Thyroiditis

Thyroiditis is a catchall term used to describe a variety of conditions that have inflammation of the thyroid gland in common. It includes pathologies that cause an acute illness with severe thyroid pain (e.g., subacute thyroiditis and infectious thyroiditis) as well as conditions in which there is no clinically evident inflammation and the manifestations primarily reflect thyroid dysfunction or a goiter (e.g., painless thyroiditis and fibrous Riedel’s thyroiditis). The etiology of thyroiditis is varied and includes autoimmune inflammation (most common), bacterial or viral infection, and drug-induced reactions. The inflammation of the thyroid leads to a sequential pathologic process that can result in signs and symptoms of hyperthyroidism followed by signs and symptoms of hypothyroidism. The resulting damage can be temporary or permanent, and the treatment depends on the underlying cause.

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Etiology and Pathophysiology

Thyroiditis, or inflammation of the thyroid gland, has multiple etiologies, including autoimmune conditions, infectious agents, and iatrogenic causes. Each causative condition has a specific pathologic mechanism.

Table: Etiology and pathophysiology of thyroiditis
CategoryEtiologyPathophysiology
AutoimmuneHashimoto’s thyroiditis
  • Associated with HLA-DR3, DR4, and DR5
  • Thyroid peroxidase (TPO) and thyroglobulin (Tg) antibodies destroy the thyroid gland.
Painless, silent, or lymphocytic thyroiditis
  • Any patient with symptoms of mild hyperthyroidism for < 2 months with a small diffuse goiter or no enlargement
  • Considered a “milder” form of Hashimoto’s thyroiditis
  • Damage to follicular cells with lymphocytic infiltration
Postpartum thyroiditis
  • < 1 year after parturition or abortion
  • No thyroid enlargement or tenderness
  • Lymphocytic infiltration of the thyroid gland with the formation of germinal centers
  • Resolves spontaneously
Riedel’s thyroiditis
  • Primary fibrosing disorder
  • Dense fibrosis that replaces normal thyroid parenchyma with macrophage and eosinophil infiltration
InfectionsSubacute granulomatous thyroiditis (De Quervain syndrome)
  • Due to viral infections (usually mumps or coxsackievirus); often follows an upper respiratory infection
  • Strong association with HLA-B35
  • Damage to follicular cells
  • Formation of granulomas and fibrosis
Acute suppurative thyroiditis
  • Gram-positive or gram-negative bacteria enter via a fistula from the piriform sinus.
  • Bacteria spread hematogenously in immunocompromised patients.
Chronic suppurative thyroiditisUsually caused by Aspergillus or Pneumocystis in immunocompromised patients
IatrogenicDrug-induced
  • Amiodarone: structurally resembles thyroid hormone and contains iodine
  • Others: α-interferon, lithium, IL-2, and tyrosine
Radiation thyroiditis
  • Presents 5–10 days after radioactive therapy used to treat Graves’ disease, head and neck cancer, or lymphoma.
  • Stored triiodothyronine (T3) and thyroxine (T4) are released as rapid destruction of thyroid tissue occurs.

Clinical Presentation

  • Goiter → mass effect leading to:
    • Discomfort and/or globus sensation
    • Dysphagia
    • Dyspnea and/or stridor
    • Hoarseness
  • Specific signs and symptoms depend on the underlying cause:
    • Hashimoto’s thyroiditis: 
      • Initially asymptomatic
      • Painless, symmetrical goiter develops.
      • Transient hyperthyroidism followed by permanent hypothyroidism
    • Riedel’s thyroiditis: presents along with symptoms of tracheal compression
    • Subacute (De Quervain) thyroiditis: fever with a painful, enlarged and tender thyroid on palpation (goiter)
    • Suppurative thyroiditis: 
      • Sudden onset of neck pain, usually unilateral
      • Fever, dysphagia, and leukocytosis
  • Triphasic clinical course: presents in painless, postpartum, and subacute thyroiditis 
    • Thyrotoxicosis occurs owing to increased release of preformed/stored thyroid hormones and suppression of TSH and lasts 4–6 weeks.
    • As stores are depleted, and TSH is already suppressed, a hypothyroidism phase begins. This phase lasts 4–6 months.
    • TSH will subsequently rise and increase thyroid hormone production, leading to normalization of thyroid function. This phase lasts for several months after onset.

The triphasic clinical course of subacute thyroiditis:
Subacute thyroiditis usually presents initially with signs of hyperthyroidism as large amounts of thyroid hormones are released from the destroyed glandular tissue. Then, as storage runs out, thyroid hormone levels begin to drop and thyroid-stimulating hormone (TSH) rises to compensate. Eventually, months after the onset of the disease, hormonal levels stabilize into a euthyroid state.
RAI: radioactive iodine.

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Table: Manifestations of hypothyroidism and hyperthyroidism
ManifestationsHypothyroidismHyperthyroidism
Metabolic
  • Cold intolerance
  • Decreased sweating
  • Weight gain (lowered basal metabolic rate)
  • Hyponatremia due to lower free water clearance
  • Heat intolerance
  • Increased sweating
  • Weight loss (increased basal metabolic rate)
Dermatologic
  • Dry, cool skin due to low blood flow
  • Coarse, brittle hair and nails and diffuse alopecia
  • Puffy facies
  • Generalized nonpitting edema (myoedema) due to increased osmotic pressure/water retention
  • Warm, moist skin (due to vasodilation)
  • Fine hair and onycholysis
  • Pretibial myxedema in Graves’ disease
OcularPeriorbital edema
  • Ophthalmopathy in Graves’ disease
  • Lid lag/retraction (sympathetic stimulation of levator palpebrae superioris)
Musculoskeletal
  • Hypothyroid myopathy
  • Carpal tunnel syndrome
  • Myxedema (small lump on the surface of muscle when hit with a hammer)
  • Thyrotoxic myopathy
  • Osteoporosis
  • Higher fracture rate
Reproductive
  • Abnormal uterine bleeding
  • Reduced libido
  • Infertility
  • Abnormal uterine bleeding
  • Gynecomastia
  • Reduced libido
  • Infertility
Neuropsychiatric
  • Hypoactivity
  • Lethargy
  • Fatigue and weakness
  • Depressed mood
  • Delayed or slow reflexes
  • Hyperactivity
  • Restlessness
  • Anxiety
  • Insomnia
  • Fine tremors
  • Overactive reflexes
GI
  • Constipation due to decreased motility
  • Decreased appetite
  • Diarrhea due to increased motility
  • Increased appetite
Cardiovascular
  • Bradycardia
  • Dyspnea on exertion
  • Decreased cardiac output
  • Tachycardia, palpitations, and tachyarrhythmias
  • Dyspnea
  • Chest pain and systolic hypertension due to higher sensitivity of beta-adrenergic receptors

Diagnosis

  • The signs and symptoms of thyroiditis will be characteristic of their respective thyroid hormone levels (hypothyroidism versus hyperthyroidism).
  • Goiter characteristics should be examined via palpation.
  • Thyroid function test results will depend on the clinical phase:
    • Thyrotoxicosis: ↑ T3 and T4, ↓ TSH
    • Hypothyroid phase: ↓T3 and T4, ↑ TSH
    • Euthyroid phase: normal levels of T3, T4, and TSH
  • Ultrasonography:
    • Infectious thyroiditis presents with abscesses.
    • Subacute thyroiditis presents with diffuse heterogeneity and low vascular flow.
  • Fine-needle aspiration:
    • Infectious thyroiditis shows fluid collection with microbes.
    • Subacute thyroiditis shows multinucleated giant cell granulomas.
  • Thyroid peroxidase and thyroglobulin antibodies will be present in Hashimoto’s thyroiditis.
  • Radioactive iodine uptake will usually be low.

Management

The type of therapy used will depend on which phase the patient presents or the specific cause of the condition.

  • Thyrotoxicosis phase: antithyroid medication should not be used
    • Nonspecific beta-blockers block peripheral conversion of T4 to T3.
    • NSAIDs in the case of painful goiters (e.g., infectious thyroiditis)
  • Hypothyroid phase: lifelong oral administration of L-thyroxine
  • Riedel’s thyroiditis may require prednisolone and surgical relief of compressive symptoms.

Differential Diagnosis

The differential diagnosis of thyroiditis depends on the differentiation/recognition of the various conditions that can produce inflammation of the thyroid gland. The following are the most common causes and their characteristic presentations.

  • Subacute thyroiditis (De Quervain’s thyroiditis): Patients present with hyperthyroidism, followed by hypothyroidism and then recovery. During the hyperthyroid phase, the patient presents with neck pain, a tender diffuse goiter, and elevated levels of T3 and/or T4.
  • Acute infectious thyroiditis with abscess formation is caused by gram-positive or gram-negative organisms, usually in immunocompromised patients. The organisms most commonly involved are staphylococci and streptococci. The patient presents with sudden onset of neck pain and tenderness that is usually unilateral and accompanied by fever and chills. Ordinarily, patients have a unilateral neck mass, which can fluctuate. Thyroid function is often normal, but thyrotoxicosis may be present.
  • Chronic infectious thyroiditis: usually presents as bilateral disease: The pain and tenderness are less prominent than in acute infections. Patients might present with hypothyroidism.
  • Radiation thyroiditis: Some patients with hyperthyroidism treated with radioiodine develop thyroid pain and tenderness 5 to 10 days later due to a radiation-induced injury and necrosis of the thyroid follicular cells and associated inflammation. Patients present with neck pain and tenderness, which is usually mild and disappears in a few days. Transient exacerbation of hyperthyroidism is possible.
  • Riedel’s thyroiditis: presents as neck discomfort or tightness with dysphagia or hoarseness and a diffuse, asymmetric goiter that is very hard, fixed, and often not clearly defined: Most patients with Riedel’s thyroiditis are euthyroid, and only a few are hypothyroid. Serum antithyroid antibody concentrations are often high in these patients.

References

  1. Hershman JM. (2020). Subacute thyroiditis (de Quervain thyroiditis; giant cell thyroiditis; granulomatous thyroiditis). Merck Manual Profession Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/thyroid-disorders/subacute-thyroiditis
  2. Hershman JM. (2020). Hashimoto thyroiditis (autoimmune thyroiditis; chronic lymphocytic thyroiditis). Merck Manual Profession Version. https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/thyroid-disorders/hashimoto-thyroiditis
  3. Slatosky J, Shipton B, Wahba H. (2000). Thyroiditis: differential diagnosis and management. American Family Physician 61:1047–1054. https://pubmed.ncbi.nlm.nih.gov/10706157/
  4. Burman KD, Ross DS, Mulder JE. (2021). Overview of thyroiditis. Retrieved March 28, 2021, from https://www.uptodate.com/contents/overview-of-thyroiditis
  5. Burman KD, Ross DS, Mulder JE. (2021). Subacute thyroiditis. Retrieved March 28, 2021, from https://www.uptodate.com/contents/subacute-thyroiditis
  6. Burman KD, Ross DS, Mulder JE. (2021). Painless thyroiditis. Retrieved March 28, 2021, from https://www.uptodate.com/contents/painless-thyroiditis
  7. Burman KD, Ross DS, Mulder JE. (2021). Postpartum thyroiditis. Retrieved March 28, 2021, from https://www.uptodate.com/contents/postpartum-thyroiditis

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