stridor, dysphagia, hypothyroidism, hypoparathyroidism, Horner’s syndrome, and occlusive phlebitis. Prognosis is generally good and the disease-specific death rate ranges in frequency from 6-10% in the patients with Riedel’s thyroiditis.

The symptoms of Riedel’s thyroiditis usually develop in the third to fifth decade of life and progresses slowly.^{[1][2][3][4][5][6]}

• Diagnosis of is often delayed for a variable period of time after the onset of clinical symptoms.
• After the initial presentation, it has been observed that the process may stabilize or even regress.
• If left untreated, patients with Riedel’s thyroiditis may progress to develop dysphagia, stridor, painless neck pressure out of proportion to the size of the goiter, and hypothyroidism.

• Common complications of Riedel’s thyroiditis include:^{[4][7][8][9][10][11][12]}
  • Hoarseness
  • Stridor
  • Dysphagia
  • Hypothyroidism
  • Hypoparathyroidism
  • Horner’s syndrome
  • Occlusive phlebitis
  • Cerebral venous sinus thrombosis

• Prognosis is generally good and the disease-specific death rate ranges in frequency from 6-10% in patients with Riedel’s thyroiditis.^[13][14][8]

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