Transcript giant cell thyroiditis

Painful thyroid
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acute pyogenic or fungal thyroiditis
subacute thyroiditis
hemorrhage into a cyst
Acute hemorrhagic degeneration in a
nodule,
Hashimoto’s disease with painful
recurrence
thyroid malignancy(lymphoma)
amiodarone-induced thyroiditis or
amyloidosis
Thyroiditis
1- Acute:
Bacterial - Fungal
Radiation
Drugs
2- Subacute:
Viral - Mycobacterial
Silent thyroiditis
3- Chronic:
Autoimmune
Reidel
Trauma
Acute Thyroiditis
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Causes
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May occur secondary to
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68% Bacterial (S. aureus, S. pyogenes)
15% Fungal
9% Mycobacterial
Pyriform sinus fistulae
Pharyngeal space infections
Persistent Thyroglossal remnants
Thyroid surgery wound infections (rare)
More common in HIV
Acute Thyroiditis
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Symptoms
Thyroid pain and tenderness
 Fever
 Dysphagia
 Dysphonia
 Warm, tender, enlarged thyroid
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Acute Thyroiditis
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Diagnosis
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FNA to drain abscess, obtain culture
RAIU normal&TFT NL (versus decreased in
DeQuervain’s)
CT or US if infected TGDC suspected
Treatment
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High mortality without prompt treatment
IV Antibiotics
• Nafcillin / Gentamycin or Rocephin for empiric therapy
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Search for pyriform fistulae (BA swallow, endoscopy)
Recovery is usually complete
Subacute Thyroiditis
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Subacute
Most common cause of
painful thyroiditis
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20% of thyrotoxic cases
De Quervain’s thyroiditis
Giant cell thyroiditis
Pseudogranulomatous
thyroiditis
Subacute painful
thyroiditis
characteristic features
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well-developed follicular
lesion that consists of a
central core of colloid
surrounded by the
multinucleated giant cells,
hence the designation
giant cell thyroiditis.
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Colloid may be found in
the interstitium or within
the giant cells.
Sub Acute Thyroiditis
Viral (granulomatous)
Mumps,
coxsackie,
influenza,
adeno and
echoviruses
Subacute thyroiditis features
5:1 female predominance
 Age of onset 20-60y
 Prodrome (myalgias, fever, pharyngitis)
 Seasonal variation (correlation with enterovirus?)
 Fever/severe neck pain
 Dysphagia,odynophagia,hoaresness
 The pain, which is aggravated by turning the
head or swallowing, characteristically radiates to the ear,
jaw, or occiput and may mimic disorders arising in these areas.
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Usually low to absent titer of anti-TPO immunoglobulins
Thyroid storm – case reports
Subacute thyroiditis features
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On palpation, at least part of the thyroid is
slightly to moderately enlarged, firm, often
nodular, and usually exquisitely tender.
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One lobe is frequently being more severely
affected than the other, and the symptoms may
be truly unilateral.
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The overlying skin may be warm and
erythematous.
Subacute Thyroiditis
DeQuervain’s, Granulomatous
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FNA may reveal multinuleated
giant cells or granulomatous
change.
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Course
Pain and thyrotoxicosis (3-6
weeks)
 Asymptomatic euthyroidism
 Hypothyroid period (weeks to
months)
Recovery (complete in 95% after
4-6 months)
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2-9% with recurrent disease
5% residual hypothyroidism
Clinical Course of Sub Acute
Thyroiditis
Subacute Thyroiditis
DeQuervain’s, Granulomatous
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Diagnosis
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Elevated ESR usually>100
Elevated/NL CBC
Anemia (normochromic, normocytic)
Low TSH, Elevated T4 > T3, Low anti-TPO/Tgb
Low RAI uptake (same as silent thyroiditis)
Treatment
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NSAID’s and salicylates.
Oral steroids in severe cases
Beta blockers for symptoms of hyperthyroidism, Iopanoic acid
for severe symptoms
PTU not indicated since excess hormone results from leak
instead of hyperfunction
Symptoms can recur requiring repeat treatment
Treatment: Subacute Thyroiditis
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large doses of aspirin (e.g., 600 mg every 4–6 h) or NSAIDs
marked local or systemic symptoms, glucocorticoids usual
starting dose is 40–60 mg prednisone, depending on severity.
The dose is gradually tapered over 6–8 weeks, in response to
improvement in symptoms and the ESR.
If a relapse occurs during glucocorticoid withdrawal, treatment
should be started again and withdrawn more gradually. In these
patients, it is useful to wait until the radioactive iodine uptake
normalizes before stopping treatment.
monitoring every 2–4 weeks using TSH and unbound T4 levels.
Symptoms of thyrotoxicosis improve spontaneously but may be
ameliorated by -adrenergic blockers.
antithyroid drugs play no role in treatment of the thyrotoxic
phase. Levothyroxine replacement may be needed if the
hypothyroid phase is prolonged, but doses should be low enough
(50 to 100 g daily) to allow TSH-mediated recovery.
Patient’s follow up
11.3.92
T4:5.3
 T3:81
 TSH:2.3
 ESR:4
 FBS:107
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Thank You for Your Attention
Thyroid nodule
Risk factors for cancer:
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Age <15, > 45
Male sex
Hx of radiation ( up to 5% of patients develop Ca)
Solitary thyroid nodule + h/o radiation = 40% will
have Ca
Family Hx or h/o diseases associated with thyroid
Ca: Cowden’s and Gardner syndromes, FAP, Pheo
and Hyperparathyroidism
Size > 4 cm
Prior h/o thyroid Ca
Thyroid nodule
Sign of malignancy:
 Rapid growth
 Hard nodule
 Fixated
 Vocal cord paralysis
 Enlarged lymph nodes
 Family h/o thyroid Ca
 Symptoms of invasion
 All - 71% risk of malignancy
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Dx of follicular neoplasm on FNA:
NCCN Practice Guidelines 2003
J. Hamming. Arch Intern Med 1990
R. Wein, Otolaryngology Clinics of NA 2005
20% thyroid Ca
US signs of
malignancy
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Microcalcifications
Solid nodule / marked
hypoechogenicity
Irregular margins
Absence of a
hypoechoic halo around
the nodule
Lymphadenopathy and
local invasion of
adjacent structures
High vascularity on
Doppler flow
Benign
nodule
Radioactive Iodine Uptake
(RAIU)
• A small amount of 131I is given orally, and
4 & 24 hr dosimetry readings are taken
from the thyroid
• Normal range: ~5-30%
• Increased RAIU
 Graves Disease
 Toxic Multinodular Goiter
 Thyroid Adenoma
• Decreased RAIU
 Subacute or Silent Thyroiditis
 Iodine-Induced
 Factitious
Ultrasonography
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Findings suggestive of malignancy:
No Presence of halo
 Irregular border
 Presence of cystic components
 Presence of calcifications
 Heterogeneous echo pattern
 Extrathyroidal extension
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No findings are definitive
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Silent Thyroiditis
Post-partum Thyroiditis
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Postpartum
thyroiditis
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2-21% of
pregnancies
Can occur up to one
year post partum
Usually transient
and returns to
euthyroid state
Treat
• Hypothyroidism
• Symptoms with
‘hyperthyroidism’
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Presence of TPO
AB increases risk
of long term
hypothyroidism
Silent Thyroiditis
Post-partum Thyroiditis
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Silent thyroiditis is termed post-partum thyroiditis if it
occurs within one year of delivery.
Clinical
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Diagnosis
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Hyperthyroid symptoms at presentation
Progression to euthyroidism followed by hypothyroidism for
up to 1 year.
Hypothyroidism generally resolves
May be confused with post-partum Graves’ relapse
Treatment
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Beta blockers during toxic phase
No anti-thyroid medication indicated
Iopanoic acid (Telopaque) for severe hyperthyroidism
Thyroid hormone during hypothyroid phase. Must withdraw
in 6 months to check for resolution.
Chronic Thyroiditis
Hashimoto’s
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Autoimmune
Initially goiter later
very little thyroid tissue
Rarely associated with
pain
Insidious onset and
progressionHashimoto’s
• Women 3.5/1000
• Men 0.8/1000
• Frequency increases
with age
• Familial history
• Associated with
autoimmune diseases
Hashimoto’s Thyroiditis
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Most common cause of goiter and hypothyroidism in the U.S.
Physical
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Lab studies
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Painless diffuse goiter
Hypothyroidism
Anti TPO antibodies (90%)
Anti Thyroglobulin antibodies (20-50%)
Acute Hyperthyroidism (5%)
Treatment
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Levothyroxine if hypothyroid
Triiodothyronine (for myxedema coma)
Thyroid suppression (levothyroxine) to decrease goiter size
• Contraindications
• Stop therapy if no resolution noted
Surgery for compression or pain.
Riedel’s Thyroiditis
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Insidious painless
Symptoms due to compression
Dense fibrosis develop
Usually no thyroid function impairment
Diagnosis
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Rare disease involving fibrosis of the thyroid glandMiddle aged women
Thyroid antibodies are present in 2/3
Painless goiter “woody”
Open biopsy often needed to diagnose
Associated with focal sclerosis syndromes (retroperitoneal, mediastinal, retroorbital, and sclerosing
cholangitis)
Treatment
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Resection for compressive symptoms
Chemotherapy with Tamoxifen, Methotrexate, or steroids may be effective
Thyroid hormone only for symptoms of hypothyroidism
Drug-Associated Thyroiditis
Most cases of thyroiditis associated with various therapeutic agents appear
to be caused by drug-induced exacerbation of underlying autoimmune
disease.
• Amiodarone
• IL-2, interferon-α,
• granulocyte/macrophage colony-stimulating factor (GM-CSF)
• lithium
• GnRH agonist leuprolide, but the pathophysiology is obscure.
Thyroiditis has been found in association with the use
of a multitargeting kinase inhibitor, sunitinib, in patients
with gastrointestinal stromal tumors or renal cell carcinoma
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exacerbations of Hashimoto’s disease may be difficult to
distinguish from subacute thyroiditis. Lack of elevation of the
erythrocyte sedimentation rate and high titers of
thyroid autoantibodies strongly suggest the former condition.
Acute pyogenic thyroiditis is distinguished by the
presence of a septic focus
elsewhere,bygreaterinflammatoryreaction in the tissues adjacent
to the thyroid, andby much greater leukocytic and febrile
responses .The RAIU and thyroid function are usually preserved
in acute pyogenic thyroiditis. Rarely, widespread infiltrating
cancer of the thyroid can manifest with aclinical and laboratory
picture almost indistinguishable from that of subacute thyroiditis.
Ultrasonography and fine-needle aspiration should be performed
if this is a consideration
Comparison of Thyroiditis
Characteristic
Silent thyroiditis
Subacute thyroiditis
Age of onset (yr)
5-93
20-60
Sex ratio (F:M)
2:1
5:1
Etiology
Autoimmune
Viral
Pathology
Lymphocytic infiltration
Giant cells, granulomas
Prodrome
Pregnancy
Viral illness
Goiter
Non-painful
Painful
Fever/malaise
No
Yes
TPO/thyroglobulin AB
High and rising
Low, absent or transient
ESR
Normal
High
RAIU
<5%
<5%
Relapse
Common
Rare
Permanent
hypothyroidism
Common
Infrequent