Subacute Thyroiditis

• Subacute thyroiditis (De Quervain's thyroiditis or granulomatous

thyroiditis) is an acute inflammatory disorder of the thyroid
gland most likely due to viral infection.
• A number of viruses, including coxsackievirus, and
adenoviruses, have been implicated, either by finding the virus
in biopsy specimens taken from the gland or by demonstration
of rising titers of viral antibodies in the blood during the course
of the infection.
• Pathologic examination reveals moderate thyroid enlargement
and a mild inflammatory reaction involving the capsule.
• Histologic features include destruction of thyroid parenchyma
and the presence of many large phagocytic cells, including giant
cells. Subacute thyroiditis is more common in the summer
months, in women, and in individuals who are HLA-Bw35
positive.
 Clinical Signs
• Subacute thyroiditis usually presents with fever, malaise, and
soreness in the anterior neck, which may extend up to the
angle of the jaw or toward the ear lobes on one or both sides
of the neck.
• Initially, the patient may have symptoms of hyperthyroidism,
with palpitations, nervousness, and sweats. There is no
ophthalmopathy.
• On physical examination, the gland is exquisitely tender, so
that the patient objects to pressure on it. There are no signs of
local redness or heat suggestive of abscess formation. Clinical
signs of thyrotoxicosis, including tachycardia, tremor, and
hyperreflexia, may be present.
 Laboratory findings
• Initially, FT4 and T3 are elevated, whereas serum TSH
and RAIU are extremely low. Because the thyroid
hormone levels in the blood are a reflection of
leakage of glandular hormonal stores, serum FT4
levels are elevated disproportionately to serum T3
levels.
• Thyroid autoantibodies are usually not detectable in
serum. As the disease progresses, FT4 and T3 drops,
TSH rises, and symptoms of hypothyroidism are
noted.
 Treatment
• In many cases, only symptomatic treatment is necessary (aspirin
or other nonsteroidal anti-inflammatory drugs). In severe cases
or in patients who do not respond to nonsteroidal agents, a
glucocorticoid such as prednisone, 20 mg three times daily for
7–10 days, may be necessary to reduce the inflammation.
• Beta-adrenergic blocking agents can be employed during the
hyperthyroid phase to treat bothersome symptoms of
hyperthyroidism.
• T4, 0.1–0.15 mg once daily, may be indicated during the
hypothyroid phase of the illness if hypothyroid symptoms are
present. T4 therapy may also prevent exacerbations of
inflammation due to elevated TSH levels.
 Chronic Thyroiditis
Hashimoto’s thyroidit
• Chronic thyroiditis (Hashimoto's thyroiditis, lymphocytic
thyroiditis) is the most common cause of hypothyroidism and
goiter. It is certainly the major cause of goiter in children and
young adults and is the cause of "idiopathic myxedema," which
represents an end stage of Hashimoto's thyroiditis, with total
destruction of the gland.
• Riedel's thyroiditis may be a very rare variant of Hashimoto's
thyroiditis, with extensive fibrosis extending outside the gland and
involving overlying muscle and surrounding tissues. Riedel's
struma presents as a stony-hard mass that must be differentiated
from thyroid cancer. It is also associated with fibrosis in other
parts of the body including the mediastinum and retroperitoneum
 Etiology & Pathogenesis
• Hashimoto's thyroiditis is thought to be an immunologic
disorder in which lymphocytes become sensitized to
thyroidal antigens and autoantibodies are formed that
react with these antigens (see Thyroid Autoimmunity,
above). In Hashimoto's thyroiditis, the three most
important thyroid autoantibodies are thyroglobulin
antibody, TPO Ab, and TSH-R blocking antibody. During
the early phases of Hashimoto's thyroiditis,
thyroglobulin antibody is markedly elevated, and TPO Ab
is slightly elevated. Later, thyroglobulin antibody may
disappear, but TPO Ab is present for many years
 Symptomps and Signs
• Hashimoto's thyroiditis usually presents with
goiter in a patient who is euthyroid or has mild
hypothyroidism. The female: male sex
distribution is about 4:1. The process is
painless, and the patient may be unaware of
the goiter unless it becomes very large. Older
patients may present with severe
hypothyroidism with only a small, firm
atrophic thyroid gland (idiopathic myxedema).
 Laboratory findings
• Circulating thyroid hormone levels are usually
normal or low, and if low, TSH will be elevated.
• The most striking laboratory finding is the high
titer of autoantibodies to thyroidal antigens in
the serum. Serum tests for either
thyroglobulin antibody or TPO Ab are positive
in most patients with Hashimoto's thyroiditis.
 Complications
• The major complication of Hashimoto's
thyroiditis is progressive hypothyroidism. Most
patients with Hashimoto's thyroiditis initially
have a small goiter and "subclinical
hypothyroidism," which is defined as normal
serum levels of FT4 and T3, but mildly elevated
serum TSH levels.
 Complications
• Rarely, a patient with Hashimoto's thyroiditis
may develop lymphoma of the thyroid gland.
Although the etiology of thyroid lymphoma is
unknown, Hashimoto's thyroiditis is a definite
risk factor.
• Thyroid lymphoma is characterized by rapid
growth of the gland despite continued T4
therapy; the diagnosis of lymphoma must be
made by surgical biopsy.
 Treatment
• The indications for treatment of Hashimoto's thyroiditis are
goiter or hypothyroidism; a patient with a positive thyroid
antibody test alone does not require therapy.
• Surgery is rarely indicated for Hashimoto's thyroiditis but
occasionally is performed if a goiter does not regress and
continues to cause compressive symptoms.
• The treatment of subclinical hypothyroidism is a matter of
debate but is often instituted because of mild symptoms;
positive antithyroid antibody titers, which predicts a high
chance of progression to hypothyroidism over time.
• Sufficient T4 is given to normalize TSH and allow regression of
the goiter.