Riedel's thyroiditis overview: Difference between revisions
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==Overview== | ==Overview== | ||
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 connective tissue|fibrous]] variant of [[Hashimoto's thyroiditis|Hashimoto's thyroiditis]]<nowiki/> 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 [[Parenchyma|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 [[Genetics|genetic factors]], medications such as [[lysergic acid]], [[ergotamine]], [[serotonin]], and other [[autoimmune disease|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 out of proportion to the size of the [[goiter]], [[hoarseness]], [[stridor]], [[dysphagia]], [[hypothyroidism]], [[hypoparathyroidism]], [[Horner's syndrome]], and [[Phlebitis|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 [[Granuloma|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 masses|neck mass]], painless [[goiter]], [[dysphagia]], [[dyspnea]], and [[hoarseness]]. Less common symptoms of Riedel's thyroiditis include [[Muscle cramps|muscular cramps]], [[Paresthesia|paresthesias]], [[fatigue]], and [[dry skin]]. Physical examination of patients with Riedel's thyroiditis is usually remarkable for hard [[Thyroid mass causes|thyroid mass]] and clinical signs of [[hypothyroidism]] such as [[fatigue]], [[bradycardia]], [[bradypnea]]. Patients may have the clinical signs of [[hypocalcemia]] such as positive [[Chvostek's sign|Chvostek sign]] and positive [[Trousseau sign]]. Laboratory findings consistent with the diagnosis of Riedel's thyroiditis include elevated [[Erythrocyte sedimentation rate|ESR]], mild elevation of [[thyroid peroxidase]] antibodies and occasionally elevated [[TSH]] levels. 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, [[Tracheal compression|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|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+ T cells|CD8+]], [[CD4+ lymphocytes|CD4+]] and [[Plasma cell|plasma cells]]. Pharmacologic medical therapies for Riedel's thyroiditis include [[corticosteroids]], [[tamoxifen]], and [[Mycophenolate sodium|mycophenolate mofetil]]. Surgery is usually reserved for patients with [[esophageal]] or [[Tracheal compression|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 connective tissue|fibrous]] variant of [[Hashimoto's thyroiditis|Hashimoto's thyroiditis]]<nowiki/> 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 [[Parenchyma|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 [[Genetics|genetic factors]], medications such as [[lysergic acid]], [[ergotamine]], [[serotonin]], and other [[autoimmune disease|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 out of proportion to the size of the [[goiter]], [[hoarseness]], [[stridor]], [[dysphagia]], [[hypothyroidism]], [[hypoparathyroidism]], [[Horner's syndrome]], and [[Phlebitis|occlusive phlebitis]]. Prognosis is generally good and the disease-specific [[Mortality rate|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 [[Granuloma|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 masses|neck mass]], painless [[goiter]], [[dysphagia]], [[dyspnea]], and [[hoarseness]]. Less common symptoms of Riedel's thyroiditis include [[Muscle cramps|muscular cramps]], [[Paresthesia|paresthesias]], [[fatigue]], and [[dry skin]]. Physical examination of patients with Riedel's thyroiditis is usually remarkable for hard [[Thyroid mass causes|thyroid mass]] and clinical signs of [[hypothyroidism]] such as [[fatigue]], [[bradycardia]], [[bradypnea]]. Patients may have the clinical signs of [[hypocalcemia]] such as positive [[Chvostek's sign|Chvostek sign]] and positive [[Trousseau sign]]. Laboratory findings consistent with the diagnosis of Riedel's thyroiditis include elevated [[Erythrocyte sedimentation rate|ESR]], mild elevation of [[thyroid peroxidase]] [[antibodies]] and occasionally elevated [[TSH]] levels. 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, [[Tracheal compression|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|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 [[Hyaline|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+ T cells|CD8+]], [[CD4+ lymphocytes|CD4+]] and [[Plasma cell|plasma cells]]. Pharmacologic medical therapies for Riedel's thyroiditis include [[corticosteroids]], [[tamoxifen]], and [[Mycophenolate sodium|mycophenolate mofetil]]. Surgery is usually reserved for patients with [[esophageal]] or [[Tracheal compression|tracheal compressive]] symptoms. | ||
==Historical Perspective== | ==Historical Perspective== | ||
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There is insufficient evidence to recommend routine [[Screening (medicine)|screening]] for Riedel's thyroiditis. | There is insufficient evidence to recommend routine [[Screening (medicine)|screening]] for Riedel's thyroiditis. | ||
==Natural History, Complications, and Prognosis== | ==Natural History, Complications, and Prognosis== | ||
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 [[Phlebitis|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. | 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 [[Phlebitis|occlusive phlebitis]]. [[Prognosis]] is generally good and the disease-specific [[Mortality rate|death rate]] ranges in frequency from 6-10% in the patients with Riedel's thyroiditis. | ||
==Diagnosis== | ==Diagnosis== | ||
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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. | 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=== | ===Ultrasound=== | ||
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|Doppler ultrasoun | 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|Doppler ultrasoun<nowiki/>d]]. | ||
===Other Imaging Findings=== | ===Other Imaging Findings=== | ||
Revision as of 14:02, 16 October 2017
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Riedel's thyroiditis Microchapters |
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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]
Overview
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 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. 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.
Historical Perspective
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.
Classification
There is no established system for the classification of Riedel's thyroiditis.
Pathophysiology
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.
Causes
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.
Differentiating Riedel's thyroiditis from Other Diseases
Riedel's thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain's thyroiditis, Hashimoto's thyroiditis, and suppurative thyroiditis.
Epidemiology and Demographics
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.
Risk Factors
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.
Screening
There is insufficient evidence to recommend routine screening for Riedel's thyroiditis.
Natural History, Complications, and Prognosis
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.
Diagnosis
Diagnostic Criteria
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.
History and Symptoms
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
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
Laboratory findings consistent with the diagnosis of Riedel's thyroiditis include elevated ESR, mild elevation of thyroid peroxidase antibodies and occasionally elevated TSH levels.
Electrocardiogram
There are no ECG findings associated with Riedel's thyroiditis.
X-ray
X-ray findings in Riedel's thyroiditis are helpful to identify esophageal or tracheal compression.
CT scan
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
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
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.
Other Imaging Findings
24-hour iodine-123 uptake is absent or decreased in Riedel's thyroiditis.
Other Diagnostic Studies
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.
Treatment
Medical Therapy
Pharmacologic medical therapies for Riedel's thyroiditis include corticosteroids, tamoxifen, and mycophenolate mofetil.
Surgery
Surgery is usually reserved for patients with esophageal or tracheal compressive symptoms.
Primary Prevention
There are no established measures for the primary prevention of Riedel's thyroiditis.
Secondary Prevention
There are no established measures for the secondary prevention of Riedel's thyroiditis.