Riedel fibrosing thyroiditis, also known as ligneous struma, Riedel struma, or chronic invasive fibrous thyroiditis, is an uncommon disorder characterized by persistent inflammation and fibrosis of the thyroid gland. This condition is marked by the gradual replacement of normal thyroid tissue with dense fibrous tissue, which destroys follicular cells within the thyroid.
Typically, Riedel fibrosing thyroiditis presents with symptoms of hypothyroidism, including weight gain, fatigue, and cold intolerance. One distinctive feature is the development of a hardened, non-tender thyroid gland, which may feel as rigid as wood or stone. Over time, the fibrotic changes extend beyond the thyroid parenchyma, affecting neighboring structures such as the airways.
Progressive fibrosis can lead to the compression and obstruction of adjacent anatomical structures. This compression can result in various symptoms, such as difficulty breathing, swallowing difficulties, and hoarseness. These obstructive manifestations arise due to the mechanical pressure exerted by the fibrotic tissue on the airways, esophagus, and vocal cords.
Epidemiology
Among the various types of thyroiditis, Riedel thyroiditis is exceptionally uncommon compared to conditions like subacute granulomatous thyroiditis or Hashimoto thyroiditis.
Its incidence is estimated to be approximately 1.06 cases per 100,000 individuals. This disorder primarily affects adult females, with a higher likelihood of occurrence between the ages of 30 and 50.
Anatomy
Pathophysiology
Riedel thyroiditis is characterized by a distinctive feature wherein the normal thyroid tissue is progressively replaced by dense fibrotic tissue. This fibrosis extends beyond the thyroid gland’s boundaries and affects neighboring structures within the neck. The trachea, parathyroid glands, neck musculature, laryngeal nerves, and blood vessels in the vicinity may all be affected by this process. One of the significant consequences of this fibrotic transformation is the loss of mobility and fixation of the thyroid gland.
Upon examination, the thyroid gland feels abnormally firm, resembling a stone or wood texture. Palpation of the thyroid reveals a rigid, unyielding consistency, distinct from the normal soft and pliable texture. Furthermore, the fibrotic changes associated with Riedel thyroiditis extend beyond the confines of the thyroid gland itself. The surrounding structures that play crucial roles in the neck’s function and anatomy also experience fibrosis. The trachea, the airway responsible for conducting air to and from the lungs, may become encased in dense fibrotic tissue. This encasement can potentially result in narrowing or compression of the tracheal lumen, leading to respiratory difficulties.
In addition to the trachea, the parathyroid glands, which regulate calcium levels in the body, can be affected by fibrosis in Riedel thyroiditis. The fibrotic process may encroach upon these small endocrine glands, impairing their ability to secrete parathyroid hormone and maintain proper calcium balance. The fibrosis can also involve the neck musculature, causing stiffness and limited range of motion in the affected area. This can contribute to discomfort and restricted movement of the neck.
Furthermore, the laryngeal nerves, responsible for controlling vocal cord movement and sensation in the larynx, can be affected by fibrosis. Compression or infiltration of these nerves by fibrotic tissue may lead to hoarseness of voice and potential laryngeal dysfunction. Lastly, the fibrotic changes can also impact blood vessels supplying the thyroid and surrounding structures. The vascular structures may become encased or compressed by fibrous tissue, potentially leading to compromised blood flow and vascular-related complications.
Etiology
The exact cause of Riedel thyroiditis remains uncertain, and varied theories have been proposed to explain its origins. One hypothesis suggests that it could be a manifestation of or distinct variation of autoimmune thyroiditis of a systemic fibrosing disorder. Another possibility is that it may be related to IgG4 associated disease.
Anti-thyroid antibodies, infiltration of eosinophils in the affected tissue, and positive response to glucocorticoid treatment strongly indicate an autoimmune component in Riedel thyroiditis. However, the absence of other specific antibodies typically associated with autoimmune disorders, the lack of a consistent association with other autoimmune conditions, normal lymphocyte counts, and usual complement levels challenge the autoimmune theory.
Riedel thyroiditis has been observed with primary sclerosing cholangitis, orbital fibrosis, and fibrotic changes in the mediastinum retroperitoneum. This association has led to speculation that Riedel thyroiditis may be part of a multifocal idiopathic fibrosclerosing disorder. However, the inconsistent occurrence of Riedel thyroiditis with further fibrosing disorders weakens this hypothesis.
Further research is needed to elucidate the precise etiology of Riedel thyroiditis and determine its relationship to autoimmune processes, fibrosing disorders, or IgG4-related diseases. The complexity of its pathogenesis suggests that multiple factors, including immune dysregulation, genetic predisposition, and environmental triggers, may contribute to the developing this rare condition.
Genetics
Prognostic Factors
Riedel thyroiditis typically carries a favorable prognosis, although the course of the disease can vary. In mild cases, the condition may remain stable over a prolonged period, spanning several years. However, it is important to note that Riedel thyroiditis can also exhibit an aggressive and rapidly progressive nature following any triggering event.
Clinical History
Clinical History
Riedel thyroiditis typically manifests with noticeable changes in the thyroid gland, characterized by its hardness and enlargement. This condition often leads to the occurrence of obstructive symptoms as a result of the thyroid gland’s impact on nearby neck structures. Various complications may arise due to the involvement of different anatomical components in the neck. One common manifestation is dyspnea, which occurs when the enlarged thyroid gland affects the trachea or windpipe. The trachea’s compression or narrowing can cause breathing difficulty, resulting in breathlessness or shortness of breath.
Esophageal involvement in Riedel thyroiditis can lead to dysphagia. As the thyroid gland encroaches upon the esophagus, it can create a blockage or impede the smooth passage of food and liquids, causing discomfort and difficulty in swallowing. The recurrent laryngeal nerve, responsible for controlling the vocal cords, may also be affected in Riedel thyroiditis. When this nerve becomes involved, it can develop a stridor. Stridor can result from the partial obstruction or paralysis of the vocal cords caused by the enlarged thyroid gland. Additionally, the vasculature surrounding the thyroid gland may be affected, potentially resulting in venous sinus thrombosis.
The involvement of the blood vessels in Riedel thyroiditis can lead to the formation of blood clots, which can obstruct normal blood flow and cause further complications. Furthermore, Riedel thyroiditis can extend beyond the confines of the thyroid gland and affect the retrobulbar tissues surrounding the eyes. This involvement can lead to exophthalmos, a condition characterized by protrusion or bulging of the eyeballs. The enlargement and inflammation of the retrobulbar tissues caused by Riedel thyroiditis contribute to the developing this eye-related symptom.
Physical Examination
Physical Examination
During a physical examination of a patient with Riedel thyroiditis, several characteristic findings may be observed. The primary feature of Riedel thyroiditis is the enlargement of the thyroid gland, which may appear significantly larger than normal and can be easily palpated during the examination. The gland may feel firm or hard to the touch due to the fibrosis characteristic of this condition.
In addition, the thyroid gland may exhibit fixity or immobility, as fibrotic tissue replaces the normal thyroid tissue, making it difficult to move or manipulate during palpation. The borders of the thyroid gland may also be irregular or poorly defined due to the fibrotic changes. Some patients may experience pain or tenderness in the affected area, which can be elicited by palpation or pressure on the thyroid gland. The enlarged thyroid gland can exert pressure on adjacent structures in the neck, leading to discomfort or a sensation of a mass.
This can cause symptoms such as difficulty in breathing due to tracheal compression, swallowing difficulties due to esophageal compression, or hoarseness or stridor due to recurrent laryngeal nerve involvement. Furthermore, if the retrobulbar tissues are involved, the physical examination may reveal eye-related manifestations such as exophthalmos or changes in eye movement.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Anaplastic thyroid carcinoma
Thyroid sarcoma
Thyroid lymphoma
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Due to the rarity of Riedel thyroiditis, there is a lack of standardized treatment protocols, and limited outcome studies have been conducted. However, glucocorticoids are commonly used as the primary medical treatment. The anti-inflammatory properties of glucocorticoids are most effective when administered early in the course of the disease.
While there are no established dosage guidelines, reports have indicated that prednisone can be effective. The response to glucocorticoid treatment varies among individuals, with some experiencing significant improvement, including relief of upper airway symptoms and the reversal of dysphonia. However, it is important to note that not all patients respond favorably to glucocorticoids, and some may show no response at all.
The lack of response could potentially be attributed to the increased fibrosis observed in the later stages of the disease, where inflammation is less prominent compared to the early stages. Tamoxifen, a selective estrogen receptor modulator, has effectively treated Riedel thyroiditis and other systemic fibrosing disorders. Tamoxifen is administered alone or in combination with prednisone. This approach has been successful in reducing the size of the fibrotic mass.
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References
https://www.ncbi.nlm.nih.gov/books/NBK537303/
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Riedel fibrosing thyroiditis, also known as ligneous struma, Riedel struma, or chronic invasive fibrous thyroiditis, is an uncommon disorder characterized by persistent inflammation and fibrosis of the thyroid gland. This condition is marked by the gradual replacement of normal thyroid tissue with dense fibrous tissue, which destroys follicular cells within the thyroid.
Typically, Riedel fibrosing thyroiditis presents with symptoms of hypothyroidism, including weight gain, fatigue, and cold intolerance. One distinctive feature is the development of a hardened, non-tender thyroid gland, which may feel as rigid as wood or stone. Over time, the fibrotic changes extend beyond the thyroid parenchyma, affecting neighboring structures such as the airways.
Progressive fibrosis can lead to the compression and obstruction of adjacent anatomical structures. This compression can result in various symptoms, such as difficulty breathing, swallowing difficulties, and hoarseness. These obstructive manifestations arise due to the mechanical pressure exerted by the fibrotic tissue on the airways, esophagus, and vocal cords.
Among the various types of thyroiditis, Riedel thyroiditis is exceptionally uncommon compared to conditions like subacute granulomatous thyroiditis or Hashimoto thyroiditis.
Its incidence is estimated to be approximately 1.06 cases per 100,000 individuals. This disorder primarily affects adult females, with a higher likelihood of occurrence between the ages of 30 and 50.
Riedel thyroiditis is characterized by a distinctive feature wherein the normal thyroid tissue is progressively replaced by dense fibrotic tissue. This fibrosis extends beyond the thyroid gland’s boundaries and affects neighboring structures within the neck. The trachea, parathyroid glands, neck musculature, laryngeal nerves, and blood vessels in the vicinity may all be affected by this process. One of the significant consequences of this fibrotic transformation is the loss of mobility and fixation of the thyroid gland.
Upon examination, the thyroid gland feels abnormally firm, resembling a stone or wood texture. Palpation of the thyroid reveals a rigid, unyielding consistency, distinct from the normal soft and pliable texture. Furthermore, the fibrotic changes associated with Riedel thyroiditis extend beyond the confines of the thyroid gland itself. The surrounding structures that play crucial roles in the neck’s function and anatomy also experience fibrosis. The trachea, the airway responsible for conducting air to and from the lungs, may become encased in dense fibrotic tissue. This encasement can potentially result in narrowing or compression of the tracheal lumen, leading to respiratory difficulties.
In addition to the trachea, the parathyroid glands, which regulate calcium levels in the body, can be affected by fibrosis in Riedel thyroiditis. The fibrotic process may encroach upon these small endocrine glands, impairing their ability to secrete parathyroid hormone and maintain proper calcium balance. The fibrosis can also involve the neck musculature, causing stiffness and limited range of motion in the affected area. This can contribute to discomfort and restricted movement of the neck.
Furthermore, the laryngeal nerves, responsible for controlling vocal cord movement and sensation in the larynx, can be affected by fibrosis. Compression or infiltration of these nerves by fibrotic tissue may lead to hoarseness of voice and potential laryngeal dysfunction. Lastly, the fibrotic changes can also impact blood vessels supplying the thyroid and surrounding structures. The vascular structures may become encased or compressed by fibrous tissue, potentially leading to compromised blood flow and vascular-related complications.
The exact cause of Riedel thyroiditis remains uncertain, and varied theories have been proposed to explain its origins. One hypothesis suggests that it could be a manifestation of or distinct variation of autoimmune thyroiditis of a systemic fibrosing disorder. Another possibility is that it may be related to IgG4 associated disease.
Anti-thyroid antibodies, infiltration of eosinophils in the affected tissue, and positive response to glucocorticoid treatment strongly indicate an autoimmune component in Riedel thyroiditis. However, the absence of other specific antibodies typically associated with autoimmune disorders, the lack of a consistent association with other autoimmune conditions, normal lymphocyte counts, and usual complement levels challenge the autoimmune theory.
Riedel thyroiditis has been observed with primary sclerosing cholangitis, orbital fibrosis, and fibrotic changes in the mediastinum retroperitoneum. This association has led to speculation that Riedel thyroiditis may be part of a multifocal idiopathic fibrosclerosing disorder. However, the inconsistent occurrence of Riedel thyroiditis with further fibrosing disorders weakens this hypothesis.
Further research is needed to elucidate the precise etiology of Riedel thyroiditis and determine its relationship to autoimmune processes, fibrosing disorders, or IgG4-related diseases. The complexity of its pathogenesis suggests that multiple factors, including immune dysregulation, genetic predisposition, and environmental triggers, may contribute to the developing this rare condition.
Riedel thyroiditis typically carries a favorable prognosis, although the course of the disease can vary. In mild cases, the condition may remain stable over a prolonged period, spanning several years. However, it is important to note that Riedel thyroiditis can also exhibit an aggressive and rapidly progressive nature following any triggering event.
Clinical History
Riedel thyroiditis typically manifests with noticeable changes in the thyroid gland, characterized by its hardness and enlargement. This condition often leads to the occurrence of obstructive symptoms as a result of the thyroid gland’s impact on nearby neck structures. Various complications may arise due to the involvement of different anatomical components in the neck. One common manifestation is dyspnea, which occurs when the enlarged thyroid gland affects the trachea or windpipe. The trachea’s compression or narrowing can cause breathing difficulty, resulting in breathlessness or shortness of breath.
Esophageal involvement in Riedel thyroiditis can lead to dysphagia. As the thyroid gland encroaches upon the esophagus, it can create a blockage or impede the smooth passage of food and liquids, causing discomfort and difficulty in swallowing. The recurrent laryngeal nerve, responsible for controlling the vocal cords, may also be affected in Riedel thyroiditis. When this nerve becomes involved, it can develop a stridor. Stridor can result from the partial obstruction or paralysis of the vocal cords caused by the enlarged thyroid gland. Additionally, the vasculature surrounding the thyroid gland may be affected, potentially resulting in venous sinus thrombosis.
The involvement of the blood vessels in Riedel thyroiditis can lead to the formation of blood clots, which can obstruct normal blood flow and cause further complications. Furthermore, Riedel thyroiditis can extend beyond the confines of the thyroid gland and affect the retrobulbar tissues surrounding the eyes. This involvement can lead to exophthalmos, a condition characterized by protrusion or bulging of the eyeballs. The enlargement and inflammation of the retrobulbar tissues caused by Riedel thyroiditis contribute to the developing this eye-related symptom.
Physical Examination
During a physical examination of a patient with Riedel thyroiditis, several characteristic findings may be observed. The primary feature of Riedel thyroiditis is the enlargement of the thyroid gland, which may appear significantly larger than normal and can be easily palpated during the examination. The gland may feel firm or hard to the touch due to the fibrosis characteristic of this condition.
In addition, the thyroid gland may exhibit fixity or immobility, as fibrotic tissue replaces the normal thyroid tissue, making it difficult to move or manipulate during palpation. The borders of the thyroid gland may also be irregular or poorly defined due to the fibrotic changes. Some patients may experience pain or tenderness in the affected area, which can be elicited by palpation or pressure on the thyroid gland. The enlarged thyroid gland can exert pressure on adjacent structures in the neck, leading to discomfort or a sensation of a mass.
This can cause symptoms such as difficulty in breathing due to tracheal compression, swallowing difficulties due to esophageal compression, or hoarseness or stridor due to recurrent laryngeal nerve involvement. Furthermore, if the retrobulbar tissues are involved, the physical examination may reveal eye-related manifestations such as exophthalmos or changes in eye movement.
Differential Diagnoses
Anaplastic thyroid carcinoma
Thyroid sarcoma
Thyroid lymphoma
Due to the rarity of Riedel thyroiditis, there is a lack of standardized treatment protocols, and limited outcome studies have been conducted. However, glucocorticoids are commonly used as the primary medical treatment. The anti-inflammatory properties of glucocorticoids are most effective when administered early in the course of the disease.
While there are no established dosage guidelines, reports have indicated that prednisone can be effective. The response to glucocorticoid treatment varies among individuals, with some experiencing significant improvement, including relief of upper airway symptoms and the reversal of dysphonia. However, it is important to note that not all patients respond favorably to glucocorticoids, and some may show no response at all.
The lack of response could potentially be attributed to the increased fibrosis observed in the later stages of the disease, where inflammation is less prominent compared to the early stages. Tamoxifen, a selective estrogen receptor modulator, has effectively treated Riedel thyroiditis and other systemic fibrosing disorders. Tamoxifen is administered alone or in combination with prednisone. This approach has been successful in reducing the size of the fibrotic mass.
https://www.ncbi.nlm.nih.gov/books/NBK537303/
medtigo
Riedel Thyroiditis
Updated :
August 24, 2023
Riedel fibrosing thyroiditis, also known as ligneous struma, Riedel struma, or chronic invasive fibrous thyroiditis, is an uncommon disorder characterized by persistent inflammation and fibrosis of the thyroid gland. This condition is marked by the gradual replacement of normal thyroid tissue with dense fibrous tissue, which destroys follicular cells within the thyroid.
Typically, Riedel fibrosing thyroiditis presents with symptoms of hypothyroidism, including weight gain, fatigue, and cold intolerance. One distinctive feature is the development of a hardened, non-tender thyroid gland, which may feel as rigid as wood or stone. Over time, the fibrotic changes extend beyond the thyroid parenchyma, affecting neighboring structures such as the airways.
Progressive fibrosis can lead to the compression and obstruction of adjacent anatomical structures. This compression can result in various symptoms, such as difficulty breathing, swallowing difficulties, and hoarseness. These obstructive manifestations arise due to the mechanical pressure exerted by the fibrotic tissue on the airways, esophagus, and vocal cords.
Among the various types of thyroiditis, Riedel thyroiditis is exceptionally uncommon compared to conditions like subacute granulomatous thyroiditis or Hashimoto thyroiditis.
Its incidence is estimated to be approximately 1.06 cases per 100,000 individuals. This disorder primarily affects adult females, with a higher likelihood of occurrence between the ages of 30 and 50.
Riedel thyroiditis is characterized by a distinctive feature wherein the normal thyroid tissue is progressively replaced by dense fibrotic tissue. This fibrosis extends beyond the thyroid gland’s boundaries and affects neighboring structures within the neck. The trachea, parathyroid glands, neck musculature, laryngeal nerves, and blood vessels in the vicinity may all be affected by this process. One of the significant consequences of this fibrotic transformation is the loss of mobility and fixation of the thyroid gland.
Upon examination, the thyroid gland feels abnormally firm, resembling a stone or wood texture. Palpation of the thyroid reveals a rigid, unyielding consistency, distinct from the normal soft and pliable texture. Furthermore, the fibrotic changes associated with Riedel thyroiditis extend beyond the confines of the thyroid gland itself. The surrounding structures that play crucial roles in the neck’s function and anatomy also experience fibrosis. The trachea, the airway responsible for conducting air to and from the lungs, may become encased in dense fibrotic tissue. This encasement can potentially result in narrowing or compression of the tracheal lumen, leading to respiratory difficulties.
In addition to the trachea, the parathyroid glands, which regulate calcium levels in the body, can be affected by fibrosis in Riedel thyroiditis. The fibrotic process may encroach upon these small endocrine glands, impairing their ability to secrete parathyroid hormone and maintain proper calcium balance. The fibrosis can also involve the neck musculature, causing stiffness and limited range of motion in the affected area. This can contribute to discomfort and restricted movement of the neck.
Furthermore, the laryngeal nerves, responsible for controlling vocal cord movement and sensation in the larynx, can be affected by fibrosis. Compression or infiltration of these nerves by fibrotic tissue may lead to hoarseness of voice and potential laryngeal dysfunction. Lastly, the fibrotic changes can also impact blood vessels supplying the thyroid and surrounding structures. The vascular structures may become encased or compressed by fibrous tissue, potentially leading to compromised blood flow and vascular-related complications.
The exact cause of Riedel thyroiditis remains uncertain, and varied theories have been proposed to explain its origins. One hypothesis suggests that it could be a manifestation of or distinct variation of autoimmune thyroiditis of a systemic fibrosing disorder. Another possibility is that it may be related to IgG4 associated disease.
Anti-thyroid antibodies, infiltration of eosinophils in the affected tissue, and positive response to glucocorticoid treatment strongly indicate an autoimmune component in Riedel thyroiditis. However, the absence of other specific antibodies typically associated with autoimmune disorders, the lack of a consistent association with other autoimmune conditions, normal lymphocyte counts, and usual complement levels challenge the autoimmune theory.
Riedel thyroiditis has been observed with primary sclerosing cholangitis, orbital fibrosis, and fibrotic changes in the mediastinum retroperitoneum. This association has led to speculation that Riedel thyroiditis may be part of a multifocal idiopathic fibrosclerosing disorder. However, the inconsistent occurrence of Riedel thyroiditis with further fibrosing disorders weakens this hypothesis.
Further research is needed to elucidate the precise etiology of Riedel thyroiditis and determine its relationship to autoimmune processes, fibrosing disorders, or IgG4-related diseases. The complexity of its pathogenesis suggests that multiple factors, including immune dysregulation, genetic predisposition, and environmental triggers, may contribute to the developing this rare condition.
Riedel thyroiditis typically carries a favorable prognosis, although the course of the disease can vary. In mild cases, the condition may remain stable over a prolonged period, spanning several years. However, it is important to note that Riedel thyroiditis can also exhibit an aggressive and rapidly progressive nature following any triggering event.
Clinical History
Riedel thyroiditis typically manifests with noticeable changes in the thyroid gland, characterized by its hardness and enlargement. This condition often leads to the occurrence of obstructive symptoms as a result of the thyroid gland’s impact on nearby neck structures. Various complications may arise due to the involvement of different anatomical components in the neck. One common manifestation is dyspnea, which occurs when the enlarged thyroid gland affects the trachea or windpipe. The trachea’s compression or narrowing can cause breathing difficulty, resulting in breathlessness or shortness of breath.
Esophageal involvement in Riedel thyroiditis can lead to dysphagia. As the thyroid gland encroaches upon the esophagus, it can create a blockage or impede the smooth passage of food and liquids, causing discomfort and difficulty in swallowing. The recurrent laryngeal nerve, responsible for controlling the vocal cords, may also be affected in Riedel thyroiditis. When this nerve becomes involved, it can develop a stridor. Stridor can result from the partial obstruction or paralysis of the vocal cords caused by the enlarged thyroid gland. Additionally, the vasculature surrounding the thyroid gland may be affected, potentially resulting in venous sinus thrombosis.
The involvement of the blood vessels in Riedel thyroiditis can lead to the formation of blood clots, which can obstruct normal blood flow and cause further complications. Furthermore, Riedel thyroiditis can extend beyond the confines of the thyroid gland and affect the retrobulbar tissues surrounding the eyes. This involvement can lead to exophthalmos, a condition characterized by protrusion or bulging of the eyeballs. The enlargement and inflammation of the retrobulbar tissues caused by Riedel thyroiditis contribute to the developing this eye-related symptom.
Physical Examination
During a physical examination of a patient with Riedel thyroiditis, several characteristic findings may be observed. The primary feature of Riedel thyroiditis is the enlargement of the thyroid gland, which may appear significantly larger than normal and can be easily palpated during the examination. The gland may feel firm or hard to the touch due to the fibrosis characteristic of this condition.
In addition, the thyroid gland may exhibit fixity or immobility, as fibrotic tissue replaces the normal thyroid tissue, making it difficult to move or manipulate during palpation. The borders of the thyroid gland may also be irregular or poorly defined due to the fibrotic changes. Some patients may experience pain or tenderness in the affected area, which can be elicited by palpation or pressure on the thyroid gland. The enlarged thyroid gland can exert pressure on adjacent structures in the neck, leading to discomfort or a sensation of a mass.
This can cause symptoms such as difficulty in breathing due to tracheal compression, swallowing difficulties due to esophageal compression, or hoarseness or stridor due to recurrent laryngeal nerve involvement. Furthermore, if the retrobulbar tissues are involved, the physical examination may reveal eye-related manifestations such as exophthalmos or changes in eye movement.
Differential Diagnoses
Anaplastic thyroid carcinoma
Thyroid sarcoma
Thyroid lymphoma
Due to the rarity of Riedel thyroiditis, there is a lack of standardized treatment protocols, and limited outcome studies have been conducted. However, glucocorticoids are commonly used as the primary medical treatment. The anti-inflammatory properties of glucocorticoids are most effective when administered early in the course of the disease.
While there are no established dosage guidelines, reports have indicated that prednisone can be effective. The response to glucocorticoid treatment varies among individuals, with some experiencing significant improvement, including relief of upper airway symptoms and the reversal of dysphonia. However, it is important to note that not all patients respond favorably to glucocorticoids, and some may show no response at all.
The lack of response could potentially be attributed to the increased fibrosis observed in the later stages of the disease, where inflammation is less prominent compared to the early stages. Tamoxifen, a selective estrogen receptor modulator, has effectively treated Riedel thyroiditis and other systemic fibrosing disorders. Tamoxifen is administered alone or in combination with prednisone. This approach has been successful in reducing the size of the fibrotic mass.
https://www.ncbi.nlm.nih.gov/books/NBK537303/
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