16.1 Introduction
Thyroiditides make up approximately 20% of all thy- roid 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 in- flammation has been ruled out, most other types of thyroiditis have either a definitive autoimmune etiol- ogy or are possibly autoimmune in nature [2].
In life, one out of 100 individuals will develop an overt autoimmune thyroiditis. Thyroid autoantibod- ies may be found in up to 10% of the general popula- tion [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. Autoan- tibodies may promote thyroid hormone dysfunctions (stimulating thyroid autoantibodies, blocking thyroid
autoantibodies). An association of autoimmune thy- roiditis with defined HLA haplotypes implies a genetic predisposition [5]. Iodine therapy, viral infections, pregnancy and menopause, stress [6], and immuno- modulating 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 thyroid- itis) or without evident inflammation but with thy- roid dysfunction or a goiter (e.g., silent thyroiditis, Hashimoto’s or Riedel’s thyroiditis).
16 Thyroiditis
Michel Adamina and Daniel Oertli
Contents
16.1 Introduction . . . 207
16.2 Autoimmune Thyroiditis . . . 208 16.2.1 Hashimoto’s Thyroiditis . . . 208 16.2.1.1 Fibrotic Hashimoto’s Thyroiditis . . . 208 16.2.1.2 Atrophic Autoimmune Thyroiditis . . . 208 16.2.2 Focal Lymphocytic Thyroiditis . . . 209 16.2.3 Postpartum Thyroiditis . . . 209
16.2.4 Subacute de Quervain’s Thyroiditis . . . 209 16.2.5 Painless Thyroiditis . . . 209
16.2.6 Riedel’s Fibrosing Thyroiditis . . . 210 16.3 Acute Infectious Thyroiditis . . . 210 16.3.1 Etiologies of Infectious Thyroiditis . . . 211 16.3.2 Surgical Treatment . . . 211
16.4 Non-autoimmune Thyroiditis . . . 211 16.4.1 Drug-induced Thyroiditis . . . 212
16.4.2 Postoperative Necrotizing Thyroiditis . . . 213 16.4.3 Radiation Thyroiditis . . . 213
16.5 Indications for Surgery . . . 214 References . . . 214
Table 16.1 Etiologies of thyroiditis 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
16.2 Autoimmune Thyroiditis
The largest community study published so far on auto- immune thyroiditis revealed elevated thyroid autoan- tibodies against thyroid peroxidase and thyroglobulin in more than 10% of a British community (Whick- ham 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 au- toimmune thyroiditis and is the archetypic exam- ple of organ-specific autoimmune disease. With a prevalence of about 3% it represents the most com- mon cause of hypothyroidism in the general popula- tion [1]. In regions where iodine intake is adequate, Hashimoto’s thyroiditis also represents the most com- mon 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 HLA- DR3, -DR4, and -DR5 is found. Many other autoim- mune diseases are associated with Hashimoto’s thy- roiditis: Graves’ disease, juvenile diabetes, Addison’s disease, pernicious anemia, rheumatoid arthritis, Sjögren’s syndrome, and systemic lupus erythemato- sus. Hashimoto’s thyroiditis mostly presents with an oligosymptomatic clinical course, a painless homoge- neous goiter, and with signs of hypothyroidism. Low concentrations of thyroid hormones with high TSH and circulating thyroid autoantibodies (against per- oxidase in 70–90% of cases and against thyroglobulin in 40–70% of cases) confirm the diagnosis [1]. Oc- casionally, a transient hyperthyroidism state may be noted, up to a marked hyperthyroidism or hashitoxi- cosis, associated with the presence of anti-TSH re- ceptor 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 sup- pressor 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 auto- antibodies to the thyrocytes accounts for complement and T lymphocyte-mediated lysis of the thyrocytes and non-regulated release of thyroxine and triiodo- thyronine, 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 as- piration biopsy from a follicular neoplasm, papillary carcinoma, or low-grade MALT lymphoma. Immu- nohistochemistry studies may help to clear the differ- ential 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, predomi- nantly 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 myx- edema, 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 (refer- ence weights: male 20 g, female 17 g [7]).
16.2.2 Focal Lymphocytic Thyroiditis
Synonyms: focal autoimmune thyroiditis, chronic un- specific thyroiditis
Focal lymphocytic thyroiditis is a coincidental finding in 50% of women’s and 25% of men’s autop- sies, without clinical relevance. This low-grade auto- immune thyroiditis is characterized by focal lympho- cytic infiltrates of less than 5% of the thyroid gland.
16.2.3 Postpartum 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 dis- ease represents an exacerbation of a preceding (un- diagnosed) autoimmune thyroiditis and is classically linked to the haplotypes HLA-DR3, -DR4, and -DR5.
It may be interpreted as rebound autoimmunity af- ter the pregnancy-associated immunosuppression.
Eighty-five percent of these patients develop autoan- tibodies against thyroid peroxidase and thyroglobu- lin, which may vanish over time. Clinically, women may show a transient hyperthyroidism state, which rapidly converts to hypothyroidism, and then to eu- thyroidism within 12 months. Treatment consists of thyroid hormone substitution when required. Thy- reostatic medication, occasionally β-blockers, may be needed in the presence of exacerbated hyperthyroid- ism. Neither prophylaxis nor predicting marker have been identified so far and women affected once have a higher probability of relapse following further preg- nancies.
Women with a known autoimmune thyroiditis prior to pregnancy and an elevated titer of autoanti- bodies against thyroglobulin during pregnancy nearly always suffer from a postpartum exacerbation of their autoimmune thyroiditis.
16.2.4 Subacute de Quervain’s Thyroiditis
Synonyms: granulomatous thyroiditis, pseudotuber- culous thyroiditis, giant cell thyroiditis
Subacute de Quervain’s thyroiditis is a self-limiting disease accounting for 0.5–3% of all thyroid patholo- gies and lasts a few weeks to 2 months [10]. Women are 3–6 times more affected than men. The peak inci- dence 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,
lassitude, and a feeling of illness. The thyroid is exqui- sitely tender and enlarged to palpation. The erythro- cyte 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, euthyroid- ism 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 infec- tion. A postviral cytokine-mediated inflammation of the thyroid is suspected because a seasonal frequency and an association with upper respiratory tract infec- tion is noted. In half of the patients antibodies against mumps, measles, influenza, adenovirus, coxsackievi- rus, or echovirus are found. Furthermore, a genetic predisposition exists with the haplotype HLA-Bw35.
The differential diagnosis encompasses acute sup- purative thyroiditis. In contrast to acute suppurative thyroiditis, the gland sonographically reveals irregu- lar hypoperfused areas instead of hyperperfused tis- sue. On fine-needle biopsy, the differential diagnosis further includes palpation thyroiditis, as well as other granulomatous diseases such as sarcoidosis, tubercu- losis, and rheumatoid diseases.
Treatment is supportive with non-steroidal antiin- flammatory agents (NSAR) and β-blockers in severe cases with hyperthyroidism. Corticosteroids are use- ful (about 40 mg hydrocortisone equivalents daily) when the NSAR medication is not successful. Symp- toms usually improve within 2–3 days after the initia- tion of corticosteroid treatment. However, it may take about 4 weeks for the disappearance of the thyroid mass.
16.2.5 Painless Thyroiditis
Synonym: subacute lymphocytic thyroiditis
Patients present with a diffuse but modest en- largement of the thyroid and function tests reveal a transient hyperthyroidism, followed by hypothyroid- ism. 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 post- partum period. Autoantibodies against thyroid per- oxidase and thyroglobulin are found, as well as an
association with HLA-DR3 and -DR5 haplotypes.
Histologic examination of a specimen reveals a lym- phocytic 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 fi- broinflammatory 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 thy- roiditis are protean, often resembling malignancy due to a goiter of remarkably hard consistency. Patients complain of a rapid indolent enlargement of the thy- roid that becomes very hard on palpation and diffi- cult to delineate. Neck discomfort and dysphagia are frequently reported. Thirty to 40% of these patients develop overt hypothyroidism. Hoarseness and hypo- parathyroidism may also appear due to involvement of the recurrent laryngeal nerve and/or the parathy- roid glands. Physical examination, laboratory analy- sis, cytology, and imaging features are not useful for differentiating between Riedel’s thyroiditis and neo- plastic 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 en- compasses anaplastic carcinoma and sarcoma of the thyroid. In contrast to the fibrotic variant of Hashi- moto’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 struc- tures. 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 thy- roid. 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, predomi- nantly 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 separa- tion 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 infec- tions are extremely rare [14]. The most common pre- disposing factor for suppurative thyroiditis is immu- nodepression in association with HIV, tuberculosis, old age, or debilitation. Other predisposing factors include preexisting thyroid diseases, such as multi- nodular 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 hyper- or hypothyroidism may appear. The erythrocyte sedi- mentation 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 bi- opsy and cultures allow for pathogen identification and guide the antibiotic treatment. Depending on the clinical context, dedicated stainings and/or immu- nohistochemistry 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 sus- picion 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 ad- enitis. In addition to fine-needle biopsy, sonography helps to establish the correct diagnosis: acute suppu- rative thyroiditis usually shows hyperperfused areas (Fig. 16.2). In contrast, sonography in de Quervain’s thyroiditis depicts only microabscesses and no hyper- perfused areas. Computed tomography (CT) and/or contrast oesography may further refine the diagnosis
(Fig. 16.3) and help to delineate the extent of surgical treatment, particularly in the case of an infected pyri- form sinus fistula.
16.3.1 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 thyroid- itis in the immunocompetent patient. Viral, fungal,
or parasitic infections occur preferentially in immu- nodepressed patients. Dedicated stainings and a high index of suspicion may be necessary to identify atypi- cal pathogens, such as Pneumocystis carinii and my- cobacteria. 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
When an abscess is identified, surgical drainage is mandatory. Surgical incision and drainage of the ab- scess are curative only in patients whose acute thy- roiditis is unrelated to a pyriform sinus fistula or thy- roglossal duct fistula. Sometimes an affected thyroid lobe needs complete resection (Fig. 16.4a–c). In pa- tients with recurrent acute thyroiditis, an undetected fistula must be postulated. Complete removal of the infected fistula is therefore required to prevent re- currence. 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.
16.4 Non-autoimmune Thyroiditis
Non-immune thyroiditis consist of a heteroge- neous and rare group of thyroid inflammatory dis- eases. Some of them are clearly iatrogenic, such as drug-induced thyroiditis, postoperative necrotizing
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 unilat- eral painful neck mass, dysphagia, and fever. Surgical incision and drainage was necessary to cure this condition
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
thyroiditis, and radiation thyroiditis. Other causes are related to a local process, such as an acute hemor- rhage into a thyroid cyst or nodule.
Palpation thyroiditis refers to a mild, self-limited thyroiditis occurring after physical examination, sur- gery, or trauma to the thyroid. It is not associated with any thyroid disease.
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 in- volved in up to 6% of sarcoidoses [18]), metastatic cancer, or a globus hystericus.
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 long- term lithium therapy [1]. Anticonvulsants (phenyt- oin, carbamazepine) may cause unspecific thyroid- itis 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-
Table 16.2 Pathogens involved in acute thyroiditis Bacteria Staphylococcus aureus (30%)
Staphylococcus pyogenes Staphylococcus pneumoniae Streptococcus
Enterobacteria
Fungi Aspergillus
Pneumocystis carinii Cryptococcus Candida
Virus EBV
CMV Measles Adenovirus Echovirus Mumps Parasites Echinococcus
Strongyloides Taenia
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
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 con- tains 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 pa- tients with preexisting thyroid disease. Amiodarone decreases the conversion of T4 to the biologically ac- tive T3. It is worth noting that if the decision is taken to cease amiodarone therapy, the drug is not elimi- nated 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 complica- tion. On histologic examination, the specimen typi- cally 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 manipula- tion of the gland at surgery or through repeated fine- needle aspiration [26]. Such manipulation could in- duce 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.
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 hemithy- roidectomy. c Opened specimen presenting abscess with asper- gilloma
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 techni- cal challenges to the endocrine surgeon. The glands are firm, rigid, and highly vascular. The tissues sur- rounding the thyroid are inflamed with lymphade- nopathy. This makes preservation of the parathyroids and recurrent nerves a highly demanding task. How- ever, 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 goi- ter 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 fine- needle biopsy may indicate a thyroid lobectomy. Sim- ilarly, the rapid growth of a chronic lymphocytic thy- roid 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 ther- apy. Open biopsy or thyroid lobectomy is sufficient in these cases to establish the definitive diagnosis.
A subacute de Quervain’s thyroiditis exception- ally 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 Hashi- moto’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.
The fibrotic variant of Hashimoto’s thyroiditis is characterized by a rapid enlargement of a preexisting goiter that may lead to the suspicion of a thyroid can- cer and to surgical resection.
Amiodarone-induced thyrotoxicosis in the setting of a rare patient with otherwise intractable arrhyth- mia is an indication for thyroidectomy.
Finally, the acute suppurative thyroiditis is a classic indication for surgical drainage followed by antibiotic therapy. Rarely lobectomy is necessary when the sup- purative process is necrotizing. An underlying thyro- glossal (pyriform) fistula should be excluded by the time of surgical exploration.
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