Professional Documents
Culture Documents
SECTION ONE
Follicular Carcinoma
Hurthle Cell Tumors
Medullary Carcinoma
Anaplastic Carcinoma
Primary Lymphoma
Rare Malignancies
Metastatic Disease
SECTION TWO: THE PARATHYROID GLANDS
ANATOMY OF THE PARATHYROID GLANDS
ENDOCRINOLOGY OF THE PARATHYROID
GLANDS
CLINICAL MANIFESTATIONS OF
PARATHYROID DISEASE
Hyperparathyroidism
Hypoparathyroidism
IMAGING OF PATHOLOGY OF THE
PARATHYROID GLANDS
Parathyroid Adenoma
Ultrasonography
Cross-Sectional Imaging
Nuclear Scintigraphy
Reoperation for Hyperparathyroidism
Parathyroid Hyperplasia
Parathyroid Carcinoma
Parathyroid Cyst
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FIGURE 40-1 Normal thyroid gland on MR imaging. A, Unenhanced axial T1-weighted MR image shows the
normal appearance of the thyroid gland (T ), which is homogeneously hyperintense to the neck musculature (m). The
normal anatomic relationship of the gland to the jugular vein (J ), carotid artery (c), esophagus (e), and musculature
(m) is shown. B, Axial T2-weighted image at the same level as A shows the normal gland to be hyperintense relative
to the neck musculature.
FIGURE 40-2
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Table 40-2
EVALUATION OF THE HYPERTHYROID PATIENT
TFTs
elevated
RAIU
(Normal)
RAIU
(Low)
RAIU
(High)
Plummers
disease
Thyroiditis
De Quervains thyroiditis
Graves
disease
Subacute lymphocytic
disease
Struma ovarii
Factitious disease
RAIU, 24-hour radioactive iodine uptake (normal, 10% to 30%); TFTs, thyroid
function tests.
Thyroid storm characterized by hypertension, tachycardia, and fever may present as a clinical emergency in
patients with unrecognized or inadequately treated thyrotoxicosis. If unrecognized, it may result in death.
Thyroid ophthalmopathy, more common in women, is
characterized by proptosis usually secondary to enlargement
of the extraocular muscle bellies, with sparing of their
tendinous insertions. Although most commonly seen in
Gravesdisease and hyperthyroidism, thyroid ophthalmopathy may occur in euthyroid and even hypothyroid patients.
The most common patterns of extraocular muscle involvement are enlargement of the inferior rectus muscle,
enlargement of both the inferior and medial rectus muscles,
and enlargement of all of the muscles (Fig. 40-3).4 There
usually is relative sparing of the lateral rectus muscles, and
isolated involvement of this muscle should raise the
suspicion of a different disease process such as myositis or
pseudotumor. Proptosis may also be related to an increase in
orbital fat secondary to edema and lymphocytic infiltration,
as well as due to an increase in the volume of the extraocular
muscles. Although most commonly symmetric, exophthalmos (proptosis) may be asymmetric or even unilateral.4
Clinical signs and symptoms include proptosis, lid retraction, decreased ocular range of motion, and corneal exposure
caused by eyelid retraction. Extraocular muscle enlargement
may result in compression of the optic nerve at the orbital
Table 40-1
COMMON MEDICATIONS THAT MAY
DECREASE THYROID IODIDE UPTAKE
Iodine-containing contrast agents
Oral cholecystographic agents
Thyroxine (Synthroid)
Cytomel (T3)
Antithyroid medications (propylthiouracil)
Iodide preparations
Antibiotics
Antihistamines
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FIGURE 40-4 Enhanced CT scan of a multinodular goiter with substernal extension and compression of the
trachea and esophagus. A, Axial CT scan at the level of the upper trachea shows diffuse nodular enlargement of the
thyroid gland that is heterogeneous in density. There is marked displacement of the trachea (T ) and esophagus (e)
from left to right. B, There is extension of goiter (arrows) behind the trachea into the middle mediastinum.
THYROID IMAGING
Nuclear scintigraphy and ultrasonography are frequently
the first imaging modalities used to assess patients with
suspected thyroid disorders. CT and MR imaging are
frequently utilized to address specific issues regarding
thyroid disease such as the extent of thyroid goiter or
extension of neoplasm outside the thyroid capsule and into
adjacent structures in the neck. They are used in assessing
for regional nodal metastases in the setting of thyroid cancer
and in the evaluation of recurrent disease following
treatment for thyroid cancer.
Nuclear Scintigraphy
Nuclear scintigraphy provides excellent functional information about the thyroid because the radionuclides used to
image the gland do so by utilizing some step of hormone
synthesis within the thyroid. The primary role of scintigraphy in the evaluation of a focal thyroid mass is to determine
whether a lesion is hot (low incidence of malignancy) or
cold (higher incidence of malignancy).6, 7 Nuclear
imaging of the thyroid gland is performed with a gamma
scintillation camera. The patient is usually placed in a
hyperextended supine position. Images are typically obtained from the chin to the sternal notch in multiple views
including anterior, posterior, and bilateral oblique projec-
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Cross-Sectional Imaging
While scintigraphy provides functional information
about the thyroid, CT and MR imaging provide important
adjunctive anatomic information that is superior to that of
nuclear imaging. These modalities not only provide better
delineation of lesions within the thyroid, but also play a
critical role in the detection of lymph node metastases, as
well as extension of thyroid disease to adjacent tissues in the
neck. Specifically, invasion of the paraspinal musculature,
esophagus, trachea, and carotid sheath structures may be
assessed 15 (Fig. 40-6). The detailed anatomic information
provided by CT and MR imaging is also valuable in guiding
the surgical approach.
For CT and MR examinations, patients are typically
scanned in the supine position with the neck mildly
hyperextended so that the hard palate is roughly perpendicular to the tabletop. When possible, the patient is scanned
with quiet breathing and swallowing suspended. Contiguous
3 mm thick axial sections are obtained from the level of the
cavernous sinuses (upper level of the external auditory
canal) to the superior mediastinum, including the aortic arch.
In cases where small lesions are being evaluated, thinner
sections (1 to 2 mm) may be obtained.
The normal thyroid gland (due to its iodide content) has a
density of approximately 80 to 100 HU on CT. That is, since
the thyroid gland normally concentrates iodine approximately100 times over the iodine concentration in the serum,
and since iodine is the basis of the CT contrast agents, the
radiodensity of the thyroid gland on noncontrast CT images
correlates well with thyroid function. Thus, a well-seen
thyroid gland usually indicates a normally functioning
Table 40-3
RADIONUCLIDES COMMONLY USED IN IMAGING THE THYROID GLAND
Radionuclide
Tc-99m
I-123
I-131 (diagnostic)
I-131 (whole body)*
I-123 (whole body)*
I-131 (treatment)
I-131 (treatment)
Administration
Dose
Half-life
Energy
Intravenous
Oral
Oral
Oral
Oral
Oral
Oral
210 mCi
200400 Ci
30100 Ci
25 mCi
12.5 mCi
100 mCi
100200 mCi
6.02 hr
13.6 hr
8.05 days
140 keV
159 keV
364 keV
*Diagnostic whole body scan following thyroidectomy to evaluate for residual thyroid tissue in the thyroid bed or to detect distant metastases; to detect ectopic thyroid tissue such
as struma ovarii; in hyperthyroid patients with no demonstrable iodine uptake in the thyroid.
Cancer treatment following thyroidectomy with the goal of ablating residual thyroid tissue (may require hospital admission, depending on the dose).
Cancer treatment with the goal of ablating thyroid metastases (may require hospital admission, depending on the dose).
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FIGURE 40-5 Recurrent thyroid cancer in a 64-year-old woman following thyroidectomy for papillary
carcinoma, tall cell variant. A, 18FDG-PET image shows a region of intense radiotracer uptake (arrow) in the base of
the right neck. B, Unenhanced axial T1-weighted MR image shows a corresponding soft-tissue mass in the right
tracheoesophageal groove (arrows), confirmed to be recurrent tumor at surgery.
FIGURE 40-6
A 68-year-old man presented with a rapidly enlarging right neck mass and facial swelling. MR
imaging revealed a right thyroid tumor with extension to the jugular vein. A, Unenhanced axial T1-weighted MR
image shows a poorly defined mass originating in the right thyroid lobe with extracapsular extension and direct
invasion of the jugular vein, which is filled with tumor (arrows). J, Left jugular vein with normal flow void; N,
metastatic disease. B, Unenhanced axial T1-weighted MR image superior to A shows tumor in the right jugular vein.
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Ultrasonography
Real-time ultrasound of the thyroid gland is usually
performed with high-resolution linear array transducers
ranging from 7.5 to 10 MHz.17 The neck is mildly
hyperextended, and the thyroid gland is imaged in its
entirety in both the transverse and longitudinal planes. The
carotid arteries and jugular veins are posterior and lateral to
the thyroid lobes, respectively, and provide excellent
anatomic markers during the examination. The thyroid gland
is normally uniformly hyperechoic.17 The more hypoechoic
a focal lesion is relative to the normal thyroid gland, the
higher the likelihood of malignancy.18
The advantages of ultrasound are three: it is accessible,
inexpensive, and noninvasive. It is a quick and highly
sensitive modality for distinguishing cystic from solid
lesions. Focal lesions meeting all of the criteria for a simple
cyst (thin wall with smooth margins, anechoic, distinct back
wall, and enhanced through transmission) are usually
benign. However, any complicated cyst may represent a
carcinoma. When calcifications are present, they appear as
foci of increase echogenicity with distal acoustic shadowing. Calcifications are nonspecific and may be seen in
benign as well as malignant lesions.18 Ultrasound may also
be used to guide fine needle aspiration of nodular
disease within the thyroid or to guide aspiration of suspicious cervical lymph nodes in the setting of thyroid cancer
(Fig. 40-7).1921
Drawbacks of ultrasound are that the quality of the
images as well as their interpretation are dependent on the
expertise of the examiner. Another limitation is that
ultrasound is not as good as cross-sectional imaging
techniques in identifying lymphadenopathy or in evaluating
for extension of thyroid disease into the soft tissues of the
neck, chest, or air-filled structures.
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Graves Disease
Graves disease is the most common of the autoimmune
disorders, occurring in approximately 0.4% of the U.S.
population.2 The peak incidence is in the third to fourth
decades of life, with a female predominance. There is a
familial predisposition. In Graves disease the thyrotropin
receptor on the follicular cells is the target for thyroid
autoantibodies, which bind to these receptors, stimulating
them as though TSH triggered the receptor. This results in
constant autonomous function of the thyroid resulting in
hyperthyroidism. Serologic tests for specific autoimmune
markers may be elevated, confirming the diagnosis. Marked
enlargement of the thyroid gland without focal nodules
referred to as diffuse toxic goiter results. There may be
prominent enlargement of a pyramidal lobe (Fig. 40-2).
Pathologically, in the thyroid gland there is diffuse
hyperplasia of the follicular epithelial cells and depletion of
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colloid. Vascularity is increased. Graves disease is associated with other autoimmune diseases of the thyroid
including Hashimotos thyroiditis.
Radionuclide scintigraphy may be useful in evaluating a
patient with suspected Graves disease as well as in
differentiating it from acute thyroiditis. Typically in Graves
disease, the thyroid gland is diffusely enlarged with intense
radiotracer uptake, often as high as 80% in 24 hours (Fig.
40-13).
The differential diagnosis includes thyroiditis, toxic
multinodular goiter, and toxic adenoma. In contrast to
Graves disease, where there is concordance between the
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FIGURE 40-15
Toxic multinodular goiter. Technetium-99m pertechnetate scans show enlargement of the thyroid gland with regions of
increased and decreased uptake.
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FIGURE 40-16 Hashimotos thyroiditis. A, Transverse ultrasound image showing heterogeneity in the
echotexture of the right lobe of the thyroid gland with a more focal region of decreased echogenicity posteriorly
(arrows). V, Jugular vein; C, carotid; T, trachea. B, Corresponding enhanced axial CT scan shows a focal region of
hypodensity (arrows) corresponding to the abnormality seen on ultrasound.
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enlargement. Radioactive iodine uptake is low, and the pattern on scintigraphy varies from no tracer uptake to diffuse
or heterogeneous uptake.34 Nuclear scans may return to normal in conjunction with resolution of the process.
Postpartum thyroiditis typically occurs 4 to 6 weeks
following delivery. It occurs in up to 5% of postpartum
women and may recur with subsequent pregnancy.52 As
with silent thyroiditis, women may present with goiter,
thyrotoxicosis, and antithyroid antibodies. The process
usually resolves after transient hypothyroidism; however,
some patients progress to chronic lymphocytic thyroiditis.
De Quervains Thyroiditis (Subacute Granulomatous
Thyroiditis)
De Quervains thyroiditis is a self-limited inflammatory
process that usually occurs following a viral upper
respiratory tract infection.2, 22 The viral infections that have
been associated with subacute thyroiditis include coxsackievirus and the mumps.53 The peak incidence is in the
second to fifth decades of life, with an occurrence three
times more frequent in women. Early in the inflammatory
process, follicles may be replaced with neutrophils forming
microabscesses. Later, macrophages and multinucleated
giant cells surround the damaged follicles, stimulating a
granulomatous process.2 Viral inclusions have not been
found in the inflamed gland. With healing, there is
regeneration of the follicles. The clinical presentation may
include painful enlargement of the thyroid gland, fever, and
thyrotoxicosis with low radioactive iodine uptake. Scintigraphy shows a variable pattern that usually reverts to normal as
the patient returns to a euthyroid state.6 On non-contrast CT,
the gland is slightly enlarged and has a lower than normal
attenuation.
Acute Suppurative Thyroiditis
Acute suppurative thyroiditis is uncommon and typically
occurs due to seeding of the thyroid gland by bacterial, and
occasionally fungal, organisms in immunocompromised or
debilitated patients.22 It may be associated with a fourth
branchial cleft abnormality, and one of the roles of imaging
is to exclude a fistula (from the pyriform sinus apex) as an
etiology of the thyroiditis.54 On cross-sectional imaging, the
affected portion of the gland (lobe[s] and/or isthmus) will be
enlarged and heterogeneous in CT density and MR signal
intensity. With disease progression, focal abscesses may
develop and there may be obliteration of the adjacent soft
tissues in the neck resulting from associated myositis and
cellulitis.55
Riedels Thyroiditis (Struma)
Riedels thyroiditis (struma) is a rare form of chronic
thyroiditis characterized by a fibrosing reaction similar to
that seen in retroperitoneal fibrosis, which destroys the
thyroid and extends into the adjacent soft tissues of the neck.
Within the fibrosing tissue is a lymphocytic and plasma cell
infiltration and a vasculitis (phlebitis).56 As a result, stridor,
dysphagia, and vocal cord paralysis may result from
recurrent laryngeal nerve involvement. In fact, Reidels
thyroiditis is one of the few nonmalignant thyroid causes of
recurrent laryngeal nerve paralysis. The cause of Reidels
thyroiditis is unknown. It is more common in women and
usually occurs in the fourth to seventh decades of life. On
Thyroid Goiter
As mentioned, the term goiter refers to any clinical
enlargement of the thyroid gland. A goiter develops because
as the thyroid gland compensates for inadequate thyroid
hormone output, the follicular epithelium undergoes compensatory hypertrophy to achieve a euthyroid state. As a
result, either hypothyroidism or hyperthyroidism may
develop. Although initially the goitrous enlargement is
diffuse, with time it usually becomes nodular. If the
impediment to thyroid hormone output abates, the thyroid
gland may revert to normal during the diffuse state.
Diffuse nontoxic goiter is a diffuse nonnodular enlargement of the thyroid associated with a euthyroid state. There
are two stages in its development. The first stage is
hyperplasia (follicular cell growth) characterized by diffuse
glandular enlargement and hyperemia. The second stage is
colloid involution, which occurs when a euthyroid state is
maintained. Endemic goiters are prevalent in iodinedeficient areas. In simple sporadic goiter, there is a female
predominance and a peak incidence at puberty.2 With time,
most simple goiters progress to multinodular goiters that
may remain nontoxic or may induce thyrotoxicosis.
Multinodular goiter is characterized by nodularity, focal
hemorrhage, focal calcifications, cyst formation, and scarring. Glandular enlargement may be asymmetric, involving
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one lobe more than the other and/or involving the isthmus.
Thyroid goiters may extend substernally and into the
anterior mediastinum.
Multiple patterns may be identified with nuclear scintigraphy (Fig. 40-15). Radioactive iodine or Tc-99m
pertechnetate may accumulate in multiple foci throughout
the gland or, less typically, in only a few nodules. Some
FIGURE 40-20 Multinodular goiter. A, Enhanced axial CT image shows asymmetry in the thyroid gland. Both
lobes are enlarged (the right greater than the left), with multiple focal regions of low density consistent with goiter.
B, Enhanced axial CT image superior to A shows nodular enlargement with a focal area of hypoattenuation within
the isthmus of the gland. The patient has an orotracheal tube in place.
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FIGURE 40-21 Multinodular goiter with substernal extension. A, Enhanced axial CT scan reveals extensive
enlargement of the thyroid gland with diffuse heterogeneous hypodensity. The patient has an orotracheal tube in
place. B, There was substernal extension of the thyroid goiter. Multiple calcifications are also noted.
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FIGURE 40-23
FIGURE 40-24 A 60-year-old woman presented with hyperthyroidism. The 24 hour uptake was 46% (upper limit of normal is 30%), and
scintigraphy showed a hot nodule with suppression of the remainder of the
gland consistent with an autonomous nodule. (Courtesy of Dr. Joseph Sam,
Department of Radiology, Ultrasound Division, University of Pennsylvania Medical Center.)
Adenomas
Thyroid adenomas are true benign neoplasms distinctly
separate from the adjacent thyroid tissue and encased by a
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Chapter 40
fibrous capsule. They are usually solitary and nonfunctioning, most commonly detected in young and middle-aged
adults. Autonomously functioning adenomas are not usually
associated with hyperthyroidism.71 Toxicity is most commonly seen with large lesions and advanced age. Follicular
adenomas slowly increase in size, usually not exceeding 4
cm.2 Sudden enlargement of a follicular adenoma is usually
related to spontaneous hemorrhage within the lesion.72
Spontaneous degeneration of an adenoma may occur, and in
fact, most thyroid cysts represent degeneration of adenomas.
The presence of carcinoma within an adenoma is rare.72
Hurthle cell adenomas are rare neoplasms composed of
granular cells and pink-staining cytoplasm. Unlike follicular
adenomas, these are not well circumscribed, and some
believe they are malignant.
If an adenoma is autonomous (independent of TSH),
ablation with I-131 may be performed, as the short-acting
beta radiation will deposit preferentially in the nodule.
Alternatively, the nodule may be surgically removed. In
either case, the risk of postprocedural hypothyroidism is
small. The previously suppressed normal thyroid tissue
resumes normal function following treatment.
Recent reports describe successful treatment of autonomous thyroid and parathyroid adenomas with 95%
ethanol injection. Results vary but generally show resolution of the hyperthyroid state without development of
hypothyroidism.7378 A potential complication is inadvertent injection of ethanol into the recurrent laryngeal nerve at
the level of the tracheoesophageal groove, which may result
in vocal cord paralysis.79
Malignant Neoplasms
The incidence of thyroid cancer in men and women
increased up to 1975. This increase was believed to reflect
the use of low-dose radiation to treat the head and neck,
particularly in children for benign diseases such as thymic
enlargement and adenoidal hypertrophy.80 There is a linear
dose-response relationship between 100 and 2000 rads.6, 81
Approximately 15% to 30% of patients who received
radiation in this dose range will develop a thyroid nodule,
and 6% to 8% will develop thyroid cancer. Long-term
follow-up is necessary, as the latent period for the
development of cancer may be as long as 30 years. Early
detection is essential since carcinoma in this population is
more aggressive and may require extensive surgical
management to achieve a cure rate equivalent to that of
nonirradiated patients.66 Thyroid carcinoma following highdose irradiation (greater than 2000 rads) is rare, likely
because irradiation at these doses destroys thyroid tissue.6
Individuals at increased risk (low-dose radiation exposure,
genetic predisposition) of developing thyroid cancer may be
screened and followed by obtaining serum calcitonin levels,
as calcitonin serves as a sensitive marker for tumor
development.
Approximately 12,000 new cases of thyroid carcinoma are diagnosed in the United States each year, and
the annual death rate is approximately 1000.82 Of interest, the prevalence of incidental thyroid carcinomas identified at autopsy is 3.9%83 and at surgery it is 10.5%.84
Differentiated thyroid carcinomas including papillary and
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FIGURE 40-25 Papillary thyroid carcinoma in two different patients. A, Enhanced axial CT scan shows a
dominant hypodense mass (M ) replacing the right lobe of the thyroid gland. Also note the pathologic ipsilateral
cervical lymph node (N ). B, A sagittal sonogram of the right lobe of the thyroid shows a dominant nodule with
heterogeneous echogenicity. There are both cystic and frond-like solid components. (Courtesy of Dr. Jill Langer,
Department of Radiology, Ultrasound Division, University of Pennsylvania Medical Center.)
Cystic nodes are different from the necrotic nodes frequently seen with metastatic squamous cell carcinoma that
have central low density but retain a thick rind of residual lymphatic tissue. Hemorrhagic or colloid-containing
nodes may be hyperintense on unenhanced T1-weighted
MR images (Fig. 40-31). Although in the vast majority of
cases regional nodal metastases from thyroid cancer occur
in the anterior and posterior cervical lymph chains,
occasionally (2%) metastases occur in retropharyngeal
nodes (Fig. 40-32). Any lymph node seen in a patient with
papillary carcinoma should raise the suspicion of metastatic
disease because of the high rate of lymphatic spread. This is
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FIGURE 40-30
Medullary Carcinoma
Medullary carcinoma arises from parafollicular C cells
that are believed to be derived from neural crest tissue in the
ultimobranchial bodies. It is relatively uncommon and has a
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FIGURE 40-33
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Primary Lymphoma
Primary lymphoma of the thyroid gland is uncommon,
representing less than 5% of all lymphomas arising in
extranodal sites and approximately 1% to 3% of all thyroid
malignancies. It usually presents in elderly women with a
long history of goiter. In addition, patients with Hashimotos
thyroiditis have an increased incidence of developing
lymphoma of the thyroid, usually the non-Hodgkins
type.46, 47 The thyroid gland may also be involved secondarily by lymphoma.
Imaging, including MR imaging, cannot reliably distinguish lymphoma from thyroiditis in patients with Hashimotos thyroiditis.1, 108 Patients usually present with a
rapidly enlarging thyroid mass and symptoms of obstruction
related to compression of the aerodigestive tract.1, 46
Thyroid lymphoma may present as multiple nodules, but
more commonly (80%) it presents as a solitary mass.1, 46
Usually it is hypoechoic on ultrasound17, 18 and hypodense
on CT.46 While lymphoma is typically cold on iodine and
technetium nuclear scintigraphy, it may show increased
uptake on gallium scans. Necrosis and calcification are
uncommon.46 On MR imaging, lymphoma is usually
hyperintense on T2-weighted images and isointense to
normal thyroid on T1-weighted images.1, 108
FIGURE 40-36
Anaplastic thyroid carcinoma. A, Unenhanced axial CT scan shows an infiltrative mass in the
left lobe of the thyroid gland Extension outside the thyroid capsule is suggested by soft-tissue stranding in the adjacent
neck fat (arrow). There is also obliteration of the fat plane between the thyroid and the esophagus (long arrow, esophageal lumen). B, Inferior image shows a necrotic metastatic lymph node (N ). C, Carotid; J, jugular vein.
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Rare Malignancies
Primary squamous cell carcinoma of the thyroid gland is
rare and may result from squamous metaplasia of epithelial
cells. Similarly, rare sporadic cases of mucoepidermoid
carcinoma may occur (Fig. 40-38). These are typically seen
in patients with a long history of goiter and have a poor
prognosis. There are no diagnostic imaging findings to
distinguish these from other neoplasms. Primary sarcomas
of the thyroid gland are extremely rare, can be radiation
induced, and have a poor prognosis. Such lesions include
liposarcomas, fibrosarcomas, leiomyosarcomas, chondrosarcomas, osteosarcomas, and angiosarcomas.
Teratomas in infants, and rarely in adults, may involve
the thyroid gland. Thymus-related lesions may also rarely
occur. About 1.5% of thyroid glands contain thymic tissue,
and intrathyroidal thymomas can occur. Similarly, spindle
and epithelial thymus-like tumors (SETTLE) and carcinoma
with thymus-like features (CASTLE) have been reported.
Even a very rare intrathyroidal paraganglioma has been
reported.
Metastatic Disease
Metastatic disease to the thyroid gland is uncommon.
Lung and breast carcinomas are the most common causes of
thyroid metastases found at autopsy, while renal carcinoma
is the most common metastasis detected clinically.109
Metastatic melanoma and colon carcinoma metastatic to the
thyroid gland have also been reported.110 Multiple thyroid
masses are usually present in the setting of metastatic
disease (Fig. 40-39). When atypical histology of a resected
thyroid mass is detected, metastatic disease should be
considered. Testing to establish the presence of thyroglobulin and/or calcitonin supporting the belief that the neoplasm
is thyroidal in origin may be extremely useful, and the
absence of these markers favors metastatic disease.
REFERENCES
FIGURE 40-38 Mucoepidermoid carcinoma of the thyroid gland in
a 76-year-old woman with a long-standing history of goiter. Axial
fat-suppressed T2-weighted image shows diffuse goiter. A 1 cm hyperintense nodule (N ) was biopsied and sdshown to be mucoepidermoid
carcinoma.
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58. Belfiore A, LaRose GL, LaPorta GA, et al. Cancer risks in patients
with cold thyroid nodules: relevance of iodine intake, sex, age, and
multinodularity. Am J Med 1992;93:363369.
59. Cerise EJ, Spears R, Ochsner A. Carcinoma of the thyroid and
nontoxic nodular goiter. Surgery 1952;31:552561.
60. McCall A, Jarosz H, Lawrence AM, et al. The incidence of thyroid
carcinoma in solitary cold nodules and in multinodular goiters.
Surgery 1986;100:11281132.
61. Shulkin BL, Shapiro B. The role of imaging tests in the diagnosis of
thyroid carcinoma. Endocrinol Metab Clin North Am 1990;19(3):
523543.
62. Noma S, Kanaoka M, Minami S, et al. Thyroid masses: MR imaging
and pathologic correlation. Radiology 1988;168:759764.
63. Huysmans DA, Hermus AR, Corstens FH, et al. Large, compressive
goiters treated with radioiodine. Ann Intern Med 1994;121(10):
757762.
64. Dworkin HJ, Meier DA, Kaplan M. Advances in the management of patients with thyroid disease. Semin Nucl Med 1995;25:
205220.
65. Huang T, Loevner LA, Yousem DM. Management of incidental
thyroid lesions detected on CT and MR imaging of the neck
performed for other purposes. Presented at the 30th Annual Scientific
Conference, American Society of Head and Neck Radiology, Los
Angeles, April 2428, 1996.
66. Harvey HK. Diagnosis and management of the thyroid nodule: an
overview. Otolaryngol Clin North Am 1990;23:303337.
67. Shamma FN, Abrahams JJ. Imaging in endocrine disorders. J Reprod
Med 1992;37:3945.
68. Klieger PS, Wilson GA, Greenspan BS. The usefulness of the
dynamic phase in pertechnetate thyroid imaging for solitary
hypofunctioning nodules. Clin Nucl Med 1992;17(8):617622.
69. Gharib H, Goellner JR, Johnson DA. FNA cytology of the thyroid: a
12 year experience with 11,000 biopsies. Clin Lab Med 1995;13:
699710.
70. Gharib H, Goellner JR. Fine needle aspiration of the thyroid: an
appraisal. Ann Intern Med 1993;11:282289.
71. Hamberger JI. Evolution of toxicity in solitary nontoxic autonomously functioning thyroid nodules. Clin Endocrinol Metab
1980;50:10891093.
72. Ross DS. Evaluation of the thyroid nodule. J Nucl Med
1991;32:21812192.
73. Livraghi T, Paracchi A, Ferrari, et al. Treatment of autonomous
thyroid nodules with percutaneous ethanol injection: preliminary
results. Radiology 1990;175:827829.
74. Monzani F, Goletti O, Caraccio N, et al. Percutaneous ethanol
injection treatment of autonomous thyroid adenoma: hormonal and
clinical evaluation. Clin Endocrinol 1992;36:491497.
75. Mazzeo S, Toni MG, DeGaudio C, et al. Percutaneous injection
of ethanol to treat autonomous thyroid nodules. AJR 1993;161:
871876.
76. Papini E, Panunzi C, Pacella CM, et al. Percutaneous ultrasoundguided ethanol injection: a new treatment of toxic autonomously functioning thyroid nodules. J Clin Endocrinol Metab
1993;76:411416.
77. Livraghi T, Paracchi A, Ferrari C, et al. Treatment of autonomous
thyroid nodules with percutaneous ethanol injection: 4-year experience. Radiology 1994;190:529533.
78. Ozdemir H, Ilgit ET, Yucel C, et al. Treatment of autonomous
thyroid nodules: safety and efficacy of sonographically guided
percutaneous injection of ethanol. AJR 1994;163:929932.
79. Solbiati L, Pra LD, Ierace T, et al. High-resolution sonography of the
recurrent laryngeal nerve: anatomic and pathologic considerations.
AJR 1985;145:989993.
80. Duffy BJ Jr, Fitzgerald PJ. Cancer of the thyroid in children: a report
of 28 cases. J Clin Endocrinol Metab 1950;10:12961311.
81. Favus MJ, Schneider AB, Stachura ME, et al. Thyroid cancer
occurring as a late consequence of head-and-neck irradiation:
evaluation of 1,056 patients. N Engl J Med 1976;294:10191025.
82. Mazzaferri EL. Management of a solitary thyroid nodule. N Engl J
Med 1993;328:553559.
83. Mazzaferri EL, de los Santos ET, Rofagha-Keyhani S. Solitary
thyroid nodules: diagnosis and management. Med Clin North Am
1988;72:11771211.
84. Pelizzo MR, Piotto A, Rubello D, et al. High prevalence of occult
papillary thyroid carcinoma in a surgical series for benign thyroid
disease. Tumori 1990;76:255257.
85. Sutton RT, Reading CC, Charboneau JW, et al. US-guided biopsy of
neck masses in postoperative management of patients with thyroid
cancer. Radiology 1988;168:769772.
86. Chen KTK, Rosai J. Follicular variant of thyroid papillary carcinoma.
A clinicopathologic study of 6 cases. Am J Surg Pathol
1977;1:123130.
87. Rosai J, Zampi G, Carcangiu ML. Papillary carcinoma of the thyroid.
A discussion of its several morphologic expressions, with particular
emphasis on the follicular variant. Am J Surg Pathol 1983;7:
809817.
88. Carcangiu ML, Zampi G, Pupi A, Castagnoli A, Rosai J.
Papillary carcinoma of the thyroid. A clinicopathologic study of 244
cases treated at the University of Florence, Italy. Cancer 1985;55:
805828.
89. Chen KTK, Rosai J. Follicular variant of thyroid papillary carcinoma:
a clinicopathologic study of six cases. Am J Surg Pathol
1977;1:123130.
90. Vickery AL. Thyroid papillary carcinoma. Pathological and
philosophical controversies. Am J Surg Pathol 1983;7:797807.
91. Hay ID. Papillary thyroid carcinoma. Endocrinol Metab Clin North
Am 1990;19:545576.
92. Hawk WA, Hazard JB. The many appearances of papillary carcinoma
of the thyroid. Cleve Clin Q 1976;43:207216.
93. Som PM, Brandwein M, Lidov M, et al. The varied appearance of
papillary carcinoma cervical nodal disease: CT and MR findings.
AJNR 1994;15:11291138.
94. Franssila KO, Ackerman LV, Brown CL, Hedinger CE. Follicular
carcinoma. Semin Diagn Pathol 1985;2:101102.
95. Roediger WEW. The oxyphil and C cells of the human thyroid gland.
Cancer 1975;36:17581770.
96. Bondeson L, Bondeson AG, Ljungberg O, Tibblin S. Oxyphil tumors
of the thyroid. Follow-up of 42 surgical cases. Ann Surg
1981;194:677680.
97. Gorman B, Charboneau JW, James EM, et al. Medullary thyroid
carcinoma: role of high-resolution US. Radiology 1987;162:147150.
98. Melvin KEW, Miller HH, Tashjian AH. Early diagnosis of medullary
carcinoma of the thyroid by means of calcitonin assay. N Engl J Med
1971;285:11151120.
99. Steiner AL, Goodman AD, Powers SR. Study of a kindred with
pheochromocytoma, medullary thyroid carcinoma, hyperparathyroidism, and Cushings disease: multiple endocrine neoplasia type 2.
Medicine 1968;47:371409.
100. Wolfe HJ, DeLellis RA. Familial medullary thyroid carcinomaand
C-cell hyperplasia. Clin Endocrinol Metab 1981;10:351365.
101. Kakudo K, Carney JA, Sizemore GW. Medullary carcinoma of
thyroid: biologic behavior of the sporadic and familial neoplasm.
Cancer 1985;55:28182821.
102. Busnardo B, Girelli ME, Simioni N, Nacamuilli D, Busetto E.
Non-parallel patterns of calcitonin and carcinoembryonic antigen
levels in the follow-up of medullary thyroid carcinoma. Cancer
1984;53:278285.
103. Dorr U, Wurstlin S, Frank-Raue K, et al. Somatostatin receptor
scintigraphy and magnetic resonance imaging in recurrent medullary
thyroid carcinoma: a comparative study. Horm Metab Res Suppl
1993;27:4855.
104. Lebouthillier G, Morais J, Picard M, et al. Tc-99m sestamibi and
other agents in the detection of metastatic medullary carcinoma of the
thyroid. Clin Nucl Med 1993;18(8):657661.
105. Krenning EP, Kwekkeboom DJ, Bakker WH, et al. Somatostatin
receptor scintigraphy with [111-In-DTPA-D-phe]- and [I-123-tyr]octreotide: the Rotterdam experience with more than 1,000 patients.
Eur J Nucl Med 1993;20:716731.
106. Dorr U, Sautter-Bihl ML, Heiner B. The contribution of somatostatin
receptor scintigraphy to the diagnosis of recurrent medullary
carcinoma of the thyroid. Semin Oncol 1994;21:4245.
107. Takashima S, Morimoto S, Ikezoe J, et al. CT evaluation of
anaplastic thyroid carcinoma. AJR 1990;154:10791085.
108. Ohnishi T, Noguchi S, Murakami N, et al. MR imaging in patients
with primary thyroid lymphoma. Am J Neuroradiol 1992;13(4):
11961198.
109. Haugen BR, Nawaz S, Cohn A, et al. Secondary malignancy of the
thyroid gland: a case report and review of the literature. Thyroid
1994;4(3):297300.
110. Czech JM, Lichtor TR, Carney JA, van Heerden JA. Neoplasms
metastatic to the thyroid gland. Surg Gynecol Obstet 1982;155:
503505.
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SECTION TWO
CLINICAL MANIFESTATIONS OF
PARATHYROID DISEASE
Hyperparathyroidism
Primary hyperparathyroidism is common, more common
in women, occurring in approximately 1 in 700 adults.8 In
most cases, patients are asymptomatic and the condition is
detected by routine screening blood tests for serum calcium
that individuals frequently have as part of their yearly
checkup. It occurs secondary to hypersecretion of PTH,
resulting in hypercalcemia. The causes of primary hyperparathyroidism include a single 1 to 3 cm parathyroid
adenoma (75% to 85% of cases), parathyroid hyperplasia
(10% to 15%), multiple parathyroid adenomas (2% to 3%),
and, rarely, parathyroid carcinomas (less than 1%).3, 911
Solitary adenomas vary widely in size, being very small
(less than 1 cm) as well as very large (several centimeters).
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FIGURE 40-40
are identified prior to surgery.3, 1214 Importantly, preoperative imaging in many cases has allowed the surgeon to treat
hyperparathyroidism successfully with only a unilateral
neck exploration.14, 15
Nonetheless, there are clearly certain situations in which
all would agree that imaging plays a very useful role. This
includes high-risk surgery patients where imaging may
permit the surgeon to resect the abnormal gland with only a
unilateral neck exploration. Alternatively, percutaneous
injection of absolute ethanol to ablate adenomas may be
performed under ultrasound guidance in patients who are
poor surgical candidates due to underlying medical illness.16, 17 The success of treatment is monitored with serum
calcium levels, which are followed until levels approach
near-normal values. Also, when hyperparathyroidism recurs
following surgery, imaging is indicated, as ectopic glands
are prevalent in this group of patients.
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There are also secondary and tertiary forms of hyperparathyroidism. Secondary hyperparathyroidism occurs in patients with long-standing renal failure leading to changes in
calcium metabolism, which in turn results in enlargement of
the parathyroid glands. In tertiary hyperparathyroidism,
hypercalcemia occurs as a sequela of secondary hyperparathyroidism due to the autonomous secretion of PTH from
chronically overstimulated parathyroid glands.
Hypoparathyroidism
Hypoparathyroidism is mainly a functional clinical disorder characterized by hypocalcemia and hyperphosphatemia secondary to a deficiency of PTH. The clinical
manifestation may be subtle and include facial contractions
brought on by tapping the facial nerve (Chvosteks sign), or
carpal contractions initiated by applying a blood pressure
cuff (Trousseaus sign). Hypoparathyroidism may be acute
and transient, usually following parathyroid or thyroid
surgery. Chronic hypoparathyroidism may be iatrogenic
(surgery), developmental (agenesis is rare), autoimmune,
infiltrative (secondary to cancers, amyloid, etc.), or part of a
group of disorders called pseudohypoparathyroidism in
which there is a resistance in the kidneys and skeleton to the
physiologic effects of PTH. There is a group of patients
that exhibit the characteristic phenotypical appearance of
pseudohypoparathyroidism (short, round facies, brachydactyly), but lack the unresponsiveness to PTH (normal calcium
and phosphate levels). These patients are said to have
pseudopseudohypoparathyroidism.
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2163
FIGURE 40-41
A pitfall in Tc-99m sestamibi scintigraphy is that thyroid lesions may concentrate sestamibi
similarly to parathyroid adenomas. A, Sestamibi scan shows increased activity in the right lobe of the thyroid gland.
B, Transverse ultrasound image reveals a well-demarcated mass in the thyroid (curved white arrows) that at surgery
was found to be a thyroid adenoma, as well as a rounded mass hypoechoic to and posterior to the thyroid that was a
parathyroid adenoma (straight arrows). J, Jugular vein; C, carotid artery.
mediastinum. This method offers superior soft-tissue discrimination and is more sensitive than CT for identifying
parathyroid adenomas. MR imaging should be performed on
a high field strength system. Accuracy may be improved and
artifacts related to heart motion reduced by using cardiac
gating. The imaging sequences utilized should include axial
T1- and T2-weighted 4 to 5 mm thick images extending
from the skull base through the mediastinum.38 The
administration of intravenous contrast material (gadolinium)
can increase lesion conspicuity.
The appearance of adenomas on MR imaging is
variable.39 Usually, adenomas are iso- to hypointense
compared to the thyroid gland on T1-weighted images, and
they are usually hyperintense on T2-weighted images. They
may enhance avidly following intravenous gadolinium
administration (Fig. 40-43). Some lesions with dense
cellularity may be iso- to hyperintense compared to muscle
on T1-weighted images and isointense on T2-weighted
images (Fig. 40-44). It is uncommon for an adenoma to be
hypointense on T2-weighted images. Pitfalls in detection of
parathyroid adenomas on MR imaging include misinterpretation of enlarged cervical lymph nodes for adenomas,38
large cervical ganglia, and a multiplicity of ectopic sites.39
Distinction between abnormal gland and vessel is less of a
problem with MR imaging due to its ability to readily
identify vascular structures (flow voids). MR imaging has a
reported accuracy of over 90%.40
Nuclear Scintigraphy
Nuclear scintigraphy to identify parathyroid adenomas
may be performed with several radionuclides including
thallium-201 (Tl-201)/Tc-99m pertechnetate subtraction
scanning, Tc-99m sestamibi subtraction imaging with I-123
(Fig. 40-45) or Tc-99m pertechnetate, or Tc-99m sestamibi
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2165
FIGURE 40-45 Parathyroid adenomas detected in two different patients by Tl-201/Tc-99m pertechnetate
subtraction imaging (A to C) and by Tc-99m sestamibi subtraction imaging with I-123 (D). A, Tc-99m pertechnetate
concentrated within the thyroid gland. B, Tl-201 concentrated within thyroid and parathyroid glands. C, Computer
techniques allow technetium concentrated in the thyroid gland to be subtracted from thallium that accumulates
within both thyroid and parathyroid tissue. After thyroid subtraction, a parathyroid adenoma is noted as a focus of
increased thallium uptake (arrows). D, Tc-99m sestamibi subtraction imaging with I-123 shows an adenoma below
the inferior pole of the left lobe of the thyroid gland. (Courtesy of Dr. Joseph Sam, Department of Radiology,
Nuclear Medicine Division, University of Pennsylvania Medical Center.)
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Chapter 40
2167
FIGURE 40-46 Ectopic parathyroid adenoma. A, Delayed image from a sestamibi scan shows increased uptake
in a surgically proven ectopic parathyroid adenoma in the superior mediastinum (arrow). B, Enhanced chest CT scan
shows the corresponding adenoma in the anterior mediastinum (arrow).
reoperation is useful despite the cost.11, 71 When preoperative imaging is performed, the success rate of surgery is
approximately 80% to 90% compared to 65% when imaging
is not performed prior to reoperation.11 In reoperations, the
sensitivity of ultrasonography, CT, MR imaging, and
scintigraphy is quite variable.4, 11, 32, 7274
One of the major differences in imaging the patient who
has failed prior surgery for detection of a parathyroid
adenoma is that scar tissue in the operative bed in the
perithyroidal region makes image interpretation as well as
anatomic detection at surgery more difficult. As with
cross-sectional imaging at initial surgery, lymphadenopathy may be mistaken for an adenoma. Because the
incidence of false-positive examinations caused by lymphadenopathy is lowest with nuclear imaging,4 sestamibi
scintigraphy as a single study is probably the most accurate
and cost-effective means to detect parathyroid adenomas.
However, because of the increased surgical risk in cases of
reoperation including vocal cord paralysis,20 as well as the
distortion of anatomic landmarks due to prior surgery, many
surgeons believe that a functional scintigraphic study
combined with an anatomic cross-sectional examination
(MR imaging is less likely than CT and ultrasound to
mistake a lymph node for an adenoma)4 is warranted, as it
provides the most accurate means of detecting parathyroid
tissue despite the fact that it is not the most cost-effective
approach. In general, MR imaging in combination with
sestamibi scintigraphy allows accurate detection of parathyroid tissue.62, 74, 75
I-123 or Tc-99m pertechnetate and Tc-99m sestamibi
subtraction images may increase the sensitivity of ectopic
parathyroid adenoma detection in cases of failed initial neck
explorations.76 Finally, the sensitivity of sestamibi imaging
in patients who require repeat surgery may be increased if
the interval between initial surgery and imaging is extended
Parathyroid Hyperplasia
Chief-cell parathyroid hyperplasia accounts for hyperparathyroidism in up to 15% of patients and may be
associated with familial hyperparathyroidism or MEN
syndromes.78, 79 MEN is a spectrum of hereditary (autosomal dominant) conditions characterized by two or more
hyperfunctioning endocrine tumors. MEN type I is associated with primary hyperparathyroidism, pancreatic islet cell
tumors, and anterior pituitary neoplasms.8082 Primary
hyperparathyroidism, which is usually multiglandular, is the
most common clinical presentation. MEN type IIA is
characterized by pheochromocytoma, medullary thyroid
cancer, and hyperparathyroidism.8083 The hyperparathyroidism of MEN type IIA is also multiglandular but is less
severe than that of MEN type I.
Chief-cell hyperplasia accounts for the majority of cases
of parathyroid hyperplasia, although uncommonly, clearcell hyperplasia may occur. Clear cells are chief cells with
an abundant amount of cytoplasmic glycogen.1 Histologically, there are numerous chief cells, occasional oxyphil
cells, and sparse adipose tissue. Usually all of the
parathyroid glands are enlarged, although usually not to
significant degrees.26, 84 Infrequently, one gland is disproportionately enlarged, and as a result may be mistaken
intraoperatively for an adenoma.
Treatment of primary parathyroid hyperplasia is removal of most if not all parathyroid tissue, with or
without autotransplantation to the forearm.30, 78 Parathyroid
hyperplasia is difficult to evaluate with any imaging
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Parathyroid Carcinoma
FIGURE 40-47 Parathyroid carcinoma invading the airway. Unenhanced axial T1-weighted MR image shows a poorly defined soft-tissue
mass (M ) just below the inferior pole of the left lobe of the thyroid gland.
The fat plane between this mass and the esophagus (e) is obliterated, and
there is extension into the left lateral wall of the adjacent airway (A ).
Parathyroid carcinoma is an unusual cause of hyperparathyroidism, accounting for less than 2% of all cases.
However, hyperparathyroidism accounts for the clinical
presentation of approximately 85% of all parathyroid
carcinomas.1 Patients usually have the typical symptoms
associated with hypercalcemia. In addition, because these
tumors are frequently large, many patients may have a
palpable neck mass at presentation. Grossly, parathyroid
carcinomas tend to be large (over 10 g), and histologically
are noted to have tumor cells with mitotic figures admixed
with fibrous tissue, as well as capsular and vascular
invasion.86
Parathyroid carcinomas have no characteristic imaging
features and may not be distinguishable from adenomas or
other soft-tissue masses. Regional cervical and mediastinal
lymph node metastases may occur in up to one third of
FIGURE 40-48
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Chapter 40
Parathyroid Cyst
Parathyroid cysts, like adenomas, most commonly arise
in the inferior parathyroid glands (65% of cases), and 95%
of these cysts occur below the level of the inferior thyroid
border. They are rare in children, more common in women,
and typically present in the fourth to fifth decades of life.1, 90
They are usually large (1 to 4 cm).
Parathyroid cysts represent only 0.6% of all thyroid and
parathyroid lesions. Nonfunctioning cysts account for the
majority of cases and present at a mean age of 43.3 years.
Functioning cysts account for 11.5% to 30% of the cases, are
more common in men, and occur at a mean age of 51.9
years.
The origin of parathyroid cysts is unclear. They may arise
from pharyngeal pouch remnants or they may be acquired.
Proposed acquired etiologies include degeneration of parathyroid adenomas into cysts and enlargement or coalescence
of parathyroid microcysts.
Similar to their appearance at gross pathology, on
imaging they are usually large and unilocular and have
variable MR imaging and CT characteristics, depending on
their protein content (Fig. 40-48).90 They may be difficult to
distinguish from cystic or necrotic lymph nodes or from
cysts derived from other sources such as solitary thyroid
cysts and cervical thymic cysts.
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