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207 16 Thyroiditis Michel Adamina and Daniel Oertli Contents 16.1 16.2 16.2.1 16.2.1.1 16.2.1.2 16.2.2 16.2.3 16.2.4 16.2.5 16.2.6 16.3 16.3.1 16.3.2 16.4 16.4.1 16.4.2 16.4.3 16.5 Introduction . . . 207 Autoimmune Thyroiditis . . . 208 Hashimoto’s Thyroiditis . . . 208 Fibrotic Hashimoto’s Thyroiditis . . . 208 Atrophic Autoimmune Thyroiditis . . . 208 Focal Lymphocytic Thyroiditis . . . 209 Postpartum Thyroiditis . . . 209 Subacute de Quervain’s Thyroiditis . . . 209 Painless Thyroiditis . . . 209 Riedel’s Fibrosing Thyroiditis . . . 210 Acute Infectious Thyroiditis . . . 210 Etiologies of Infectious Thyroiditis . . . 211 Surgical Treatment . . . 211 Non-autoimmune Thyroiditis . . . 211 Drug-induced Thyroiditis . . . 212 Postoperative Necrotizing Thyroiditis . . . 213 Radiation Thyroiditis . . . 213 Indications for Surgery . . . 214 References . . . 214 autoantibodies). An association of autoimmune thyroiditis with defined HLA haplotypes implies a genetic predisposition [5]. Iodine therapy, viral infections, pregnancy and menopause, stress [6], and immunomodulating drugs (interferon-α, interleukin-2) have also been linked to autoimmune thyroiditis. Except for Graves’ disease, most autoimmune thyroiditides initially present with a limited hyperthyroid state, and thereafter return to euthyroidism or definitively fall to permanent (subclinical or overt) hypothyroidism. Thus, over 90% of cases of clinical hypothyroidism are caused by an autoimmune thyroiditis. Conversely, about 1–10% of cases of hyperthyroidism are related to a thyroiditis. Clinically, patients may present either with an acute illness with severe thyroid pain (e.g., subacute de Quervain’s thyroiditis, acute suppurative thyroiditis, radiation thyroiditis, traumatic thyroiditis) or without evident inflammation but with thyroid dysfunction or a goiter (e.g., silent thyroiditis, Hashimoto’s or Riedel’s thyroiditis). Table 16.1 Etiologies of thyroiditis 16.1 Introduction Thyroiditides make up approximately 20% of all thyroid diseases [1] and are caused by multiple factors (Table 16.1). Autoimmune diseases represent the most common etiologies. According to the clinical course, thyroiditides have been subdivided into acute, subacute, and chronic forms. Once a suppurative inflammation has been ruled out, most other types of thyroiditis have either a definitive autoimmune etiology or are possibly autoimmune in nature [2]. In life, one out of 100 individuals will develop an overt autoimmune thyroiditis. Thyroid autoantibodies may be found in up to 10% of the general population [3,4]. These autoantibodies are mainly directed against thyroid peroxidase or thyroglobulin. They are not the cause of the disease, but the consequence of a lost immune tolerance to the thyroid gland. Autoantibodies may promote thyroid hormone dysfunctions (stimulating thyroid autoantibodies, blocking thyroid Autoimmune thyroiditis Chronic lymphocytic thyroiditis (Hashimoto’s) Fibrotic variant of Hashimoto’s thyroiditis Atrophic thyroiditis (primary myxedema) Variants of autoimmune thyroiditis Postpartum thyroiditis Silent or painless thyroiditis Subacute de Quervain’s thyroiditis Fibrotic Riedel’s thyroiditis Non-immune thyroiditis Acute infectious thyroiditis Radiation thyroiditis Palpation/trauma-induced thyroiditis Sarcoidosis Vasculitis Postoperative necrotizing thyroiditis Drug-induced thyroiditis Carcinoma-associated thyroiditis 208 Michel Adamina and Daniel Oertli 16.2 Autoimmune Thyroiditis The largest community study published so far on autoimmune thyroiditis revealed elevated thyroid autoantibodies against thyroid peroxidase and thyroglobulin in more than 10% of a British community (Whickham study) [3]. On the one hand, in 7.5% of this community, elevated TSH together with a euthyroid state indicated a subclinical hypothyroidism, which became overt hypothyroidism in 1.9% of the study’s population. On the other hand, subclinical or overt hyperthyroidism was shown in 2% of people in the Whickham community. Women showed a 10 times higher prevalence of autoimmune thyroiditis, but this gender difference declined with age so that, for people over 75 years of age, 16% of the men and 20% of the women showed subclinical hypothyroidism. 16.2.1 Hashimoto’s Thyroiditis Synonyms: chronic lymphocytic thyroiditis, struma lymphomatosa Hashimoto’s thyroiditis is the most frequent autoimmune thyroiditis and is the archetypic example of organ-specific autoimmune disease. With a prevalence of about 3% it represents the most common cause of hypothyroidism in the general population [1]. In regions where iodine intake is adequate, Hashimoto’s thyroiditis also represents the most common cause of goiter. The peak incidence culminates in the fifth decade of life and the prevalence increases with age. Women are 10–20 times more affected than men. A genetic association with the haplotypes HLADR3, -DR4, and -DR5 is found. Many other autoimmune diseases are associated with Hashimoto’s thyroiditis: Graves’ disease, juvenile diabetes, Addison’s disease, pernicious anemia, rheumatoid arthritis, Sjögren’s syndrome, and systemic lupus erythematosus. Hashimoto’s thyroiditis mostly presents with an oligosymptomatic clinical course, a painless homogeneous goiter, and with signs of hypothyroidism. Low concentrations of thyroid hormones with high TSH and circulating thyroid autoantibodies (against peroxidase in 70–90% of cases and against thyroglobulin in 40–70% of cases) confirm the diagnosis [1]. Occasionally, a transient hyperthyroidism state may be noted, up to a marked hyperthyroidism or hashitoxicosis, associated with the presence of anti-TSH receptor antibodies. Like all autoimmune diseases, the clinical picture is one of relapsing episodes, with up to one quarter of the patients showing a spontaneous recovery. Hashimoto’s thyroiditis is probably related to an acquired defect of the thyroid’s specific T suppressor lymphocytes, resulting in the emergence of helper T lymphocytes directed against the gland, and the production of autoantibodies against various components of the thyroid. The binding of these autoantibodies to the thyrocytes accounts for complement and T lymphocyte-mediated lysis of the thyrocytes and non-regulated release of thyroxine and triiodothyronine, resulting in the transient hyperthyroidism occasionally noted. Later, the destruction of thyroid parenchyma may lead to permanent hypothyroidism. A causal treatment is unknown and substitutive thyroid hormone therapy is indicated when overt hypothyroidism (i.e., in about 20% of patients) is identified. Most patients require lifelong replacement therapy. On fine-needle biopsy, Hürthle cells or oncocytes are frequently seen. Hashimoto’s thyroiditis may at times be difficult to distinguish on a fine-needle aspiration biopsy from a follicular neoplasm, papillary carcinoma, or low-grade MALT lymphoma. Immunohistochemistry studies may help to clear the differential diagnosis. 16.2.1.1 Fibrotic Hashimoto’s Thyroiditis A fibrotic variant of Hashimoto’s thyroiditis accounts for up to 10% of the clinical presentations, predominantly in elderly patients with preexisting goiter. The disease is characterized by a rapid increase of goiter size, which may lead to the suspicion of malignancy and to subsequent surgery. Nevertheless, the extensive fibrotic changes and metaplasia noted on specimen or biopsies are always limited to the gland, in contrast to the invasive Riedel’s fibrosing thyroiditis. 16.2.1.2 Atrophic Autoimmune Thyroiditis Synonyms: primary myxedema, idiopathic myxedema, atrophic Hashimoto’s thyroiditis The atrophic autoimmune thyroiditis is the cause of primary myxedema and should not be confused with endstage fibrotic Hashimoto’s thyroiditis. Most of the cases proceed over years without overt signs or symptoms. The related hypothyroidism then becomes clinically obvious around the fourth to sixth decade of life. Women are 5 times more affected than men. On histologic specimen, the thyroid gland weighs less than 5 g, whereas in some milder asymptomatic cases, the thyroid gland weighs around 10 g (reference weights: male 20 g, female 17 g [7]). 16 Thyroiditis A postpartum thyroiditis occurs in 2–16% of women 4–6 months following delivery (by definition within one year after parturition or abortion) [8,9]. The disease represents an exacerbation of a preceding (undiagnosed) autoimmune thyroiditis and is classically linked to the haplotypes HLA-DR3, -DR4, and -DR5. It may be interpreted as rebound autoimmunity after the pregnancy-associated immunosuppression. Eighty-five percent of these patients develop autoantibodies against thyroid peroxidase and thyroglobulin, which may vanish over time. Clinically, women may show a transient hyperthyroidism state, which rapidly converts to hypothyroidism, and then to euthyroidism within 12 months. Treatment consists of thyroid hormone substitution when required. Thyreostatic medication, occasionally β-blockers, may be needed in the presence of exacerbated hyperthyroidism. Neither prophylaxis nor predicting marker have been identified so far and women affected once have a higher probability of relapse following further pregnancies. Women with a known autoimmune thyroiditis prior to pregnancy and an elevated titer of autoantibodies against thyroglobulin during pregnancy nearly always suffer from a postpartum exacerbation of their autoimmune thyroiditis. lassitude, and a feeling of illness. The thyroid is exquisitely tender and enlarged to palpation. The erythrocyte sedimentation rate is markedly elevated. Initially, the local inflammation process leads to a destruction of thyroid follicles with a transient hyperthyroidism, due to the breakdown of stored thyroglobulin. Later on, hypothyroidism emerges as the thyroid is not able to cope with the body’s demand for thyroid hormones. Finally, as the subacute thyroiditis heals, euthyroidism returns. Subacute de Quervain’s thyroiditis tends to recur, although at a low rate of 4% [11]. Permanent hypothyroidism requiring substitutive therapy is then noted in 15% of the patients [11]. The etiology of subacute de Quervain’s thyroiditis remains uncertain, but evidence implicates viral infection. A postviral cytokine-mediated inflammation of the thyroid is suspected because a seasonal frequency and an association with upper respiratory tract infection is noted. In half of the patients antibodies against mumps, measles, influenza, adenovirus, coxsackievirus, or echovirus are found. Furthermore, a genetic predisposition exists with the haplotype HLA-Bw35. The differential diagnosis encompasses acute suppurative thyroiditis. In contrast to acute suppurative thyroiditis, the gland sonographically reveals irregular hypoperfused areas instead of hyperperfused tissue. On fine-needle biopsy, the differential diagnosis further includes palpation thyroiditis, as well as other granulomatous diseases such as sarcoidosis, tuberculosis, and rheumatoid diseases. Treatment is supportive with non-steroidal antiinflammatory agents (NSAR) and β-blockers in severe cases with hyperthyroidism. Corticosteroids are useful (about 40 mg hydrocortisone equivalents daily) when the NSAR medication is not successful. Symptoms usually improve within 2–3 days after the initiation of corticosteroid treatment. However, it may take about 4 weeks for the disappearance of the thyroid mass. 16.2.4 16.2.5 16.2.2 Focal Lymphocytic Thyroiditis Synonyms: focal autoimmune thyroiditis, chronic unspecific thyroiditis Focal lymphocytic thyroiditis is a coincidental finding in 50% of women’s and 25% of men’s autopsies, without clinical relevance. This low-grade autoimmune thyroiditis is characterized by focal lymphocytic infiltrates of less than 5% of the thyroid gland. 16.2.3 Postpartum Thyroiditis Subacute de Quervain’s Thyroiditis Synonyms: granulomatous thyroiditis, pseudotuberculous thyroiditis, giant cell thyroiditis Subacute de Quervain’s thyroiditis is a self-limiting disease accounting for 0.5–3% of all thyroid pathologies and lasts a few weeks to 2 months [10]. Women are 3–6 times more affected than men. The peak incidence is between the second and fifth decade of life. Patients complain of moderate to severe pain in the neck of sudden onset that irradiates to the jaw, ear, face, and down to the thorax; they present with fever, Painless Thyroiditis Synonym: subacute lymphocytic thyroiditis Patients present with a diffuse but modest enlargement of the thyroid and function tests reveal a transient hyperthyroidism, followed by hypothyroidism. The painless thyroiditis is self-limited and rarely necessitates thyroid hormone substitution therapy. Women are again more often affected than men with a peak of incidence in middle life and in the postpartum period. Autoantibodies against thyroid peroxidase and thyroglobulin are found, as well as an 209 210 Michel Adamina and Daniel Oertli association with HLA-DR3 and -DR5 haplotypes. Histologic examination of a specimen reveals a lymphocytic infiltration with destruction of follicles; this is in contrast to Hashimoto’s thyroiditis. Neither giant cell granulomas (typical for a subacute thyroiditis) nor an association with a viral infection are present. 16.2.6 Riedel’s Fibrosing Thyroiditis Riedel’s thyroiditis is a rare chronic thyroiditis in which the thyroid gland is replaced by fibrous tissue. The underlying etiologic mechanisms are unclear. An autoimmune component is suspected, due to elevated titers of thyroid autoantibodies. The prevailing view is that Riedel’s thyroiditis is part of a multifocal fibroinflammatory process also involving other tissues (mediastinum, liver, lung, retroperitoneum, orbital). Women in middle to advanced ages are more affected than men. The clinical manifestations of Riedel’s thyroiditis are protean, often resembling malignancy due to a goiter of remarkably hard consistency. Patients complain of a rapid indolent enlargement of the thyroid that becomes very hard on palpation and difficult to delineate. Neck discomfort and dysphagia are frequently reported. Thirty to 40% of these patients develop overt hypothyroidism. Hoarseness and hypoparathyroidism may also appear due to involvement of the recurrent laryngeal nerve and/or the parathyroid glands. Physical examination, laboratory analysis, cytology, and imaging features are not useful for differentiating between Riedel’s thyroiditis and neoplastic diseases or the fibrotic variant of Hashimoto’s thyroiditis [12]. Histologic examination is necessary to establish the final diagnosis and surgical biopsy is mandatory. The differential diagnosis further encompasses anaplastic carcinoma and sarcoma of the thyroid. In contrast to the fibrotic variant of Hashimoto’s thyroiditis where fibrosis is strictly limited to the gland, Riedel’s thyroiditis displays a dense fibrotic replacement of thyroid parenchyma that penetrates the capsule and extends into contiguous neck structures. Once the diagnosis is confirmed, treatment is supportive with thyroid hormone substitution, when required. 16.3 Acute Infectious Thyroiditis Synonym: acute suppurative thyroiditis Infectious thyroiditis is a rare disease of the thyroid. A bacterial or a fungal infection is the main cause, though only a few hundred cases are reported worldwide. Mycobacterial, parasitic, and viral forms of thyroiditis have also been described, predominantly in immunodepressed hosts. The thyroid gland appears to be relatively resistant to infection. A rich vascular supply and an extended lymphatic drainage, as well as a fibrous capsule and an anatomic separation from the other structures of the neck by fascial planes, represent protective mechanisms. The high iodine content of the gland may account for some bactericidal effect. Infection of the gland occurs either through hematogenous spread from a primary focus or by direct extension from adjacent neck structures such as infected tonsil, pharynx, thyroglossal duct cyst, or through a pyriform sinus fistula, especially in children [13]. Other less common sources of infection include neck trauma or lymphatic spread; surgical site infections are extremely rare [14]. The most common predisposing factor for suppurative thyroiditis is immunodepression in association with HIV, tuberculosis, old age, or debilitation. Other predisposing factors include preexisting thyroid diseases, such as multinodular goiter, autoimmune thyroiditis, and thyroid cancers [14–16]. Patients are febrile with a sudden onset of disease, a painful, mostly unilateral enlargement of the thyroid, and local inflammatory signs (Fig. 16.1). The thyroid hormone tests are usually normal, but a slight hyperor hypothyroidism may appear. The erythrocyte sedimentation rate and acute phase proteins are elevated, and leucocytosis is present. Neck sonography reveals patchy hyperperfused areas in the thyroid with liquid content when an abscess is present. A fine-needle biopsy and cultures allow for pathogen identification and guide the antibiotic treatment. Depending on the clinical context, dedicated stainings and/or immunohistochemistry or in situ hybridization techniques may be necessary to identify the causative pathogen. Immunodepressed patients tend to present with more chronic thyroid infections, bilateral disease, and less prominent signs and symptoms: a high index of suspicion and aspiration biopsy are invaluable to pose the correct diagnosis and initiate correct treatment. The differential diagnosis of a painful anterior neck mass with febrile status encompasses subacute de Quervain’s thyroiditis, hemorrhage into a thyroid nodule, an infected thyroglossal or branchial cleft cyst, an infected cystic hygroma, and cervical adenitis. In addition to fine-needle biopsy, sonography helps to establish the correct diagnosis: acute suppurative thyroiditis usually shows hyperperfused areas (Fig. 16.2). In contrast, sonography in de Quervain’s thyroiditis depicts only microabscesses and no hyperperfused areas. Computed tomography (CT) and/or contrast oesography may further refine the diagnosis 16 Thyroiditis Fig. 16.1 Clinical picture of a 31-year-old female with acute infectious thyroiditis. Steroid therapy was initiated for a subacute de Quervain’s thyroiditis. Six weeks later, the patient developed a unilateral painful neck mass, dysphagia, and fever. Surgical incision and drainage was necessary to cure this condition or parasitic infections occur preferentially in immunodepressed patients. Dedicated stainings and a high index of suspicion may be necessary to identify atypical pathogens, such as Pneumocystis carinii and mycobacteria. Table 16.2 lists the pathogens commonly involved in acute thyroiditis. In children, an acute suppurative thyroiditis is caused in up to 90% of the cases by a pyriform sinus fistula [17]. 16.3.2 Surgical Treatment (Fig. 16.3) and help to delineate the extent of surgical treatment, particularly in the case of an infected pyriform sinus fistula. When an abscess is identified, surgical drainage is mandatory. Surgical incision and drainage of the abscess are curative only in patients whose acute thyroiditis is unrelated to a pyriform sinus fistula or thyroglossal duct fistula. Sometimes an affected thyroid lobe needs complete resection (Fig. 16.4a–c). In patients with recurrent acute thyroiditis, an undetected fistula must be postulated. Complete removal of the infected fistula is therefore required to prevent recurrence. Injection of 0.5% methylene blue solution through a Nélaton’s catheter into the fistula usually enables the complete resection of the fistula tract. When the origin of the fistula is difficult to identify, transection of the inferior pharyngeal constrictor muscle makes intervention easier. 16.3.1 16.4 Fig. 16.2 Thyroid sonography in acute infectious thyroiditis of the patient shown in Fig. 16.1. Hyperperfused areas and a liquid collection in the left thyroid lobe are shown. Fine-needle biopsy revealed Streptococcus constellatus, Peptostreptococcus, and fusobacteria Etiologies of Infectious Thyroiditis A bacterial infection (mainly gram-positive bacteria) contracted through hematogenous spread or neck trauma is the most common cause of acute thyroiditis in the immunocompetent patient. Viral, fungal, Non-autoimmune Thyroiditis Non-immune thyroiditis consist of a heterogeneous and rare group of thyroid inflammatory diseases. Some of them are clearly iatrogenic, such as drug-induced thyroiditis, postoperative necrotizing 211 212 Michel Adamina and Daniel Oertli Fig. 16.3 Thyroid aspergilloma in an immunodepressed kidney transplant patient. CT scan of the neck reveals a diffuse enlargement of the right thyroid gland with abscess formation Table 16.2 Pathogens involved in acute thyroiditis Bacteria Staphylococcus aureus (30%) Staphylococcus pyogenes Staphylococcus pneumoniae Streptococcus Finally, a few thyroiditides are caused by systemic diseases, such as a vasculitis-associated thyroiditis (phenytoin therapy may precipitate a hypersensitive thyroid vasculitis), a sarcoidosis (the thyroid is involved in up to 6% of sarcoidoses [18]), metastatic cancer, or a globus hystericus. Enterobacteria Fungi Aspergillus Pneumocystis carinii Cryptococcus Candida Virus EBV CMV Measles Adenovirus Echovirus Mumps Parasites Echinococcus Strongyloides Taenia thyroiditis, and radiation thyroiditis. Other causes are related to a local process, such as an acute hemorrhage into a thyroid cyst or nodule. Palpation thyroiditis refers to a mild, self-limited thyroiditis occurring after physical examination, surgery, or trauma to the thyroid. It is not associated with any thyroid disease. 16.4.1 Drug-induced Thyroiditis Chronic iodine therapy may cause a drug-induced thyroiditis with follicular hyperplasia. Likewise, lithium therapy may cause a goiter with or without hypothyroidism in 5–15% of patients under longterm lithium therapy [1]. Anticonvulsants (phenytoin, carbamazepine) may cause unspecific thyroiditis with subclinical or clinical hypothyroidism. Patients with chronic hepatitis or with cancer treated using interferon-α will develop a painless thyroiditis in about 1–5% of cases [19]. Elevated antithyroid antibodies are noted in a higher percentage in these patients and permanent hypothyroidism as well as Grave’s disease may appear [20]. Prior interferon-α therapy in the presence of antithyroid antibodies is associated with a higher probability of a subsequent antibody titer elevation and thyroid dysfunction [21]. These changes usually occur within 3 months of interferon-α therapy and seldom thereafter. As a practical matter, TSH should be measured prior to initiation of interferon-α therapy and periodically during treatment. For immunomodulation, interleukin-2 is also used in malignant melanoma, renal cell cancer, and leuke- 16 Thyroiditis Fig. 16.4 a Intraoperative finding of the patient depicted in Fig. 16.3 showing inflammatory swelling of the right thyroid lobe with aspergilloma. b Removed lobe after right hemithyroidectomy. c Opened specimen presenting abscess with aspergilloma mia, alone or in combination with chemotherapy. In several studies, interleukin-2 therapy has been linked to the development of a painless thyroiditis in about 2% of the patients treated [22]. Finally, the antiarrhythmic drug amiodarone contains 35% iodine and may cause thyroid dysfunctions in several different ways [23]. Amiodarone may cause a thyrotoxic crisis, due to its high iodine content (usually in patients with preexisting nodular goiter). Conversely, amiodarone may cause hypothyroidism via the antithyroid action of iodine, especially in patients with preexisting thyroid disease. Amiodarone decreases the conversion of T4 to the biologically active T3. It is worth noting that if the decision is taken to cease amiodarone therapy, the drug is not eliminated for months due to a very long half-life. 16.4.2 Postoperative Necrotizing Thyroiditis Postoperative necrotizing thyroiditis is a rare surgical complication [24,25]. No predictive marker or factor has been identified and the very rich vascular supply of the thyroid usually prevents this rarest complication. On histologic examination, the specimen typically shows postoperative granulomas, as found in other organs (bladder, prostate) following surgery. Postoperative necrotizing thyroiditis is related to a trauma of the thyroid, through vigorous manipulation of the gland at surgery or through repeated fineneedle aspiration [26]. Such manipulation could induce an acute thyroiditis, which in turn may lead to thyrotoxicosis or to a necrotizing thyroiditis. 16.4.3 Radiation Thyroiditis Radiation thyroiditis occurs in a dose-related fashion after radioiodine or external beam radiation therapy. Follicle destruction due to radiation injury may cause a transient hyperthyroidism, followed eventually by hypothyroidism. Neck pain and tenderness usually develop 5–10 days following treatment. Symptoms are mild and subside spontaneously in a week. 213 214 Michel Adamina and Daniel Oertli 16.5 Indications for Surgery Surgical interventions are exceptionally indicated for the management of a thyroiditis, accounting for less than 1% of all thyroid procedures [27]. Patients with autoimmune thyroiditis may pose significant technical challenges to the endocrine surgeon. The glands are firm, rigid, and highly vascular. The tissues surrounding the thyroid are inflamed with lymphadenopathy. This makes preservation of the parathyroids and recurrent nerves a highly demanding task. However, it is rather the exception than the rule to pose a surgical indication for an autoimmune thyroiditis, as most patients are effectively managed with thyroid hormone replacement therapy. In the rare instance where a large Hashimoto’s goiter may develop and become symptomatic, near-total thyroidectomy is an option [2,27,28]. Moreover, as thyroiditis patients bear a higher risk of developing thyroid carcinoma, a cold nodule suspicious on fineneedle biopsy may indicate a thyroid lobectomy. Similarly, the rapid growth of a chronic lymphocytic thyroid gland is suggestive of non-Hodgkin’s lymphoma. While total thyroidectomy may surgically cure a stage I lymphoma (i.e., confined to the thyroid), most thyroid lymphomas involve regional lymph nodes and distant sites and require multimodal systemic therapy. Open biopsy or thyroid lobectomy is sufficient in these cases to establish the definitive diagnosis. A subacute de Quervain’s thyroiditis exceptionally deserves surgical consideration. This indication is given when intractable neck pain is present in spite of a consequent analgesic and substitution therapy with thyroxin over 6 months. Thyroidectomy may then be indicated for definitive cure [27]. Riedel’s fibrosing thyroiditis often requires an open biopsy to confirm the diagnosis and rule out an anaplastic carcinoma (or the fibrotic variant of Hashimoto’s thyroiditis). However, thyroidectomy can be highly demanding because of the dense fibrotic reaction extending beyond the thyroid that puts the surrounding structures at risk for injury. Surgery is therefore confined to diagnosis of thyroiditis and exclusion of malignancy or to decompression of the trachea and the esophagus by isthmectomy and/or lobectomy. 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