Chapter 19. Acute and Subacute Thyroiditis
John H. Lazarus, M.D., Professor of Medicine, Llandough
Hospital, Cardiff, Wales
Revised September 2009
The diagnostic term thyroiditis includes a group of inflammatory or
inflammatory-like conditions. The terminology that has been employed is
confusing, and no classification is ideal. We prefer the following
nomenclature, which takes into account the cause when known.
1. Infectious thyroiditis, also referred to as either acute or chronic,
and which in fact may be either, along with the qualifying term
suppurative, nonsuppurative, or septic thyroiditis. It includes all
forms of infection, other than viral, and is caused by invasion of the
thyroid by bacteria, mycobacteria, fungi, protozoa, or flatworms.
The disorder is rare.
2. DeQuervain's thyroiditis, commonly known as subacute thyroiditis
but also termed subacute nonsuppurative thyroiditis,
granulomatous, pseudotuberculous, pseudo-giant cell or giant cell
thyroiditis, migratory or creeping thyroiditis, and struma
granulomatosa. This condition, most likely of viral origin, lasts for
a week to a few months, with a tendency to recur. The eponym was
selected because of its uncertain cause.
3. Autoimmune thyroiditis, commonly referred to as chronic,
Hashimoto's, or lymphocytic thyroiditis and also known as
lymphadenoid goiter and struma lymphomatosa. This indolent
disease usually persists for years and in the Western world is the
principal cause of non-iatrogenic primary hypothyroidism.
Nonspecific focal thyroiditis, characterised by local lymphoid cell
infiltration without parenchymal changes, may be a variant of the
autoimmune disease. The condition is covered in detail in Chapter
8. Another form of thyroiditis, also believed to be of autoimmune
cause, has recently been described. It has been variably referred to
as painless, silent, occult, subacute, subacute nonsuppurative, and
atypical (silent) subacute thyroiditis, as well as hyperthyroiditis,
transient thyrotoxicosis with low thyroidal RAIU and lymphocytic
thyroiditis with spontaneously resolving hyperthyroidism. There is
no agreement on an inclusive name. The features of this disease
entity overlap deQuervain's thyroiditis and Hashimoto's
thyroiditis. The clinical course, with the exception of a very high
erythrocyte sedimentation rate and pain in the thyroid are
indistinguishable from deQuervain's thyroiditis. Yet, histologically,
the condition cannot be differentiated from a milder form of
Hashimoto's disease. This condition often occurs in the postpartum
period and is also termed postpartum thyroiditis. All forms of
autoimmune thyroiditis are considered in Chapter 8.
4. Riedel's thyroiditis, another disorder of unknown etiology.
Synonyms include Riedel's struma, ligneous thyroiditis and
invasive fibrous or chronic sclerosing thyroiditis. This condition is
characterised by overgrowth of connective tissue which often
extends into neighboring structures.
5. Miscellaneous varieties of thyroid
inflammation or infiltration including local manifestations of a
generalized disease processes. Among these are sarcoid and
amyloid involvement of the thyroid. Radiation and direct trauma
to the thyroid gland may also cause thyroiditis.
The thyroid gland is remarkably resistant to infection. This has been
attributed to its high vascularity, the presence of large amounts of iodine in
the tissue, the fact that hydrogen peroxide is generated within the gland as a
requirement for the synthesis of thyroid hormone and its normal
encapsulated position away from external structures. However, in certain
situations, particularly in children (1,2-4), a persistent fistula from the
pyriform sinus may make the left lobe of the thyroid particularly susceptible
to abscess formation (4-10). Recurrent left-sided thyroid abscess has also been
reported due to a fourth branchial arch sinus fistula (11). In a review of 526
cases of congenital fourth branchial arch anomalies (11a) it was noted that
they presented with acute suppurative thyroiditis in 45% of cases. Acute
thyroiditis from a periapical abscess of an inferior molar has been reported
(11b). In the immuno-compromised host, fungal infection may occur (12-15).
Occasionally, acute bacterial suppurative thyroiditis occurs in children
receiving cancer chemotherapy (16). Rarely, infection will occur in a cystic or
degenerated nodule. As will be discussed, the principal differential diagnosis
is generally between acute, meaning infectious, and subacute, meaning post-
viral (non-infectious) inflammation of the gland.
Virtually any bacterium can infect the thyroid (Table 1). Streptococcus,
staphylococcus, pneumococcus, salmonella, klebsiella (17-19,19a,b),
bacteroides, t. pallidum, pasteurella spp (20), multocida (21) and m.
tuberculosis (22-25) have all been described. The subject has been extensively
reviewed (13,26,27). In addition, certain fungi, including coccidioides immitis,
aspergillus, actinomycosis, blastomycosis (28 30,30a), candida albicans,
nocardia (31), actinobacter baumanii (32) cryptococcus (33) and pneumocystis
(33a) have also been associated with thyroiditis. In the latter cases, the hosts
have often been immuno-compromised, either due to malignancy or to AIDS
(34, 35). Rarely acute suppurative thyroiditis is due to thyroid abscess with
deep neck infection. (35) Malignancy may also be associated with thyroid
abscess due to a fistulous connection (37) and a thyroid abscess due to
clostridium septicum is almost always associated with carcinoma of the colon
(38). Metastatic breast cancer has been described as presenting clinically with
acute thyroiditis (39). Recently, the role of diagnostic fine needle thyroid
aspiration has been emphasised, firstly as a factor in the cause of acute
suppurative thyroiditis with associated thyrotoxicosis in a patient with atopic
dermatitis (40) and also being causative in a case of secondary infection with
necrosis in a patient with papillary thyroid carcinoma (41) and an intrathyroid
abscess in a multinodular goiter which grew E. coli (42). Care should be taken
when performing FNAC in patients who may be susceptible to tracking of
infection into the thyroid.
Most commonly, however, especially in children, infection of the thyroid
gland is a result of direct extension from an internal fistula from the pyriform
sinus (4-6, 27, 43, 44). This tract is thought to represent the course of migration
of the ultimo branchial body from the site of its embryonic origin in the fifth
pharyngeal pouch (7). Careful histopathological studies of these fistulae have
demonstrated that they are lined by squamous columnar or ciliated
epithelium and occasionally form branches in the thyroid lobe (4, 6). In
addition, occasional cells positive for calcitonin have been found in the
fistulae and increased numbers of C-cells were noted in the thyroid lobe at the
point of termination of the tract. The predominance of acute thyroiditis in the
left lobe of the thyroid gland, particularly in infants and children, is explained
by the fact that the right ultimo branchial body is often atrophic and does not
develop in the human (as well as in other species such as reptiles). The reason
for this phenomenon is not known. Acute thyroiditis may involve a normal
gland,arise in a multinodular goiter (44a) or even Hashimoto’s thyroiditis . At
times, no source of infection can be demonstrated. The possibility of a
persistent thyroglossal duct should be considered for patients with midline
infections (45). Acute thyroiditis has arisen as the intial presentation of
juvenile systemic lupus erythematosus (45a) and has also occurred due to
septic emboli derived from infective endocarditis (45b).
Pathological examination reveals characteristic changes of acute
inflammation. With bacterial infections, heavy polymorphonuclear and
lymphocytic cellular infiltrate is found in the initial phase, often with necrosis
and abscess formation. Fibrosis is prominent as healing occurs. In material
obtained by fine needle aspiration, the infectious agent may be seen on a
gram, acid fast or appropriate fungal stains (5).
Although acute thyroiditis is quite rare (about 2 patients per year in a large
tertiary care hospital), cases of suppurative thyroiditis are increasing due to
the higher incidence of immunocompromised patients. It may be somewhat
more common in the pediatric age group, although it is still quite unusual.
The dominant clinical symptom is pain in the region of the thyroid gland
which may subsequently enlarge and become hot and tender. The patient is
unable to extend the neck and often sits with the neck flexed in order to avoid
pressure on the thyroid gland. Swallowing is painful. There are usually signs
of infection in structures adjacent to the thyroid, local lymphadenopathy as
well as temperature elevation and, if bacteremia occurs, chills. Gas formation
with suppurative thyroiditis has been noted (46). Symptoms are generally
more obvious in children than in adults. Adults may present with a vague
slightly painful mass in the thyroid region without fever, which may raise the
possibility of a malignancy. Suppurative thyroiditis may even spread to the
chest producing necrotizing mediastinitis and pericarditis in the absence of a
pyriform sinus fistula (36). It may occur more commonly in the fall and winter
following upper respiratory tract infections.
In general, there are no signs or symptoms of hyper- or hypothyroidism.
However, exceptions to both have been reported particularly if the thyroiditis
is generalized, such as occurs with fungal processes (33) or mycobacterial
infections. At times, even in patients with bacterial thyroiditis, destruction of
the thyroid gland is sufficient to release thyroid hormone in amounts
sufficient to cause symptomatic hyperthyroidism (21, 22). The adult thyroid
gland contains approximately 600 ug of T4/g (47). Given a typical 15 to 20 g
gland, sufficient hormone can be released to cause transient thyrotoxicosis.
Pain in the anterior neck will usually lead to a consideration of the possibility
of thyroiditis. Since the major differential diagnosis will lie between acute
suppurative thyroiditis and subacute thyroiditis, it is critical to compare the
history, physical, and particularly laboratory data in these two conditions (see
Table3). In general, the patient with acute thyroiditis appears septic, has
greater and more localized pain in the thyroid gland, may have an associated
upper respiratory infection, has lymphadenopathy and may be immuno-
compromised. Localization of the tenderness to the left lobe should suggest
the possibility of an infection as should any erythema or apparent abscess
formation. The presence of an elevated white blood count with a shift to the
left would argue for infection, however, elevations in sedimentation rate are
common in both acute and subacute thyroiditis. As mentioned, patients with
bacterial thyroiditis are not hyperthyroid, but exceptions do occur. This is
more common, but, by no means universal in patients with subacute
Table 1 Microbiology of Acute Suppurative Thyroiditis
Gram negative bacilli
Depending on the age and clinical circumstances, one may wish to proceed
withinvasive or non-invasive studies. The most discriminating tests for
recognizing a difference between the two conditions are either an iodine
uptake or scan showing a very low value in subacute thyroiditis with a
normal value found in the patient with localized bacterial thyroiditis (27). If a
thyroid ultrasound shows a localized process, a needle aspiration can be
performed. This will be definitive. A CT scan may be useful in identifying the
location of the abscess, but this is required only in unusual situations (48).
Gallium scans are sometimes performed in the course of an evaluation for a
fever of unknown origin. Localization of gallium to the thyroid gland would
be a very useful finding confirming thyroid inflammation as the source of the
problem. If an infectious process is identified, particularly of the left lobe of a
younger individual, then a barium swallow should be performed with
attention to the possibility of a fistulous tract located on the left side between
the pyriform sinus and the thyroid gland. During a CT scan procedure the
patient can be asked to blow into a syringe which may help to identify a
piriform sinus fistula (49.A ‘light guided procedure’ to visualize the tract may
also help (49a). In general bacterial infections tend to be localized whereas the
post viral subacute thyroiditis is more often generalized, although
intermediate conditions can certainly exist.
Occasionally, pain from an infectious process elsewhere in the neck will
present as anterior neck tenderness. For example, a retropharyngeal abscess
may present with typical symptoms of acute thyroiditis. The thyroid gland,
however, will have a normal uptake, be normal on scan, and only on CT scan
will the retropharyngeal abscess be recognized. The tendency for the pain of
thyroid inflammation to be referred to the throat or ears should be kept in
mind, although recognition of the anatomic source of the problem is usually
not such a difficult issue in patients with acute thyroiditis due to their
localized symptoms. While patients with tuberculosis or parasitic infections
tend to have a more indolent course, these infections can present with acute
symptoms and this possibility should be considered if the epidemiology is
consistent. For example, thyroidal echinococcosis occurs in countries in which
this parasite is endemic (50). Trypanosomiasis of the thyroid has also been
The diagnosis and choice of antibiotic therapy are often aided by microscopic
examination and appropriate staining of a fine needle aspirate. The procedure
is best done under ultrasound guidance so that the source of the specimen is
identified. It may also serve as a mechanism for drainage of an abscess and
can be repeated to facilitate healing. Some abscesses will require surgical
exploration and drainage. The choice of therapy will also depend on the
immune status of the patient. Systemic antibiotics are required for severe
infections. Candida albicans thyroiditis can be treated with amphotericin B
and 5 fluconazol 100 mg daily. The proper treatment of an acute thyroiditis in
children generally requires the surgical removal of the fistula (4-6).
Combining this with partial thyroidectomy may further decrease the
recurrence rate (11a). This almost always leads to a permanent cure of the
In some patients with thyroiditis, the destruction may be sufficiently severe
that hypothyroidism results (44a). Thus, patients with a particularly diffuse
thyroiditis should have follow-up thyroid function studies performed to
determine that this has not occurred. Surgical removal of a fistula or branchial
pouch sinus (51) is required to prevent recurrence.
Subacute thyroiditis, sometimes referred to as granulomatous or De
Quervain's thyroiditis, is a spontaneously remitting inflammatory condition
of the thyroid gland that may last for weeks to several months (27, 52, 53). It
has a tendency to recur. The gland is typically involved as a whole, and
thyroidal RAIU is much depressed. Transient hyperthyroxinemia, elevation of
the serum Tg concentration and the erythrocyte sedimentation rate and
sometimes the WBC during the early acute phase are characteristic if not
A cause can rarely be established. A tendency for the disease to follow upper
respiratory tract infections or sore throats has suggested a viral infection.
Earlier suggestions that the disease may represent a bacterial infection have
been disproven. An autoimmune reaction is also unlikely. The development
during the illness of cell-mediated immunity against various thyroid cell
particulate fractions or crude antigens appears to be related to the release of
these materials during tissue destruction (54, 55).
Although the search for a viral cause has usually been unrewarding, a few
cases seem to be due to the virus that causes mumps (52, 56). The disease has
occurred in epidemic form. High titers of mumps antibodies have been found
in some patients with subacute thyroiditis, and occasionally parotitis or
orchitis is associated with thyroiditis. The mumps virus has been cultured
directly from thyroid tissue involved by subacute thyroiditis. Although the
mumps virus seems to be one discrete etiologic factor, the disease has been
reported in association with other viral conditions including measles,
influenza, adenovirus infection, infectious mononucleosis (57), myocarditis,
cat scratch fever, and coxsackie virus (Figure 1) (58). Two comprehensive
studies (59, 60) failed to find evidence of enteroviruses in 27 patients and
Epstein-Barr virus or cytomegalo virus in 10 patients, respectively but a single
case report has implicated EB virus in a case of subacute thyroiditis with
typical clinical features (61) and cytomegalo virus has now been reported in
Figure 1. Viral antibody titers in subacute thyroiditis. The graph
shows serial viral antibody titers in 32 patients who had 4-fold
changes in the dilution of these antibodies. Only the single viral
antibody showing the greatest change in dilution during the
period of observation is depicted for each patient. The antibody
titers are characteristically high at the onset of the illness and
gradually diminish. (From Volpe et al,  with permission.)
Numerous attempts to culture viruses from cases not associated with mumps
have failed. Virus-like particles have been demonstrated in the follicular
epithelium of a single patient suffering form subacute thyroiditis (58).
However, viral antibody titers to common respiratory tract viruses are often
elevated in these patients. Since the titers fall promptly, and multiple viral
antibodies may appear in the same patient, the elevation probably is an
anamnestic response to the inflammatory condition. (Figure 1, above).As
stated in a recent review (62a) it seems that the thyroid could respond with
thyroiditis after invasion by a variety of different viruses but no single agent
is likely to be causative.
Histo-compatibility studies show that 72% of patients with subacute
thyroiditis manifest HLA-Bw35 (63). Familial occurrence of subacute
thyroiditis associated with HLA-B35 has been reported (6467). Thus, the
susceptibility to subacute thyroiditis is genetically influenced and it has also
been suggested that subacute thyroiditis might occur by transmission of viral
infection in genetically predisposed individuals (61). A reported association
between subacute thyroiditis and acute febrile neutrophilic dermatosis
(Sweet's syndrome) (68) may imply a common role for cytokines in both these
New treatments, particularly those in which there is manipulation of the
immune system, have led to the development of subacute thyroiditis (69).
Infusion of interleukin 2 caused hyperthyroxinemia with a low radioiodine
uptake in six patients who received this in combination with TNF or
interferon (70). The patients proceeded to pass through the pattern of
hyperthyroidism and transient hypothyroidism, with a re-establishment of
normal thyroid function typical of the patient with autoimmune painless
thyroiditis. However, none of the patients had detectable antithyroid
antibodies. This condition is thus intermediate between subacute lymphocytic
(painless) thyroiditis (Chapter 13) and subacute thyroiditis which is typically
painful. A patient who developed subacute thyroiditis after influenza
vacccination (71) suggests immune alteration as a contributary factor. In
patients with chronic hepatitis C studies following interferon therapy (IFN)
showed that a minority (15%) developed a destructive thyroiditis while others
had a mild elevation of TSH (70). IFN can exacerbate previous thyroid
autoimmunity and cause destructive thyroidal changes de novo. Subacute
thyroiditis has alsobeen noted in patients treated with combination therapy of
IFN plus ribavirin for this disease (72, 73), as well as during treatment of
hepatitis B with Interferon (74). Peginterferon alpha-2a has also been
reported to cause subacute thyroiditis (75) and the condition is seen in
Takayasu's arteritis suggesting an immune abnormality (76). On the other
hand, subacute thyroiditis has been reported in patients receiving long term
immunosuppressive therapy suggesting a minimal role for autoimmunity in
the condition (77, 78). Other reports of subacute thyroiditis for example with
renal cell carcinoma (79) or after gastric bypass (80) do not contribute to its
The thyroid gland may be adherent to its capsule or to the strap muscles but it
can usually be dissected free, a feature distinguishing subacute thyroiditis
from Riedel's thyroiditis. The involved tissue appears yellowish or white and
is more firm than normal.
The gland is enlarged, and the enlargement is usually bilateral and uniform,
but it may be asymmetrical, with predominant involvement of one lobe.
Although the lesion may extend to the capsular surface, it can also be
confined to the thyroid parenchyma and merely be palpable as a suspiciously
The macroscopic pathologic picture of subacute thyroiditis frequently bears a
striking resemblance to cancer. The lesion is firm to dense in consistency, pale
white in color, and has poorly defined margins that encroach irregularly on
the adjacent normal thyroid. Microscopically, one sees a mixture of subacute,
chronic, and granulomatous inflammatory changes associated with zones of
parenchymal destruction and scar tissue. Early infiltration with
polymorphonuclear leukocytes is replaced by lymphocytes and macrophages.
The normal follicles may be largely replaced by an inflammatory reaction, but
a few small follicles containing colloid remain (Fig. 2, below). Three
dimensional cytomorphological analysis of fine needle aspiration biopsy
samples from patients with subacute thyroiditis examined with scanning and
transmission electron microscopy has shown a loss of a uniform, honeycomb
cellular arrangement; variation in size and decrease or shortening of
microvilli in follicular cells together with the appearance of round or ovoid
giant cells (81). The most distinctive feature is the granuloma, consisting of
giant cells clustered about foci of degenerating thyroid follicles (Fig. 2). The
early literature contains accounts of tuberculous thyroiditis, a diagnosis
largely based on the granulomatous tissue reaction, from which the
descriptive but unfortunate term pseudotuberculous thyroiditis arose (82).
Data on the mechanism of inflammation and the pathogenesis of subacute
thyroiditis at the cellular level are sparse. However, expression of Bcl 1-2
family proteins in 11 patients with SAT suggests that apoptotic mechanisms
may be involved in the development of SAT (83). Growth factor rich
monocytes/macrophages (containing VEGF, beta FGF, PDGF and TGF beta 1)
are involved in the granulomatous stage (84). EGF is important in the
regenerative stage as it has mitogenic effects on the thyrocyte. VEGF and
betaFGF contribute to the angiogenesis at both these stages of the disease.
Factors influencing the severity of the acute phase response during the course
of SAT include serum interleukin -1 receptor antagonist which may have a
significant anti-inflammatory role (85; also, a decrease in TNF alpha results in
earlier resolution of experimentally induced granulomatous thyroiditis (86).
The role of TNF- related apoptosis-inducing ligand (TRAIL) in promoting
resolution of this condition is also being investigated (86a).
Mast cells play an important part in the repair process of thyroid tissue
affected by the disease via production of growth factors and biomolecules
which modulate thyroid folliculogenesis and angiogenesis (69).
Figure 2. Subacute thyroiditis. Note the discrete granulomas, with
giant cells, and the diffuse fibrosis (85 X).
Subacute thyroiditis is encountered infrequently, but each year a handful of
cases will be identified in a busy thyroid clinic. Woolner et al (82) collected
162 cases diagnosed on clinical grounds at the Mayo Clinic over a 5-year
period; during the same time, 1,250 patients with Graves' disease were seen.
Thus, the disease had approximately one-eighth the incidence of Graves'
disease in this clinic population. During an evaluation of subtypes of
hypothyroidism over a 4 year period in Denmark an incidence of subacute
thyroiditiis of 1.8% was found in a cohort of 685 patients with
hypothyroidism (88, 89). Although the disease has been described at all ages,
it is rare in children (89, 90). Female patients outnumbered male patients in a
ratio of 1.9-6:1, with a preponderance of cases in the third to fifth decades (26,
52, 82, 91, 92) and it has been noted as a rare cause of hyperthyroidism in
pregnancy (93). In 160 patients studied during 37 years at the Mayo Clinic an
age and sex adjusted incidence of 4.9 cases/100,000/yr was noted (91).
Characteristically, the patient has severe pain and extreme tenderness in the
thyroid region. A small minority of patients have been noted to present with
painless or minimally painful subacute thyroiditis following viral
symptomatology (94). These may be regarded as atypical subacute thyroiditis
patients but their natural history of the disease is not known. When the
symptom is difficulty in swallowing, the disorder may be initially mistaken
for pharyngitis. Transient vocal cord paresis may occur (95) At times, the pain
begins in one pole and then spreads rapidly to involve the rest of the gland
("creeping thyroiditis"). It may radiate to the jaw or the ears. Malaise, fatigue,
myalgia and arthralgia are common. A mild to moderate fever is expected,
and at times a high, swinging fever causes temperatures to rise daily above
104°F (40.0°C). The disease may reach its peak within 3 to 4 days and subside
and disappear within a week, but more typically, a gradual onset extends
over 1 to 2 weeks and continues with a fluctuating intensity for 3 to 6 weeks.
Several recurrences of diminishing intensity extending over many months
may be the unhappy fate of the patient.
The thyroid gland is typically enlarged two or three times the normal size or
larger and is tender to palpation, sometimes exquisitely so. It is smooth and
firm. Occasionally the condition may be confined to one lobe (96, 97).
Approximately one-half of the patients present during the first weeks of the
illness, with symptoms of thyrotoxicosis, including nervousness, heat
intolerance, palpitations, - even ventricular tachycardia (98), tremulousness,
and increased sweating. These symptoms are caused by excessive release of
thyroid hormone from the thyroid gland during the acute phase of the
inflammatory process. At least 2 cases of thyroid storm due to subacute
thyroiditis have been described (99, 100). As the disease process subsides,
transient hypothyroidism occurs in about one-quarter of the patients.
Ultimately thyroid function returns to normal and permanent
hypothyroidism occurs in less than 10 percent of the cases (26, 27, 52).
Occasionally the condition may be painless and present as fever of unknown
origin (101). Some clinical and laboratory features recorded in 2 recent series
of SAT are shown in Table 2 (101a,101b). Liver function test abnormalities are
found in half the patients and return to normal in a few months (101c).
TABLE 2. CLINICAL FEATURES OF SUBACUTE THYROIDITIS
Feature Japan Israel
Number 852 56
Females(%) 87 70
Season summer-autumn no effect
Recurrence 1.60% 9.00%
Temp >380 28.00%
Thyrotox symptoms 60.00%
Hypothyroid phase 55.00%
Labs-peak levels 1 week
Bilat hypoechogenicity 50.00% 70.00%
Disease duration (days)
ATA: Antithyroid antibodies. US: Thyroid ultrasound. --: no data
Data derived from refs 101a&b.
Table 3 provides a comparison between the clinical and laboratory findings of
patients with subacute and acute thyroiditis (27, 102-107). Laboratory
examination may disclose a moderate leukocytosis. A curious and striking
elevation of the erythrocyte sedimentation rate, at times above 100 mm/hr, or
serum C-reactive protein (108) is a useful diagnostic clue. Short of tissue
diagnosis, most helpful is the characteristic combination of elevated
erythrocyte sedimentation rate, high serum T4, T3, and TG concentrations in
the presence of low thyroidal RAIU, and an absent or low titer of circulating
TG antibodies. While the estimation of thyrotropin receptor antibodies
(TRAb) in a thyrotoxic patient may be clinically useful in Graves' disease
there have been reports of positive TRAb in patients with subacute thyroiditis
although the frequency of positivity is low (109-112). Mild anemia and
hyperglobulinemia may be present. The value of a 99m-Tc-pertechnetate
scintigraphy as a marker of disease actviity and severity has been noted (113).
Further imaging studies have shown diffuse increased uptake of Tc-99m
sestamibi in the thyroid region of patients in the acute phase (thyrotoxic) of
subacute thyroiditis suggesting increased perfusion; at the same time Tc-99m
pertechnetate uptake was markedly reduced. It is possible that Tc-99m
sestamibi uptake in the early phase may reflect the inflammatory process
associated with the disease (114). In the same patients color Doppler
ultrasonography showed an absence of vascularization in the acute phase and
its use in the differential diagnosis of unclear cases has been emphasised (115,
116). Subacute thyroiditis may obscure the coexistence of papillary carcinoma
in cases presenting with ultrasonographically diffuse hypoechoic areas (116a).
Subacute thyroiditis with thyrotoxicosis may also be distinguished from
Graves' hyperthyroidism by using T1- and T2- diffusion weighted magnetic
resonance imaging (117) although this investigation may not be available or
even desirable in all centers. Fine needle aspiration biopsy is often diagnostic
although patients are often alarmed at the prospect of this test due to the pain
in the thyroid. However FNA may be helpful in ruling out malignancy (116).
Table 3. Features Useful in Differentiating Acute Suppurative
Thyroiditis and Subacute Thyroiditis
Characteristic Acute Subacute
History Preceding upper respiratory 88% 17%
Fever 100% 54%
Characteristic Acute Subacute
Symptoms of thyrotoxicosis Uncommon 47%
Sore throat 90% 36%
Physical Painful thyroid swelling 100% 77%
on of the
Left side affected 85% not specific
Migrating thyroid Possible 27%
Erythema of overlying skin 83% not usually
Laboratory Elevated white blood cell 57% 25-50%
Elevated erythrocyte 100% 85%
Abnormal thyroid hormone 5-10% 60%
Alkaline phosphatase, Rare common
Characteristic Acute Subacute
Needle Purulent, bacteria or fungi ~100% 0
Lymphocytes, macrophages, 0 ~100%
some polys, giant cells
123I uptake low Uncommon ~100%
Radiologic Abnormal thyroid scan 92% —
Thyroid scan or ultrasound 75% —
helpful in diagnosis
Gallium scan positive ~100% ~100%
Barium swallow showing Common 0
CT scan useful Rarely not indicated
Clinical Clinical response to Transient 100%
Course glucocorticoid treatment
Incision and drainage 85% No
Recurrence following 16% No
Characteristic Acute Subacute
Pyriform sinus fistula 96% No
Modified from Szabo and Allen (27), see also Shabb & Solti (118)
A.S., a 46-year old woman, noted the onset of a tender, slowly enlarging
swelling in the low anterior neck in December. There was no antecedent
infection or virus-like syndrome. She was aware of associated increased
nervousness, mild tremor, increased sweating, and anorexia, without
alteration in weight. In January, increasing pain that radiated to the back of
her head and orbits necessitated medical consultation. A family history of
thyroid disease was not elicited.
On physical examination she appeared to be in pain, BP was 155/80, and pulse
112/min and regular. Clinically, she appeared to be euthyroid. The thyroid
gland was estimated to be 40 grams in weight and was tender, firm, and
slightly irregular. The remainder of the examination was non-contributory.
Laboratory data included an erythrocyte sedimentation rate of 58 mm/min,
FT4I of 16.1 m g/dl (normal, 3.6 to 9.3 m g/dl), TT4 level of 14.9 m g/dl (normal
4.2 to 9.4), and a Tg antibody titer of 1/40.
Figure 3 (below) shows a sequence of 125
I and Am scans obtained
throughout the course of her illness. On presentation, there was no 125I
uptake seen on thyroid scintiscan, with an RAIU of 1 percent. At the same
time, the 241Am scan showed virtually no stable iodine in the thyroid. A
241Am scan repeated in March showed continuing low 127I levels in the
thyroid, at which time the serum TT4 level was 1.7 mg/dl and the FT4I was 0.8
m g/dl. The 241Am scans on these two dates demonstrate mainly background
radiation scatter. With the resolution of her clinical syndrome over the next
few months, the results of the thyroid scans were seen to return to normal.
The result of the 125I scintiscan in June was completely normal, with an RAIU
of 20 percent, at which time her TT4 level and FT4I had returned to the
normal range. The 241Am scan 3 months later showed some reaccumulation
of 127I, but the stable iodine store was still reduced. The last 241Am scan 14
months after onset demonstrated total repletion of her thyroidal 127I stores.
At this time, the gland was normal in size (weight 20 g) and consistency.
Figure 3. Serial 125
I scintiscans and 241
Am fluorescent scans in a
patient during the course of subacute thyroiditis. The first two
fluorescent scans, done at a high sensitivity setting without
background subtraction, have much neck "background" but
demonstrate virtually no I in the thyroid. (From Rapoport et al,
 with permission.)
If subacute thyroiditis affects only one part of the thyroid gland, the serum T4
concentration and thyroidal RAIU may be entirely normal. A thyroid scan
will demonstrate failure of the involved areas of the gland to concentrate
iodide. When the thyroid is diffusely involved, which is more typical, a
dramatic disturbance in iodine metabolism is observed.
During the initial phase of the disease, the RAIU is depressed or entirely
absent and the concentrations of serum T4 and T3 are often elevated. Due to
the concomitant release of nonhydrolyzed iodoproteins from the inflamed
tissue, the serum T3 level is also high. During this phase the serum TSH level
is low, and the TSH response to TRH is suppressed (103) due to the high
levels of circulating thyroid hormone. Iodide that is collected and metabolized
by the gland is rapidly secreted because of the decreased ability to store
colloid (105). At this time, the involved tissue shows decreased but not
necessarily depleted stores of iodine, as determined by x-ray fluorescence
(102, 105). Administration of TSH usually fails to produce a normal increase
in RAIU. Evidently, thyroid cell damage reduces the ability of the gland to
respond to TSH. As the process subsides, the serum T4, T3, and TG levels
decline, but the serum TSH level remains suppressed. The normal
concentrations of SHBG in the hyperthyroid phase probably reflect the short
duration of exposure to increased thyroid hormone (120).
Later, during the recovery phase, the RAIU becomes elevated with the
resumption of the ability of the thyroid gland to concentrate iodide. The
serum T4 concentration may fall below normal; the TSH level may become
elevated. Usually after several weeks or months, all the parameters of thyroid
function return to normal (Fig.4). Restoration of iodine stores appears to be
much slower and may take more than a year after the complete clinical
remission (102, 105). In about 2% of patients subacute thyroiditis may trigger
auto-reactive B cells to produce TSH receptor antibodies, resulting in TSH
antibody associated thyroid dysfunction in some patients (112).
Figure 4. Thyroid function in a patient during the course of
deQuervain's (subacute) thyroiditis. During the thyrotoxic phase
(days 10 to 20), the serum TG concentration was greatly elevated,
the FTI was high, and TSH was suppressed; the erythrocyte
sedimentation rate was 86 mm/hr, and the thyroidal RAIU was 2
percent. The TG level and FTI declined in parallel. During the
phase of hypothyroidism (days 30 to 63), when the FTI was below
normal, a modest transient increase in the serum TG level occurred
in parallel with the increase in serum TSH. All parameters of
thyroid function were normal by day 150, 5 months after the onset
Diagnosis is usually not difficult. With an acutely enlarged, tender thyroid, an
RAIU near zero, and elevated serum T4 and Tg concentrations and ESR, the
diagnosis is almost certain. Circulating thyroid autoantibodies are absent or
the titer is low. Among the diagnostic alternatives, infectious thyroiditis must
be considered and the possibility of invading bacteria excluded (see Table 2).
The thyroid in Hashimoto's thyroiditis may be slightly tender and painful, but
this event is rare, and the typical disturbances in iodine metabolism and
erythrocyte sedimentation rate are rarely found. Hemorrhage into a cyst in a
nodular thyroid gland may be confused with subacute thyroiditis although
the condition may be associated with an autonomously functioning nodule
(119). Hemorrhage is usually more sudden and transient, a fluctuant mass
may be found in the involved region, and the erythrocyte sedimentation rate
is normal. Occasionally, subacute thyroiditis mimics hyperthyroidism in a
patient whose RAIU is suppressed by iodine. This event occurs particularly in
transient thyrotoxicosis induced by iodine (106). The sudden onset of
subacute thyroiditis, the presence of toxic symptoms without the typical signs
of long-term hyperthyroidism, the tender gland, the constitutional symptoms,
and the high erythrocyte sedimentation rate are helpful in making the
differentiation. In some instances, measurement of antibodies and thyroid-
stimulating immunoglobulins, and observation of the course of the illness
may be required to confirm the diagnosis.
The single disease entity that is probably most difficult to differentiate from
subacute thyroiditis is a variant of lymphocytic thyroiditis (107). This
condition is unrelated to iodine ingestion and most likely is a variant of
autoimmune thyroiditis. The patient presents with goiter, mild thyrotoxicosis,
and a low RAIU. The course of the disease is indistinguishable from that of
subacute thyroiditis and proceeds from a thyrotoxic phase through a
hypothyroid phase to spontaneous remission with normalization of thyroid
function. The goiter is typically painless, and there are no associated systemic
symptoms. This condition has been formerly confused with subacute (de
Quervain's) thyroiditis, whence come the misleading terms silent, painless, or
atypical subacute thyroiditis. The most helpful distinguishing features, short
of histologic examination of biopsy material, are the absence of pain and a
normal erythrocyte sedimentation rate. (See also Chapter 13.) Localized
subacute thyroiditis, with induration, mild tenderness, and depressed iodine
binding visualized on scan, can be very suggestive of thyroid cancer. Usually
the degree of pain and tenderness, elevated erythrocyte sedimentation rate
and leukocytosis, and remission or spread to other parts of the gland make
clinical differentiation possible. Gray-scale and color Doppler sonography
may be helpful in this situation (115, 121) or even magnetic resonance
imaging (117). The hypoechoic area can reflect the degree of inflammation
and thyroid hormone levels(117a). However, a fine needle aspiration is
required for a definitive differentation between these two processes (119).
In some patients, no treatment is required. However, for many, some form of
analgesic therapy is required to treat the symptoms of the disease until it
resolves. At times, this relief of symptoms can be achieved with non-steroidal
anti-inflammatory agents or aspirin. However, if this fails, as it often does
when the symptoms are severe, prednisone administration should be
employed (26, 52). Large doses promptly relieve the symptoms through non-
specific anti-inflammatory effects. Treatment is generally begun with a single
daily dose of 40 mg prednisone. After one week of this treatment, the dosage
is tapered over a period of 6 weeks or so. The relief of the tenderness in the
neck is so dramatic as to be virtually diagnostic of the problem as being due to
subacute thyroiditis. As the dose is tapered, most patients have no
recrudescence of symptoms, but occasionally this does occur and the dose
must be increased again. Alternatively oral cholecystographic agents (such as
sodium ipodate or sodium iopanoate) may be used safely and effectively for
the management of hyperthyroidism in these patients even when they have
relapsed after corticosteroid therapy (122). The recurrent rate of subacute
thyroiditis after cessation of prednisolone therapy is about 20% but no
difference has been found in routine laboratory data between recurrent and
non-recurrent groups of patients (123). Levothyroxine administration may be
useful in situations where the patient is not already hyperthyroid due to the
release of thyroidal contents into the circulation. It is thought that TSH
suppression will reduce the thyroid stimulation which might otherwise
prolong the inflammatory process. It is also necessary to administer thyroid
hormones, at least transiently, if the patient enters a phase of hypothyroidism
subsequent to the acute inflammation. TSH-suppressive doses of
levothyroxine should only be administered when there is evidence that
exacerbation of the condition occurs when TSH is present. Otherwise, the
return of thyroid function to normal, which presumably is facilitated by TSH,
may be prevented or delayed. During the recovery process, there may be a
marked but transient increase in the 24 hour radioactive iodine uptake which
can reach levels typical of Graves' Disease. This occurs prior to re-
establishment of normal thyroid function and should not be confused with
hyperthyroidism due to Graves' Disease. Surgical intervention is not the
primary treatment for subacute thyroiditis. Experience from the Mayo clinic
(124) has shown that if surgery is performed for a clinically indeterminate
thyroid nodule resection is safe and with low morbidity. Because of the
possibility of associated papillary cancer further cytological examination
should be performed in patients presenting with a persistent hypoechoic area
larger than 1 cm by ultrasonography (116a).
In 90% or more of patients, there is a complete and spontaneous recovery and
a return to normal thyroid function. However, the thyroid glands of patients
with subacute thyroiditis may exhibit irregular scarring between islands of
residual functioning parenchyma, although the patient has no symptoms. Up
to 10% of the patients may become hypothyroid and require permanent
replacement with levothyroxine. In a retrospective study of 252 patients with
SAT permanent hypothyroidism occurred in 5.9% and all these had bilateral
hypoechogeneic areas on thyroid ultrasound at initial presentation suggesting
that this may be a useful prognostic marker for the development of thyroid
dysfunction after SAT (124a). However, permanent hypothyroidism is
significantly less common in SAT compared to the outcome noted in
amiodarone induced thyrotoxicosis type 2 (the destructive thyroiditis) (125). It
is of interest that elevated levels of serum Tg may persist well over a year
after the initial diagnosis, indicating that disordered follicular architecture
and/or low grade inflammation can persist for a relatively long period (126).
In 1896 Riedel described a chronic sclerosing thyroiditis, occurring especially
in women, that tends to progress inexorably to complete destruction of the
thyroid gland and frequently causes pressure symptoms in the neck (127-129).
It is exceedingly rare. In the Mayo Clinic series (100) it occurred
approximately one-fiftieth as frequently as Hashimoto's thyroiditis. It is more
frequent in women (F:M 3.1:1) and is found most often in the 30- to 60 year
age group. The thyroid gland is normal in size or enlarged, usually
symmetrically involved, and extremely hard. Occasionally involvement may
be unilateral. Diagnostic confusion with sarcoma of the thyroid region has
been reported (131) and it may occur in a multinodular goiter mimicking
thyroid cancer (132). Although the etiology is unknown the disease may
develop in the course of subacute thyroiditis (133) and a case of concurrent
Riedel’s, Hashimoto’s and acute thyroiditis has been reported (133a). On
pathologic examination the gland is replaced by dense fibrosis in which are
scattered solitary follicular cells and occasional acini with small amounts of
colloid. The fibrosis binds the thyroid firmly to the trachea and the strap
muscles, from which it can be separated only with the greatest difficulty
(ligneous thyroiditis) (134). The fibrosis may compress the trachea or
esophagus. The disease may remain stable over many years, or it may
progress slowly and produce hypothyroidism. Dyspnea, dysphagia,
hoarseness, and aphonia are caused by the local pressure, and if there is
enough pressure on both recurrent laryngeal nerves, there may be stridor.
Sometimes the disease is asymptomatic and discovered only incidentally. The
pathologic process may advance to complete replacement of the gland, and
then symptoms and signs of hypothyroidism appear. Involvement of the
parathyroid glands by the fibrotic process may result in hypoparathyroidism
(135-139). Rarely, Riedel's thyroiditis may be associated with similar
fibrosclerotic processes in other areas, including the lacrimal glands, orbits
(140), parotid glands, mediastinum, lung, myocardium, retroperitoneal
tissues, and bile ducts in varying combinations in the syndrome of multifocal
fibrosclerositis (141, 142,142a). Fluorine-18 fluorodeoxyglucose [FDG]
positron emission tomographic images have shown metabolic activity in an
abdominal mass and increased glucose metabolism in the thyroid, probably
resulting from active inflammation involving lymphocytes, plasma cells and
fibroblast proliferation (143). FDG metabolic activity can also be used to
assess a patient's response to therapy (144). This mixture of inflammatory cell
infiltrate and fibrosis can also be visualised using dynamic magnetic
resonance imaging with gadpentate dimeglumine (145) and appropriate T1-
and T2- weighted images (146). Subcutaneous fibrosclerosis has also been
noted but it is very rare (147). The occurrence of cerebral sinus thrombosis
suggests that Riedel's thyroiditis may cause venous stasis, vascular damage,
and possibly hypercoaguability (148). The results of laboratory tests of
thyroid function are usually normal, but about one-third are hypothyroid.
The erythrocyte sedimentation rate is not elevated, as in subacute thyroiditis,
and there is no leukocytosis. Antithyroid antibodies are present in 67% of
reported cases (129) and a mixed population of B- and T-cells is present in the
thyroid, suggesting an autoimmune etiology or association. The B cell
proliferation has been shown to be polyclonal (149). The occurrence of
marked tissue eosinophilia and the extracellular deposition of eosinophil
granule major basic protein suggests a role for eosinophils and their products
in the development of fibrosis in Riedel's thyroiditis (150). Fibrosis may also
be related to the action of TGF beta 1, as seen in murine thyroiditis (151). The
manifestations of Riedel’s thyroiditis can be confusing as exemplified by a
patient who, over 18 months after biopsy proven Riedel’s thyroiditis,
developed hyperthyroidism, spontaneous primary hypoparathyroidism,
acute compressive neck symptoms requiring emergency isthmusectomy,
vocal cord paralysis, syncopal-like episodes, and Horner’s syndrome due to
compression of the right carotid sheath. This patient is under therapy with
glucocorticoids and tamoxifen (138).
Management of Riedel's Thyroiditis
Although there is no specific therapy for Riedel's thyroiditis, several
management strategies are available dependent on the clinical features of the
disease in the individual patient. Corticosteroid therapy has been found to be
effective in some cases (141,152-156), probably those with active
inflammation. Initial doses of up to 100mg per day of prednisolone have been
used but sustained improvement has been reported with lower doses of 15-60
mg per day (141). There are no controlled trials of steroid therapy in Riedel's
and although some patients obtain long term benefit after steroid withdrawal
(157) others may relapse (158). The reasons for this variation are unclear but
inflammatory activity and duration of disease may be relevant factors. In
those who fail to respond to steroid therapy or relapse after withdrawal
tamoxifen therapy should be tried. Three reports have described an
encouraging response with this agent, admittedly in only a small number of
patients (159-161). It is possible that tamoxifen acts in Riedel's by inhibition of
fibroblast proliferation through the stimulation of TGF beta. Combination
therapy with prednisolone and tamoxifen is also effective (162). There are no
data on effective therapy with other immunosuppressive agents.
As hypothyroidism is rare in Riedel's, thyroxine therapy is usually not
required and is not thought to influence the course of the disease. Surgical
intervention may be necessary to release the trachea or perform tracheotomy
in the case of severe stridor. Unilateral lobectomy has been performed for
unilateral disease (163) and larger resections should be considered in some
instances (164). It is recommended that surgical exploration and biopsy are
usually required to exclude malignancy which may be suspected at
RARE INFLAMMATORY OR INFILTRATIVE DISEASES
In addition to the varieties of thyroiditis already mentioned, which are
diseases specifically of the thyroid gland, generalized or systemic diseases
may also involve the thyroid gland (26). The lesions of sarcoid may appear in
the thyroid gland of patients with systemic sarcoidosis, and huge deposits of
amyloid occasionally causes goiter in amyloidosis. Amyloid goiter with
transthyretin activity has been reported (164a). Amyloid goiter may be readily
diagnosed by fine needle aspiration biopsy (165). Painless thyroiditis has
been noted in a woman with rheumatoid arthritis and secondary amyloidosis
infiltrating the thyroid gland (166). Radiotherapy for tonsillar carcinoma has
been reported to result in thyroiditis (167) and radiation during 131 I therapy
produces thyroiditis, which is occasionally symptomatic. This situation is
discussed in Chapters 11 and 18. Irradiation to the thyroid during therapy for
breast cancer or lymphoma can also induce hypothyroidism. Therapy should
be directed toward the primary disease rather than the thyroid, but
administration of thyroid hormone may be necessary if destruction of thyroid
tissue is sufficient to produce hypothyroidism. Finally, surgery to the neck
has been reported to cause thyroiditis but this is rare (168, 169).
The thyroid, like any other structure, may be the seat of an acute or chronic
suppurative or nonsuppurative inflammation. Various systemic infiltrative
disorders may leave their mark on the thyroid gland as well as elsewhere.
Infectious thyroiditis is a rare condition, usually the result of bacterial
invasion of the gland. Its signs are the classic ones of inflammation: heat, pain,
redness, and swelling, and special ones conditioned by local relationships,
such as dysphagia and a desire to keep the head flexed on the chest in order
to relax the paratracheal muscles. The treatment is that for any febrile disease,
including specific antibiotic drugs if the invading organism has been
identified and its sensitivity to the drug established. Otherwise, a broad-
spectrum antibiotic may be used. Surgical drainage may be necessary and a
search for a pyriform sinus fistula should be made, particularly in children
with thyroiditis involving the left lobe. Subacute (granulomatous) thyroiditis
is a more common and protracted disease that usually involves the thyroid
symmetrically. The gland is swollen and tender, and the systemic reaction
may be severe, with fever and an elevated erythrocyte sedimentation rate.
During the acute phase of the disorder, tests of thyroid function disclose a
diminished thyroidal RAIU and increased serum concentrations of T4, T3,
and Tg. The cause of this disease has been established in only a few instances
in which a viral infection has been the initiating factor. There may be repeated
recurrences of diminishing severity. Usually, but not always, the function of
the thyroid is normal after the disease has subsided. Subacute thyroiditis may
be treated with rest, non-steroidal anti-inflammatory drugs or aspirin, and
thyroid hormone. If the disease is severe and protracted, it is usually
necessary to resort to administration of glucocorticoids, but recurrence may
follow their withdrawal. Riedel's thyroiditis is a chronic sclerosing
replacement of the gland that is exceedingly rare. The process involves the
immediately adjacent structures, making any surgical attack very difficult.
The cause is unknown, and no treatment is available beyond resecting the
isthmus of the thyroid gland to relieve the symptoms of tracheal or
esophageal compression. Sarcoid may involve the thyroid, and amyloid may
be deposited in the gland in quantities sufficient to cause goiter. In all of these
diseases it may be necessary to give the patient levothyroxine replacement
therapy if the function of the gland has been impaired.
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